The epileptic focus was induced in Chinchilla rabbits by stimulation of the Hippocampus with electric stimuli.  

In order to relate possible behavioral deficits to neurobiological changes, we examined H1R-KO and wild-type (WT) mice in terms of acetylcholine esterase (AChE) activity in subregions of the Hippocampus and AChE and tyrosine hydroxylase (TH) expression in the striatum. Neurochemical assays revealed that the H1R-KO mice had significantly lower levels of AChE activity in the dentate gyrus (DG) and CA1 subregions of the Hippocampus as compared with the WT mice. In conclusion, homozygous H1R-KO mice display severe long-term memory deficits in, both, ELM and PM, which coincide with changes in AChE activity in the Hippocampus as well as DA turnover in the cerebellum.  

In this study, dosing of transgenic mice (J20 strain) with mutated human APP (Swedish mutations: K670N and M671L and Indiana mutation: V717F) transgene, with nicotine in drinking water for 20 weeks did not have a significant effect on total levels of Abeta 40 or 42 in Hippocampus or cortex.  

Proestrous (WT or betaERKO), versus diestrous, mice had higher E(2) and progestin levels in plasma, Hippocampus, and cortex. Thus, enhanced performance in cognitive tasks and anti-anxiety-like behavior of proestrous mice may require actions of ERbeta in the Hippocampus and/or cortex..  

In the present study, we investigated spatial learning ability and memory function-related gene expressions in mouse Hippocampus after the exposure of animals to nanoparticle-rich diesel exhaust (NRDE) with or without a bacterial cell wall component. After the completion of the test, the animals were sacrificed and the Hippocampus was collected from each mouse; the expressions of NMDA receptor subunits (NR1, NR2A and NR2B), proinflammatory cytokines (IL-1beta and TNF-alpha) and the oxidative stress marker heme oxygenase 1 were then investigated using real-time RT-PCR. The relative mRNA levels of the NMDA receptor subunits and proinflammatory cytokines were higher in Hippocampus of NRDE/LTA (+) group compared to clear air/LTA (-) group. These results indicate that co-exposure of NRDE and LTA could affect spatial learning and memory function-related gene expressions in mouse Hippocampus..  

However, there were significant differences in the side of Hippocampus and precuneus.  

We injected the retrograde tracer cholera toxin subunit B into either the dorsal Hippocampus or the medial septum (MS) and used triple labeled immunofluorescence to determine if nonserotonergic raphe cells projecting to these structures contained VGLUT3. Consistent with previous studies, only about half of retrogradely labeled MR neurons projecting to the Hippocampus contained serotonin, whereas a majority of the retrogradely labeled nonserotonergic cells contained VGLUT3. In addition, these results demonstrate a dissociation between glutamatergic and serotonergic MR afferent inputs to the MS and Hippocampus suggesting divergent and/or complementary roles of these pathways in modulating cellular activity within the septohippocampal network.  

We observed developmental and species-specific variations in the expression of 3R- and 4R-tau within the frontal cortex and Hippocampus.  

Examination of the Hippocampus showed heterogeneity in the population with regard to expression of S100ss and glutamine synthetase. Furthermore, different subpopulations of NG2+ cells in the Hippocampus could be recognized by their electrophysiological properties.  

To test this, adult C57BL/6J and DBA/2J prefrontal cortex, Hippocampus, ventral striatum, and midbrain fatty acid composition was determined by gas chromatography. After correction for multiple comparisons, C57BL/6J mice exhibited significantly lower DHA composition in the Hippocampus and ventral striatum, but not prefrontal cortex or midbrain, and significantly greater regional arachidonic acid (ARA, 20:4n-6):DHA ratios, relative to DBA/2J mice. C57BL/6J mice exhibited significantly smaller oleic acid:stearic acid ratio in the Hippocampus and ventral striatum relative to DBA/2J mice.  

We assessed the expression of Bcl-2 family members at both mRNA and protein levels as well as the Caspase-3 activity, in order to investigate the occurrence of apoptosis in Hippocampus of STZ-induced diabetic rats. The result showed that mRNA and protein levels of Bcl-2 and Bcl-x(L) were lower in Hippocampus of diabetic group than that of the control group, whereas expressions of Bax in Hippocampus of diabetic rats were higher than that of controls at both mRNA and protein levels (P < .01). Therefore, the induction of diabetes is associated with increased ratios of Bax/Bcl-2, Bax/Bcl-x(L), and increased caspase-3 activity in Hippocampus which shows that apoptosis is favored in hippocampal region..  

Treatment of rats for 14 days with 20 mg/kg per day protriptyline or 7.5 mg/kg per day sertraline reduced NET and SERT expression, respectively, in cerebral cortex and Hippocampus; these treatments also induced a persistent antidepressant-like effect on forced-swim behavior.  

Here we show that voluntary exercise induces uncoupling protein 2 (UCP2) mRNA expression and mitochondrial oxygen consumption in coupled as well as uncoupled respiratory states in the Hippocampus.  

Here, we determined the contribution of chromatin remodeling to learning-induced changes in brain-derived neurotrophic factor (bdnf) gene expression in the adult Hippocampus. Infusions of zebularine (a DNA methyltransferase inhibitor) significantly altered bdnf DNA methylation and triggered changes in exon-specific bdnf mRNA levels, indicating that altered DNA methylation is sufficient to drive differential bdnf transcript regulation in the Hippocampus. In addition, NMDA receptor blockade prevented memory-associated alterations in bdnf DNA methylation, resulting in a block of altered bdnf gene expression in Hippocampus and a deficit in memory formation.  

This protein tyrosine phosphatase is enriched in the synapses of the striatum, Hippocampus, cerebral cortex, and other brain regions.  

Functional magnetic resonance imaging studies of recognition memory have often been interpreted to mean that the Hippocampus supports recollection and that the adjacent perirhinal cortex supports familiarity. First, we identified regions in both Hippocampus and perirhinal cortex in which activity varied as a function of subsequent item memory strength while source memory strength was held constant at chance levels.  

In addition to its effects on neuronal survival and differentiation, brain-derived neurotrophic factor (BDNF) plays an important role in modulating synaptic transmission and plasticity in many brain areas, most notably the neocortex and Hippocampus.  

Homozygous stau1(tm1Apa) mutant mice are viable and show no obvious deficits in development, fertility, health, overall brain morphology, and a variety of behavioral assays, e.g., Hippocampus-dependent learning.  

Lesions were found particularly in the cerebellar peduncles (non-suppurative meningoencephalitis), followed by the corpus callosum, Hippocampus and thoracic spinal cord.  

The Hippocampus (CA3 field) was studied in rats with different behavioral characteristics.  

Septal cholinergic neurons project to the Hippocampus and release acetylcholine, a neurotransmitter involved in learning and memory.  

We explored navigational skills in both early and late blind individuals and structural differences in the Hippocampus, a brain region well known to be involved in spatial processing. Remarkably, we not only show that blind individuals possess superior navigational skills than controls on the route learning task, but we also show for the first time a significant volume increase of the Hippocampus in blind individuals [ F(1,36) = 6.314; P

Several studies point towards an important role of the Hippocampus and, additionally, other brain structures (e.  

The Hippocampus is also believed to play an important role in the affective and motivational components of pain perception. The aim of the present study was to investigate the participation of cholinergic, opioidergic and GABAergic systems of the dorsal Hippocampus (DH) in the modulation of nociception in guinea pigs.  

The aim of the study was to evaluate the effect of selenium on restraint stress-induced oxidative damage in Hippocampus, striatum and frontal cortex. selenium-dependent glutathione peroxidase (Se-GPx), glutathione reductase (GR), glutathione S-transferase (GST) and catalase were evaluated in the frontal cortex, striatum and Hippocampus. Selenium pre-treatment exhibited restoration of antioxidant enzymes activity, GSH content and decrease in the level of lipid peroxidation in Hippocampus, striatum and frontal cortex in both 1 h and 4 h restraint stress groups. Selenium per se had no effect on GSH, lipid peroxidation level or activities of antioxidant enzymes in Hippocampus, striatum and frontal cortex. In conclusion, selenium pre-treatment protected the brain against restraint stress-induced oxidative damage at 4 h in Hippocampus, striatum and frontal cortex..  

It is widely expressed in the Hippocampus and facilitates hippocampal plasticity by regulating neurogenesis.  

VASCULAR ENDOTHELIAL GROWTH FACTOR IS UP-REGULATED AFTER STATUS EPILEPTICUS AND PROTECTS AGAINST SEIZURE-INDUCED NEURONAL LOSS IN Hippocampus: Nicoletti JN, Shah SK, McCloskey DP, Goodman JH, Elkady A, Atassi H, Hylton D, Rudge JS, Scharfman HE, Croll SD. In addition, we administered exogenous VEGF in one experiment and blocked endogenous VEGF in another to determine whether VEGF exerts a neuroprotective effect against status epilepticus-induced cell loss in one vulnerable brain region, the rat Hippocampus. Our data revealed that VEGF is dramatically up-regulated in neurons and glia in Hippocampus, thalamus, amygdala, and neocortex 24 h after status epilepticus.  

METHODS: The sodium channel blocker, tetrodotoxin (TTX), was chronically infused into the developing neocortex or Hippocampus of infant rats by way of an osmotic minipump starting on postnatal day 10-12.  

Neurology20076924:2256-226518071146 OBJECTIVE: The goal of this work was to evaluate the relationship between neuronal injury/loss in the Hippocampus, thalamus, and putamen in temporal lobe epilepsy (TLE) patients using (1)H magnetic resonance spectroscopic imaging. METHODS: (1)H spectroscopic images from the Hippocampus and thalamus of controls and patients with TLE were acquired at 4 T. The spectroscopic imaging data were reconstructed using an automated voxel-shifting method based on anatomic landmarks providing four, six, and three loci for the Hippocampus, thalamus, and putamen, respectively. NAA/Cr in the ipsilateral Hippocampus was significantly correlated with the ipsilateral and contralateral anterior and posterior thalami, putamen, and contralateral Hippocampus. The degree of injury/loss in the ipsilateral and contralateral thalamus and putamen is directly correlated with that of the ipsilateral Hippocampus. This is consistent with the hypothesis that the impairment and damage associated with recurrent seizures as measured by N-acetyl aspartate originating in the Hippocampus results in injury and impairment in other subcortical structures..  

Pharmacological antagonism of the ionotropic purinergic P2X7R has been studied for effects on inflammatory reactivity and neuronal viability in amyloid-beta1-42-injected rat Hippocampus.  

Furthermore, a differential expression of the Bcl-2 and Bax proteins was found in the differentiating and migrating zones of the cortex, Hippocampus, thalamus, and cerebellum.  

Study A is complemented by 4 interrelated add-on projects focusing on attachment style (study B1), on cost-effectiveness (study B2), on variation in the serotonin transporter gene in SP (study C1) and on structural and functional deviations of the Hippocampus and amygdala (study C2).  

The down-regulation of DNMT1 expression induced by nicotine in the FC is also observed in the Hippocampus but not in striatal GABAergic neurons.  

It remains unclear how HSV-1 induces tissue damages in memory formation-associated brain tissues such as the Hippocampus. In this study, we examined HSV-1 infection in the Hippocampus using a rat HSV-1 infection model. We found profound pathological changes in the Hippocampus and large numbers of HSV-1 antigen-positive cells in the dentate gyrus (DG) subfield of HSV-1-infected rats. To understand the precise mechanism of HSV-1-induced tissue damages in the Hippocampus, we employed rat organotypic hippocampal slice cultures (OHC) as an in vitro HSV-1 infection model. Longitudinal analysis indicated that granule cells in DG subfield were extremely vulnerable to HSV-1 infection among neuronal cells in the Hippocampus.  

Hippocampus is the most important brain structure for neurocognitive functions. It has been shown that radiation affects the hippocampal neurogenesis due to either induce the apoptosis or reduce the precursor cell proliferation in the Hippocampus. It has also been shown that tianeptine is able to reduce apoptosis and cytoprotective against the effects of proinflammatory cytokines in the Hippocampus.  

RESULTS/CONCLUSION: CB(1) agonists and fatty acid amide hdyrolase (FAAH) inhibitors share mechanisms with other antidepressants: the ability to enhance central serotonergic and noradrenergic transmission and promote neurogenesis in the Hippocampus.  

After testing CPP, mice were sacrificed and phosphorylated ERK and CREB in the frontal cortex, Hippocampus, and striatum were examined by immunohistochemistry. Pretreatment with DRz164 significant attenuated the morphine-induced activation of ERK and CREB in the frontal cortex, Hippocampus, and striatum.  

Next, we evaluate the feasibility of using different lines of thy1::Clomeleon transgenic mice to image synaptic inhibition in several different brain regions: the Hippocampus, the deep cerebellar nuclei (DCN), the basolateral nucleus of the amygdala, and the superior colliculus (SC). However, in contrast to the Hippocampus, the responses in these three regions were largely insensitive to antagonists of inhibitory neurotransmitter receptors.  

Seven showed signal intensity abnormalities, with prominent involvement of the Hippocampus, and six showed additional involvement of the amygdala. Among the seven HHV6-negative patients, six had abnormalities in the Hippocampus but only two showed extrahippocampal involvement, which was restricted to the amygdala.  

Although the Hippocampus and olfactory bulb are most commonly studied in the context of adult neurogenesis, there is an increasing body of evidence in support of neurogenesis occurring outside of these two regions. The current study expands on previous data by showing newborn neurons with a mature phenotype are located in several olfactory and limbic structures outside of the Hippocampus and olfactory bulb, where we previously described doublecortin/bromodeoxyuridine immature neurons.  

Reevaluation of the extent of the pathology, as well as new data from animal models, suggests that the seizure focus extends, at least in some cases, beyond the Hippocampus and amygdale, which are usually removed at the time of surgery.  

In control pups, c-fos expression was low in most brain regions, but robust Arc hybridization was found in several areas including cingulate cortex, Hippocampus and caudate.  

In the case of the Hippocampus, integration of new cells in to the existing neuronal circuitry may be involved in memory processes and the regulation of emotionality. Importantly, while short sleep deprivation may not affect the basal rate of cell proliferation, one study in rats shows that even mild sleep restriction may interfere with the increase in neurogenesis that normally occurs with Hippocampus-dependent learning.  

The present study shows that traumatic brain injury (TBI) triggers inflammation and elicits changes in mRNA expression of CYP4Fs in the frontal and occipital lobes and the Hippocampus.  

Abstract This study investigated the contributions of the reverse mode of the sodium-calcium exchanger (NCX) and the type 1 sodium-proton antiporter (NHE-1) to acute astrocyte and neuronal pathology in the Hippocampus following fluid percussion traumatic brain injury (TBI) in the rat. Stereological analysis of the CA2/3 sub-regions of the Hippocampus demonstrated that higher doses of KB-R7943 (2 and 20 nmoles) significantly reduced astrocyte GFAP immunoreactivity compared to vehicle-treated animals. The results provide additional evidence of acute astrocyte pathology in the Hippocampus following TBI, while suggesting that activation of NHE-1 and the reverse mode of NCX contribute to both astrocyte and neuronal pathology following experimental TBI..  

Correspondingly, anti-choline acetyltransferase immunohistochemistry demonstrated a severe loss of cholinergic terminals in the Hippocampus accompanied by a mild cholinergic neuronal atrophy and loss in the medial septum and the nucleus of the vertical limb of the diagonal band of Broca. A major synaptic degeneration in the Hippocampus was confirmed by ultrastructural analysis.  

The aim of the present study is to examine whether electric injury causes decreasing in the number of pyramidal neurons in the rat Hippocampus and whether this decreasing can be demonstrated by stereological method. On the third day, the rats were decapitated; the brains were removed, and sectioned horizontally through the Hippocampus and samples chosen according to the systematic random sampling strategy. The results showed that the total number of pyramidal neurons in three subdivision of the Hippocampus (CA3-2 and CA1) was 242,141+/-31,167, 193,388+/-24,795 and 187,448+/-28,300 in the first, second and third groups, respectively. In conclusion, electrocution causes loss of the pyramidal neuronal in CA3-2 and CA1 subdivisions of the rat Hippocampus in this study..  

Risperidone (at 1.0 and 3.0 mg/kg/day) increased AMPA receptors in medial prefrontal cortex and caudate-putamen of juvenile animals, whereas risperidone (at 3.0 mg/kg) increased AMPA receptors in caudate-putamen and Hippocampus of adults.  

Since the Hippocampus is one of the main structures in the development of this epilepsy model, the 5-HT levels in this region were also determined after drug administration.  

Retrosplenial cortex (RSC) together with the Hippocampus is a component of the spatial memory circuit.  

PDE4D long isoforms and Ndel1 show a similar sub-cellular distribution in Hippocampus and cortex and locate to post-synaptic densities.  

Various lines of research suggest that neurotrophic processes in the Hippocampus are key mechanisms in major depressive disorder and are of relevance for response to antidepressive treatment. We performed proton magnetic resonance spectroscopy (1H-MRS) of the Hippocampus at 3 T in 18 unmedicated subjects with unipolar major depressive episodes and in 10 age- and gender-matched healthy volunteers. Our data provide first evidence for a reduction of Gln in the Hippocampus of subjects with major depression. Furthermore, we provide first evidence in patients with major depression for neurorestorative effects in the Hippocampus by pharmacological treatment expressed by a correlation of NAA and Cho increases with treatment response.  

Newborn cells of the adult dentate gyrus in the Hippocampus are characterized by their abundant expression of polysialic acid (PSA), a carbohydrate attached to the neural cell adhesion molecule (NCAM). To identify the roles of PSA in the development of adult progenitors of the dentate gyrus, we injected endoneuraminidase N (endoN) into the Hippocampus of adult rats to specifically cleave PSA from NCAM.  

These changes can be explained by overactive hippocampal CRF(1), in view of the finding that the application of the nonselective CRF receptor antagonist [ Glu(11,16)] astressin ([ Glu(11,16)]Ast) into the dorsal Hippocampus of mutant mice returned the levels of the phosphorylated proteins to baseline.  

A change in neuronal network excitability within the Hippocampus is one of the hallmarks of temporal lobe epilepsy (TLE).  

Our data underscore the importance of Reelin as a factor that promotes the maturation of target neuronal populations and the development of excitatory circuits in the postnatal Hippocampus.  

RESULTS: Low NAA levels in the left dorsal Hippocampus predicted persistent PTSD-like symptoms (both contextual freezing and hyperarousal), while animals with pretraumatic high levels of NAA decreased their fear reactions to control levels in consequence of re-exposure to associative and nonassociative cues. N-AA levels in the right dorsal Hippocampus, in contrast, were only partially predictive of the individual susceptibility to develop PTSD-like symptoms.  

Adult neurogenesis in the dentate gyrus plays a critical role in Hippocampus-dependent spatial learning. It remains unknown, however, how new neurons become functionally integrated into spatial circuits and contribute to Hippocampus-mediated forms of learning and memory. Functionally, this genetic manipulation specifically affected different Hippocampus-dependent learning and memory tasks, including contextual fear conditioning, and selectively reduced synaptic plasticity in the dentate gyrus.  

METHOD: Wistar male rats were randomly divided into control group, model group, paroxetine group, and Pingyu capsule low, middle and high doses groups; rats in all groups but the control group were fed in single cage for 21 days and were given such irritations as lightening stroke on pelma, ice water swimming, pyretic fumigation and tail clipping during this period; lobe cortex and Hippocampus of all rats were taken out for detection of the cAMP content by means of radioactive immunization, PKA and PKC content by Elisa, and the PKA and PKC activity by radioactive isotope. RESULT: Content of cAMP in lobe cortex and Hippocampus, content and activity of PKA in Hippocampus, and content of PKC in lobe cortex of rats in the model group were lower than those in the normal group.  

Synaptotagmin-I and clathrin were determined by cDNA microarry analysis and Western blotting in the Hippocampus of phenytoin-resistant and phenytoin-nonresistant kindled rats, which were associated with the exocytosis and endocytosis of the synaptic vesicle traffic. Results: Microarry analysis showed both synaptotagmin-I and clathrin mRNA were up-regulated at least 3.06 fold accompanied with their correspondent proteins increased by 52.3 +/- 6.4 % and 76.7 +/- 12.4 % respectively in the Hippocampus of phenytoin-resistant rats as compared with those in phenytoin-nonresistant rats. Conclusions: The increased expressions of synaptotagmin-I and clathrin in the Hippocampus of phenytoin-resistant kindled rats play a role in the development of intractable epilepsy..  

RESULTS: SERT levels were non-significantly decreased (-14% to -33%) in caudate, putamen and thalamus (normal in Hippocampus), and, unlike the robust striatal dopamine reduction, there was marked overlap between control and MA user ranges.  

We recorded spontaneous multiple unit activities (MUAs) of the Hippocampus and prefrontal cortex in urethane-anesthetized rats and analyzed cross-correlograms between these MUAs to investigate the functional connectivity of neuronal activities. Results of these analyses reveal a significant correlation between MUAs in these regions, in which the firing initiated from either Hippocampus (type H-P) or prefrontal cortex (type P-H) according to the significant peak of cross-correlograms. These results suggest that the correlation between the Hippocampus and prefrontal cortex MUAs that are related to the burst firing might reflect functional connectivity..  

To determine the neuroanatomical basis for the relationship among such states, we assessed surface conformations of the Hippocampus in AD, mild cognitive impairment (MCI) and subjective memory impairment (SMI). These results suggest that Hippocampus degeneration develops gradually in AD, and may be observable long before dementia is apparent..  

In this study, we observed glial fibrillary acidic protein (GFAP), a marker for astrocytes, immunoreactivity in the dentate gyrus and Hippocampus proper (CA1-3 region) of adult (2-3 years of age) and aged (10-12 years of age) dogs.  

Both drugs induced phosphorylation of the Ser9-residue, thereby, inactivating GSK-3beta in the rat Hippocampus.  

Multiple roles of CaMKII have been identified in the Hippocampus, yet its role in developing neurons is less well understood.  

Following this training condition c-Fos immunohistochemistry revealed increased activation of the CA1 area of the Hippocampus and the orbitofrontal cortex.  

This paper describes the construction of a computational anatomical atlas of the human Hippocampus. The main subfields of the Hippocampus (cornu ammonis fields CA1, CA2/3; the dentate gyrus; and the vestigial hippocampal sulcus) are labeled in the images manually using a combination of distinguishable image features and geometrical features. The atlas is provided as an online resource with the aim of supporting subfield segmentation in emerging Hippocampus imaging and image analysis techniques.  

Only a slight induction of c-Fos was seen in the Hippocampus for the higher doses used (100-200 mg/kg).  

The present studies determined whether specific manipulation of neurosteroid levels in the Hippocampus would alter seizure susceptibility in an animal model genetically susceptible to severe ethanol (EtOH) withdrawal, withdrawal seizure-prone (WSP) mice. Male WSP mice were surgically implanted with bilateral guide cannulae aimed at the CA1 region of the Hippocampus one week prior to measuring seizure susceptibility to the convulsant pentylenetetrazol (PTZ), given via timed tail vein infusion.  

RESULTS: The RT-PCR results showed that Brn-3a mRNA transcription level decreased significantly in neural cells from cerebral Hippocampus in every lead treatment group compared with the control group (P < 0.05).  

Results Histological examination showed that ischemic preconditioning significantly reduced delayed neuronal death in the Hippocampus CA1 region (P < 0.01 vs 10-min ischemia group).  

Volumetric measures of Hippocampus and WML were manually performed.  

RESULTS: The BZD receptor binding potential was decreased in multiple areas of the frontal, temporal, and parietal cortices and was increased in the Hippocampus/parahippocampal region in subjects with PD vs controls. The most significant decrease was located in the dorsal anterolateral prefrontal cortex (DALPFC); the most significant increase, in the Hippocampus/parahippocampal gyrus. In subjects with PD, the severity of panic and anxiety symptoms correlated positively with BZD receptor binding in the DALPFC but negatively with binding in the Hippocampus/parahippocampal gyrus.  

RESULTS: Compared with controls, patients showed significantly more decline in gray matter density of the Hippocampus, anterior cingulum, left amygdala, and right dorsomedial prefrontal cortex. Patients who remitted during the 3-year period had less volume decline than nonremitted patients in the left Hippocampus, left anterior cingulum, left dorsomedial prefrontal cortex, and bilaterally in the dorsolateral prefrontal cortex. CONCLUSION: This study supports findings from animal studies of neuroplastic stress-related processes that occur in the Hippocampus, amygdala, dorsomedial prefrontal cortex, dorsolateral prefrontal cortex, and anterior cingulum during depressive episodes..  

Stepwise regression analyses focused on morphometric and metabolic characteristics of the episodic memory network: Hippocampus, entorhinal, parahippocampal, retrosplenial, posterior cingulate, precuneus, inferior parietal, and lateral orbitofrontal cortices.  

Proper odor identification depends on higher order structures, such as the Hippocampus, for olfactory cognitive or memory processing. DAT binding potentials (BP) were assessed in the Hippocampus, amygdala, ventral and dorsal striatum. We found that correlation coefficients between total UPSIT scores and regional brain DAT BP were highest for the Hippocampus (Rs=0.54, P=0.002) and lower for the amygdala (Rs=0.44, P=0.02), ventral (Rs=0.48, P=0.008) and dorsal striatum (Rs=0.39, P=0.03). These findings indicate that mesolimbic dopamine innervation of the Hippocampus may be a determinant of selective hyposmia in PD..  

We show that OCT can provide the necessary guidance to perform microsurgery such as the selective transection of the Schaffer collateral inputs to the CA1 region of the Hippocampus with minimal perturbation of overlying structures. We also show that OCT allows visual monitoring of the successful delivery of viral vectors to specific subregions of the Hippocampus..  

The amygdala and Hippocampus were dissected. KEY FINDINGS: Ten days after injection of lidocaine, lipid peroxidation increases in the Hippocampus because the ROS are enhanced from day 5, whereas in the amygdala lipid peroxidation and the ROS were enhanced only on the first day postinjection. Lidocaine causes an increased concentration of GSH and GSSG in the Hippocampus from the first day. In the Hippocampus the catalase activity was enhanced, whereas the total SOD and Cu-Zn SOD activities were decreased. SIGNIFICANCE: In this research we demonstrated that lidocaine affects the redox environment and promotes increases of the oxidative markers both in the Hippocampus and amygdala but in a different pattern..  

Using functional magnetic resonance imaging (fMRI), we compared 12 adolescents with Cushing syndrome with 22 healthy control adolescents on amygdala and anterior Hippocampus activation during an emotional faces encoding task. Compared to healthy adolescents, patients with Cushing syndrome showed greater left amygdala and right anterior Hippocampus activation during successful face encoding. This first study of cerebral function in adolescents with chronic endogenous hypercortisolemia due to Cushing syndrome demonstrates the presence of functional alterations in amygdala and Hippocampus, which are not associated with affective or memory impairments.  

cAMP and cGMP contents of VTA, cortex and Hippocampus of the rat brains were determined by radioimmunoassay. Compared with the controls, cAMP content in the region of VTA, cortex and Hippocampus of the morphine dependent rats were significantly higher (P < 0.05), while cGMP contents in those regions were significantly lower (P < 0.05). cAMP contents in the area of VTA, cortex and Hippocampus of the morphine dependent rats were significantly reduced, while cGMP contents were significantly increased by ig Cedemex.  

A pattern of alpha activity as estimated by sLORETA was shown in the right amygdala, uncus, Hippocampus, BA37, insular cortex and orbitofrontal regions during the SPESA condition.  

Specifically, increased activity in the open field is associated with increased variance of log-transformed measures of gene expression in the Hippocampus, a brain region involved in open field activity. The same association of the variance of gene expression levels with behavioral variability is found with levels of gene expression in the Hippocampus of genetically heterogeneous outbred populations of mice, suggesting that variation in the large-scale organization of gene expression levels may also be relevant to phenotypic differences in outbred populations such as humans.  

Here, we characterized the PK of the active metabolite of oxcarbazepine, 10,11-dihydro-10-hydroxy-carbamazepine (MHD) in plasma and in the Hippocampus.  

METHODS: We evaluated the effects of minocycline on dendritic spine development in the Hippocampus of young Fmr1 KO mice, and in primary cultures of hippocampal neurons isolated from those mice. Our data suggest that these effects of minocycline may relate to its inhibitory action on MMP-9 expression and activity, which are higher in the Hippocampus of Fmr1 KO mice.  

Both concentrations of NAAG and NAA in the male rat cerebrum (13 weeks old) were 5.7+/-0.30 and 2.1x10(2)+/-9.2nmol/mg protein, respectively (n=6), while those in the Hippocampus were 6.8+/-0.48 and 1.9x10(2)+/-8.5nmol/mg protein, respectively (n=5).  

For example, high levels of expression were observed in the avian amygdala and Hippocampus, areas which express high levels of CB1 in mammals.  

METHODS: Functional magnetic resonance imaging (fMRI) hemodynamic responses to novelty and reward (monetary incentive) from the substantia nigra/ventral tegmental area (SN/VTA), the nucleus accumbens (NAcc), and the Hippocampus of 29 subjects were correlated with novelty-seeking scores.  

Finally, the relationship between the PPC and the Hippocampus from a systems and dynamic point view is presented..  

Furthermore, increased production of high inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions were detected in the Hippocampus and cerebral cortex of copper and cholesterol co-treated mice by immunohistochemical analysis.  

Further, COX-2(-/-) mice exposed to NMDA showed neuronal damage, detected by Fluoro Jade B (FJB) staining, in the CA3 region of the Hippocampus.  

At the end of the behavioral testing, in order to study cell proliferation and differentiation in the Hippocampus, mice were injected with 5-bromo-2-deoxyuridine (BrdU) and sacrificed 1 or 28 days after the last BrdU injection. Aluminum exposure impaired learning and memory in wild mice and increased the total number of proliferating cells in the dentate gyrus of Hippocampus.  

The present study examined how expression of KiSS1 and GPR54 is regulated in rat Hippocampus, using in vivo and in vitro preparations.  

RESULTS: To better understand the molecular changes associated with these morphological and behavioral phenotypes, we performed a DNA microarray transcriptome profiling of the Hippocampus and the frontal cortex of the PSEN1/PSEN2 double knock-out mice and littermate controls at five different ages ranging from 2-8 months. While these events may progress differently in the Hippocampus and frontal cortex, the most critical expression signatures are common across the two brain regions, and involve a strong upregulation of cathepsin and complement system transcripts.  

However, GPR125 expression was transiently increased (almost 2-fold) at 4 h after traumatic brain injury (TBI) followed by a decrease (approximately 4-fold) from 2 days onwards in the choroid plexus as well as increased expression (2-fold) in the Hippocampus that was delayed until 1 day after injury.  

Hyperintensity on T2-weighted and fluid attenuated inversion recovery images in the Hippocampus and piriform lobe was consistent with excitotoxic edema, whereas similar imaging features in other forebrain areas corresponded to areas of inflammation or liquefaction on histopathology.  

We examined the effect of occlusal disharmony in senescence-accelerated (SAMP8) mice on plasma corticosterone levels, spatial learning in the water maze, fos induction, hippocampal neuron number, expression of glucocorticoid receptors (GR) and glucocorticoid receptor messenger ribonucleic acid (GRmRNA) in Hippocampus and inhibitor of glucocorticoid (metyrapone). Bite-raised aged mice had significantly greater plasma corticosterone levels than age-matched control mice as well as impaired spatial memory and decreased Fos induction and a number of neurons in Hippocampus. These datas suggest that the bite-raised condition may enhance the aging process in Hippocampus, thereby leading to impairment of spatial memory by stress..  

These include the Hippocampus and the anterior cingulate cortex in posttraumatic stress disorder and the orbitofrontal cortex in obsessive-compulsive disorder.  

The authors studied the ultrastructure of oligodendroglia and myelinated fibers and assessed quantitatively their density and proportion of pathologically changed myelinated fibers in the CA3 region of the Hippocampus in 25 cases with schizophrenia and 25 control cases without mental pathology.  

Recent evidence suggests that rats require an intact Hippocampus in order to recognize familiar objects when they encounter them again in a different context.  

Phosphatidylinositol 3-kinase (PI3K) and its downstream targets, including Akt (also known as protein kinase B, PKB), mammalian target of rapamycin (mTOR), the 70-kDa ribosomal S6 kinase (p70S6k), and the eukaryotic initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1), may play important roles in long-term synaptic plasticity and memory in many brain regions, such as the Hippocampus and the amygdala.  

Arrhythmic hamsters may have failed to perform this task because of chronic inhibitory signaling from the SCN that interfered with the plastic mechanisms that encode learning in the Hippocampus..  

Here we show that NRG-1 stimulates dopamine release in the Hippocampus and reverses early-phase LTP via activation of D4 dopamine receptors (D4R).  

Gene expression profiles were assessed in the Hippocampus, entorhinal cortex, superior-frontal gyrus, and postcentral gyrus across the lifespan of 55 cognitively intact individuals aged 20-99 years.  

Compared to controls, an increase of HIF-1alpha-immunoreactive neurons and HIF-2alpha-positive glial cells and vascular endothelial cells was observed in hypoxic cerebral cortex and Hippocampus.  

In this study we evaluated the effects of the novel, potent non-competitive metabotropic glutamate receptor (mGluR) 1 antagonist (3aS,6aS)-6a-naphthalen-2-ylmethyl-5-methyliden-hexahydro-cyclopental[ c]furan-1-on (BAY 36-7620) on different types of synaptic plasticity in the hippocampal cornu ammonis (CA) 1-region and on Hippocampus-dependent spatial learning.  

Immunoblot analysis showed that Daam1 is enriched in the mouse Hippocampus and co-fractionates in brain lysates with dendritic and synaptic proteins.  

This paradigm significantly increased plasma corticosterone levels, and the glutamate efflux in the Hippocampus as measured by in vivo microdialysis. Immunohistochemical staining with beta-tubulin III showed that repeated immobilization caused marked morphological alterations in the Hippocampus and medial prefrontal cortex that were prevented by simultaneous treatment with agmatine (50mg/kg/day), i.p.). Likewise, endogenous agmatine levels measured by high-performance liquid chromatography in the prefrontal cortex, Hippocampus, striatum and hypothalamus were significantly increased by immobilization, as compared to controls. These results demonstrate that the administration of exogenous agmatine protects the Hippocampus and medial prefrontal cortex against neuronal insults caused by repeated immobilization.  

The expression of brain-derived neurotrophic factor (BDNF), synapsin I, cyclic-AMP response element binding protein (CREB), and calcium-calmodulin-dependent protein kinase II (alpha-CAMKII) were all significantly decreased compared with sham injury levels within the ipsilateral Hippocampus after CCI. No significant molecular level changes were found in the contralateral Hippocampus.  

Fimbria-fornix (FF), the septo-hippocampal pathway, was transected to model Alzheimer's disease (AD), which is characterized by loss of cholinergic afferent fibers in Hippocampus. Various alternations may happen in the deafferented Hippocampus. In this study, we determined the expression of Brn-4 in Hippocampus after FF lesion. Hybridization and immunohistochemistry indicated that Brn-4 signals in Hippocampus and dentate gyrus (DG) of the deafferented side were significantly stronger than the normal side. More Brn-4 positive cells were identified in the DG of deafferented Hippocampus. In vitro Brn-4 antibody attenuated the role of extract from deafferented Hippocampus in promoting differentiation of hippocampal progenitors into MAP-2 positive neurons. This study demonstrated that after FF lesion, Brn-4 in the deafferented Hippocampus was upregulated and might play an important role in inducing local progenitors to differentiate into neurons, which may compensate for the loss of cholinergic afferent fibers or other dysfunctions.  

The effects of selective ibotenate lesions of the complete Hippocampus (CHip), the hippocampal ventral pole (VP), or the medial prefrontal cortex (mPFC) in male rats were assessed on several measures related to energy regulation (i.e., body weight gain, food intake, body adiposity, metabolic activity, general behavioral activity, conditioned appetitive responding).  

We have used laser-capture microdissection and microarray hybridization to characterize gene expression in the three principal neuron layers of rat Hippocampus. Taken together, these data suggest that unique physiological characteristics of major cell layers, such as neuronal activity, neuronal plasticity, and vulnerability to neurodegeneration, are reflected in substantial transcriptional heterogeneity within the Hippocampus.  

According to one theory, the Hippocampus plays a specific role in supporting episodic retrieval, that is, the re-experiencing of an event as part of one's personal past. This theory predicts that as episodic memories fade over time and are reduced to feelings of familiarity, activity in the Hippocampus should no longer be associated with retrieval.  

Then, we evaluated the changes of heme oxygenase-1 (HO-1), a sensitive oxidative marker, as well as interleukin (IL)-1beta, IL-6, and inductible nitric oxide synthase (iNOS) mRNA in the hypothalamus and Hippocampus of rats using real-time PCR after peripheral injection of LPS (2.0 mg/kg).  

Further, increases in 5-HT levels in dorsal Hippocampus, basolateral amygdala, nucleus accumbens, and striatum were likewise potentiated, and GR205171 similarly facilitated the influence of fluoxetine upon levels of 5-HT, as well as dopamine and noradrenaline.  

The neonatal Hippocampus exhibits regularly recurring waves of synchronized neuronal activity in vitro. All AS-active neurons increase their firing rates during periods of myoclonic twitching of the limbs, and a subset of these neurons exhibit a burst of activity immediately after limb twitches, suggesting that the twitches themselves provide sensory feedback to the infant Hippocampus, as occurs in the infant spinal cord and neocortex. We hypothesize that the phasic motor events of active sleep provide the developing Hippocampus with discrete sensory stimulation that contributes to the development and refinement of hippocampal circuits as well as the development of synchronized interactions between Hippocampus and neocortex..  

Patients with noncomorbid conduct disorder showed decreased activation in paralimbic regions of the insula, Hippocampus, and anterior cingulate as well as the cerebellum relative to patients with noncomorbid ADHD and healthy comparison subjects.  

Recognition performance was positively correlated with BOLD signal in the left posterior Hippocampus, parahippocampal-retrosplenial gyrus and left superior frontal cortex regardless of risk factors.  

Using electron microscopy and electrophysiology, we now report that lack of alphaGDI impairs several steps in synaptic vesicle (SV) biogenesis and recycling in the Hippocampus.  

Using Freesurfer software, the volumes of MT [ Hippocampus, amygdala] and DGM [ thalamus, caudate] structures were calculated.  

The levels of NO in Hippocampus and striatum tissues were assessed by spectrophotometric method. The levels of DA in Hippocampus and striatum tissues were assessed by high-performance liquid chromatography with electrochemical detection. The protein levels of BDNF in Hippocampus tissue were assessed by Western blotting. The results showed that the cognitive capability of mice was significantly different between the DHA-treated groups and the control group; the protein level of BDNF was significantly increased in the Hippocampus; the levels of NO and DA were significantly increased in Hippocampus and striatum tissues. In conclusion, during aging, DHA supplementation can improve the cognitive function in mice and can increase the protein level of BDNF in Hippocampus tissue and the levels of NO and DA in Hippocampus and striatum tissues.  

The concentration of the astrocytesoluble and filament glial fibrillary acidic protein (GFAP) decreased in the posterior part of the hemispheres, including the thalamus, Hippocampus and cortex of the rats treated with L.  

Neurotoxicity in the Hippocampus and prefrontal cortex was examined using NeuN staining. NeuN staining showed no evidence of neuronal loss in either prefrontal cortex or Hippocampus after withdrawal from chronic alcohol treatment.  

Significantly higher T2-relaxation values, indicating tissue injury, appeared in anxious OSA versus nonanxious OSA subjects in subgenu, anterior, and mid-cingulate, ventral medial prefrontal and bilateral insular cortices, Hippocampus extending to amygdala and temporal, and bilateral parietal cortices. Brain injury emerged in anxious OSA versus nonanxious controls in bilateral insular cortices, caudate nuclei, anterior fornix, anterior thalamus, internal capsule, mid-Hippocampus, dorsotemporal, dorsofrontal, ventral medial prefrontal, and parietal cortices.  

The aim of the present study was to investigate the Na+-K+-ATPase activity in the Hippocampus and cortex of rats with KA-induced convulsions. Na+-K+-ATPase activity inhibition in the Hippocampus of the LTG pretreated rats on the fifth experimental day was statistically less pronounced than in KA treated rats. Conclusion: KA systemic application induced Na+, K+- ATPase activity inhibition in the rat Hippocampus and cortex and LTG pre-treatment showed a partially protective effect on the enzyme activity..  

In this study, neurogenesis and the proliferation of astrocytes in the subgranular zone of the Hippocampus were explored using unilateral amygdala-kindled rats with or without muscimol, a gammaaminobutyric acid a (GABAa) agonist injection into the bilateral anterior thalamic nuclei (AN).  

Pharmacological studies showed that NR2B-containing NMDARs are not required for LTP, while genetic studies reported that over-expression of NR2B-NMDARs enhances LTP and Hippocampus-dependent memory.  

Intergroup differences in neocortical neuronal activities were less pronounced than in Hippocampus.  

We complemented the investigation by calculating the gray matter volume of regions of interest (ROIs) in the bilateral Hippocampus. RESULTS: The VBM analysis provided evidence of a reduction in gray matter volume in the Hippocampus and thalami.  

Such findings, in concert with previous neuropsychological and neuroimaging studies, implicate an age-related deficit in the functioning of frontal and medial temporal lobe structures, with particular emphasis on the Hippocampus..  

This study confirmed that NG2 immunoreactive OPCs were continuously distributed in cerebral cortex and Hippocampus during different postnatal developmental stages. These cells rapidly increased in number over the postnatal 7 days and migrate extensively to populate with abundant processes both in developing cortex and Hippocampus.  

In this study, we investigated the expression profiles of the two major isoforms, synGAPalpha1 and synGAPbeta, in the adult rat brain and cultured neurons of the rat Hippocampus. The distribution of the synGAPalpha1 and beta (beta1-4) isoforms in the adult rat brain was clearly different in cerebellum, Hippocampus, cerebral cortex, septum and olfactory bulb.  

Animals were sacrificed 45min following their last injection and FGFR1 gene expression was assessed in the Hippocampus and prefrontal cortex by mRNA in situ hybridization. HR-bred rats exhibited increased FGFR1 mRNA in the Hippocampus compared to LR-bred rats. Furthermore, cocaine decreased FGFR1 mRNA in the Hippocampus and increased FGFR1 mRNA in the prefrontal cortex. In the Hippocampus, cocaine decreased gene expression in HR-bred rats without affecting LR-bred rats, whereas in the prefrontal cortex cocaine increased gene expression in LR-bred rats without affecting HR-bred rats.  

At adulthood, intermale aggressive interactions in mice, representing a psychosocial stressful condition, has been shown to markedly alter NGF and BDNF levels both in plasma as well as in selected brain areas, including the hypothalamus and Hippocampus.  

Monoamine levels and activity (as indexed by turnover ratio) were measured in prefrontal cortex (PFC), CA1 and CA3 regions of the Hippocampus (areas important for memory), and medial preoptic area (mPOA, an area important in display of maternal behaviors). In the CA1 and CA3 regions of the Hippocampus, monoamine levels and turnover ratios were generally higher during pregnancy, particularly on GD9.  

Decreased expression of IGFBP4 was obvious in the cerebral cortex, Hippocampus, cerebellar cortex and inferior olive of SOD1(G93A) transgenic mice.  

These results are consistent with the finding that Hippocampus is a critical part of a fronto-temporal circuit involved in auditory gating..  

Abstract The medial prefrontal cortex (mPFC), Hippocampus, and amygdala are implicated in the regulation of affect and physiological processes, including hypothalamic-pituitary-adrenal (HPA) axis function. For the control group, voxelwise analyses found a relationship between current density in beta and gamma bands and steeper cortisol slope (indicative of more adaptive HPA axis functioning) in regions of the Hippocampus, parahippocampal gyrus, and mPFC.  

Consistent with previous findings, we report a significant increase in response latencies when naming categorically related objects within blocks, an effect associated with increased perfusion fMRI signal bilaterally in the Hippocampus and in the left middle to posterior superior temporal cortex.  

Abstract The Hippocampus and the basal ganglia are thought to play fundamental and distinct roles in learning and memory, supporting two dissociable memory systems. Interestingly, however, the Hippocampus and the basal ganglia have each, separately, been implicated as necessary for reversal learning-the ability to adaptively change a response when previously learned stimulus-outcome contingencies are reversed. Here, we compared the contribution of the Hippocampus and the basal ganglia to distinct aspects of learning and reversal. These results suggest that both the Hippocampus and the basal ganglia support reversal learning, but in different ways. The failure of the amnesic subjects to reverse their response or to learn a new cue is consistent with a more general role for the Hippocampus in configural learning, and suggests it may also support the ability to respond to changes in cue-outcome contingencies..  

At the imaging level, there was a main effect of valence with increased activity in the medial-temporal lobe (amygdala and Hippocampus) during both encoding and retrieval of aversive relative to neutral stimuli.  

Differences in size and topography of dorsal CA1 multiple-unit responses reflected the ability of the Hippocampus to discriminate between stimuli in trained animals, corresponding to the performance of the behavioral discrimination. During JM trials, the rhythmicity of the neural response was further modulated by the type of the prior trial, suggesting the coding of sequential events by the Hippocampus.  

The majority of research regarding contextual learning and memory has focused on the contributions of the Hippocampus and related medial temporal lobe structures.  

The emergence of stereotypies was examined in juvenile rhesus monkeys (Macaca mulatta) who, at 2 weeks of postnatal age, received selective bilateral ibotenic acid lesions of the amygdala (N = 8) or Hippocampus (N = 8). However, between 1 to 2 years of age, both amygdala- and Hippocampus-lesioned subjects began to exhibit stereotypies. When observed as juveniles, both amygdala- and Hippocampus-lesioned subjects consistently produced more stereotypies than the control subjects in a variety of contexts. More interesting, neonatal lesions of either the amygdala or Hippocampus resulted in unique repertoires of repetitive behaviors. Amygdala-lesioned subjects exhibited more self-directed stereotypies and the Hippocampus-lesioned subjects displayed more head-twisting.  

These results showed an increased ratio of Bax/Bcl-2 and activated caspase-3 in Hippocampus and dorsal lumbar spinal cord of animals treated with pain and IMO stress; these effects were reduced in adrenalectomized animals.  

As seen previously talnetant, produced a dose dependent increase in extracellular levels of both dopamine (DA) and norepinephrine (NE) in both prefrontal cortex (PFC) and Hippocampus in a similar manner to the atypical risperidone. Combination studies revealed an additive effect of talnetant on risperidone-induced changes in both NE and DA levels in the PFC but not the Hippocampus.  

In particular, 17beta-estradiol was shown to affect GABAergic synaptic transmission in Hippocampus of adult animals in vivo but much less is known on the impact of this hormone on the GABAergic system in the developing brains.  

Other activated areas included prefrontal cortex, Broca's area, premotor cortex, supplementary motor area, superior temporal gyrus, insular, basal ganglion, and Hippocampus.  

We studied regional gray matter density in the Hippocampus in Parkinson's disease (PD) patients. A region of interest (ROI) of the Hippocampus following voxel-based morphometry (VBM) procedures was used to perform group comparisons, single- case individual analysis and correlations with learning scores. In PDD patients, hippocampal gray matter loss involved the entire Hippocampus and in PD+VH this reduction was mainly confined to the hippocampal head. These results suggest that in PD the neurodegenerative process in the Hippocampus starts in the head of this structure and later spreads to the tail and that, in addition, memory impairment assessed by Rey's Auditory Verbal Learning Test (RAVLT) correlates with hippocampal head gray matter loss..  

Long lasting changes in the strength of synaptic transmission in the Hippocampus are thought to underlie certain forms of learning and memory.  

In addition to the Hippocampus, Abeta(1-40) was found to potentiate K(+)-evoked glutamate release from cortical slices, whereas in the striatum the effect did not reach significant levels.  

Abeta peptide deposits are initially found in all the neocortical areas, then involve the Hippocampus and the subcortical nuclei.  

We have performed a comparative study of the content of glutamate (Glu), aspartate (Asp), taurine (Tau), glycine (Gly) and gamma-amino-butyric acid (GABA) in the cortex, Hippocampus, and striatum of the DBA/2J, Balb/c and C57BL/6 mice brain. The levels of Glu, Tau and GABA in DBA/2J Hippocampus was lower than those in other experimental strains.  

The mammalian telencephalon, which comprises the cerebral cortex, olfactory bulb, Hippocampus, basal ganglia, and amygdala, is the most complex and intricate region of the CNS.  

It is well known that theta rhythms (3-8 Hz) are the fingerprint of Hippocampus, and that neural activity accompanying encoding of words differs according to whether the items are later remembered or forgotten [ "subsequent memory effect" (SME)]. Here, we tested the hypothesis that temporal synchronization of theta rhythms among Hippocampus, amygdala, and neocortex is related to immediate memorization of repeated words. Spectral coherence of the intracerebral EEG activity was computed in order to assess the temporal synchronization of the theta (about 3-8 Hz) rhythms among Hippocampus, amygdala, and temporal-occipital neocortex. We found that theta coherence values between amygdala and Hippocampus, and between Hippocampus and occipital-temporal cortex, were higher in amplitude during successful than unsuccessful immediate recall. Furthermore, these theta and gamma effects were not observed in an additional (control) subject with drug-resistant TLE and a wide lesion to Hippocampus. In conclusion, a successful immediate recall to the RAVLT was associated to the enhancement of temporal synchronization of the theta (gamma) rhythms within a cerebral network including Hippocampus, amygdala, and temporal-occipital neocortex.  

We used synaptosomal fractionation with Western blotting and immunohistochemistry to examine the anatomical, subcellular, and subsynaptic expression patterns of caspase 3 in both the anterior cingulate cortex and Hippocampus of control and AD patients.  

RESULTS: The hallucinating patients showed differential neural activities in various areas including the amygdala, the Hippocampus, the cingulate, the prefrontal cortex, and the parietal cortex, compared with the nonhallucinating patients and the normal controls. In particular, compared with the nonhallucinators, the hallucinators revealed reduced activation in the left amygdala and the bilateral Hippocampus during the processing of crying sounds. CONCLUSION: Our findings suggest that the persistence of AHs in schizophrenia may induce functional disturbances of the emotion-related interconnected neural networks, including reduced responsiveness in the amygdala and Hippocampus to negative stimuli..  

However, the presence of both mutations in a parkin-deficient and hTauVLW double mutant mouse causes a tau neuropathology, reactive astrocytosis, and neuronal loss in the cortex and Hippocampus, as well as lesions in nigrostriatal and motor neurons.  

In addition, a late (3 weeks) loss of dopamine in the prefrontal cortex, but not in the Hippocampus, was seen.  

Immunohistochemical examinations of BrdU in their dorsal Hippocampus at PNDs 42 and 112 revealed that the number of BrdU immunopositive cells in the offspring of prenatally stressed rats was significantly smaller than in the offspring of unstressed ones. These results together with our previous finding that prenatal psychological stress can alter specific behaviors suggest that prenatal psychological stress can suppress neurogenesis in the dorsal Hippocampus of rats of both sexes at PND 35 even though impairment in the behavioral task has not yet appeared..  

The aim of this study was to investigate the effects of acute and chronic exercise on thiobarbituric acid reactive substances, as an indicator of lipid peroxidation, in the Hippocampus, which has a high concentration of glucocorticoid receptors, and prefrontal cortex and striatum, which have high dopamine content. Regular treadmill exercise performed at different strengths was shown not to cause oxidative stress in prefrontal cortex, striatum and Hippocampus regions of brain. As a result, we propose that acute and chronic exercise do not cause oxidant stress in prefrontal cortex, striatum and Hippocampus and chronic exercise has a favorable effect on Hippocampus, possibly by decreasing superoxide radical formation..  

In this study, we have investigated the effects of long-term intake of aluminium chloride (AlCl(3)) on the electrophysiological, behavioral, biochemical and histochemical functions of Hippocampus.  

Recent work has demonstrated that primiparous rats exhibit decreased dendritic arborizations in the Hippocampus, and enhanced Hippocampus-dependent spatial memory performance at the time of weaning compared to nulliparous and, to a lesser degree, multiparous rats.  

The analysis shows that increased activity in the Hippocampus and the parahippocampal cortex predicts subsequent memory strength. During retrieval, activity in the Hippocampus increases in association with strong memory. The results are consistent with the claim that the Hippocampus selectively subserves recollection, whereas adjacent structures subserve familiarity [ Eichenbaum, H., Yonelinas, A., & Ranganath, C. When the fMRI data are interpreted in terms of the alternative theory, the fMRI results do not point to selective roles for the Hippocampus or the adjacent MTL structures.  

The aims of this study were to investigate NCAM-mediated signaling transduction pathways and the levels of the phosphorylated (Ser133) active form of the CREB in the brain structures (the pre- and frontal cortex, basolateral amygdala, and Hippocampus) involved in the memory formation in NCAM-deficient mice. Immunohistochemical analysis revealed reduced levels of pCREB in the prefrontal cortex (PFC), frontal cortex (FC), CA3 subregion of the Hippocampus (CA3) and basolateral nucleus of amygdala (BLA) in NCAM-/- mice. NCAM-/- mice had also reduced levels of the phosphorylated CaMKII and CaMKIV in PFC/FC and the Hippocampus, which are the downstream signaling molecules of NCAM.  

The relative high level of mitochondrial alpha-Syn in Hippocampus, striatum and substantia nigral neurons may have special pathophysiological significance, which deserves further investigation..  

All five subtypes of muscarinic acetylcholine receptors (mAChR; M(1)-M(5)) are expressed in the Hippocampus, where they are involved both in cognitive functions and in synaptic plasticity, such as long-term potentiation (LTP).  

Here we studied the expression of importin beta1 (impbeta1) in the rat Hippocampus after acute and chronic seizures induced by the glutamate agonist kainic acid (KA). After chronic seizures, the overall levels of impbeta1 mRNA and protein did not change in the whole Hippocampus. These data show a differential regulation of impbeta1 expression after acute and chronic seizure activity in the rat Hippocampus.  

Here, we examined whether ginsenosides affected KA-induced mitochondrial dysfunction and oxidative stress in the rat Hippocampus.  

In Hippocampus, varying results have been obtained on the extent and site of cannabinoid actions on excitatory transmission, ranging from no effect to complete obliteration of synaptic responses.  

The results of this study show that acute systemic injection of safranal reduces the extracellular concentrations of glutamate and aspartate in the rat Hippocampus following KA administration..  

Our results demonstrated that NVP and EFV significantly inhibited CK activity in cerebellum, Hippocampus, striatum and cortex of mice.  

Results: The highest levels of this splice form were found in the hypothalamic supraoptic nucleus (SON), pontine nuclei, medulla oblongata, gray matter of the spinal cord, the Hippocampus, glomeruli of the cerebellum, the nucleus basalis of Meynert (NBM), and the tuberomamillary nucleus (TMN). In the Hippocampus, the NBM, and the TMN, TADDI-ir was higher in postmenopausal women than in women

Proneurotrophins, which are potent apoptosis-inducing ligands for p75(NTR), were increased in the Hippocampus, particularly in astrocytes, by pilocarpine-induced seizures; and infusion of anti-pro-NGF dramatically attenuated neuronal loss after seizures. After seizure-induced injury, NRIF(-/-) mice showed an increase in p75(NTR) expression in the Hippocampus; however, these neurons failed to undergo apoptosis in contrast to wild-type mice.  

To assess VGF function in the Hippocampus, we tested heterozygous and homozygous VGF knock-out mice in two different learning tasks, assessed long-term potentiation (LTP) and depression (LTD) in hippocampal slices from VGF mutant mice, and investigated how VGF C-terminal peptides modulate synaptic plasticity.  

The nucleus accumbens (NAc) is an integral part of limbic circuits proposed to play a central role in the pathophysiology of schizophrenia, and is positioned to integrate information from limbic and cortical regions, including the medial prefrontal cortex (mPFC) and the Hippocampus. The ventral subiculum (vSub) of the Hippocampus, in particular, is proposed to gate information flow within the NAc, a factor that is disrupted in models of schizophrenia.  

We examined the requirement of multiple kinases and NMDA receptor interacting proteins for gene expression in mouse Hippocampus slices.  

Atrophic changes of the Hippocampus are typically regarded as an early sign of Alzheimer's dementia (AD).  

To identify age-related proteins in small regions of mouse brain, we improved a proteomics approach, fluorogenic derivatization-liquid chromatography-tandem mass spectrometry (FD-LC-MS/MS), and applied the method to the differential proteome analysis of aging in cerebral cortex, Hippocampus and brainstem.  

Of the structures that receive direct projections from the cortex, the thalamus, caudate nucleus, nucleus accumbens, and Hippocampus showed changes specific to subjects with schizophrenia, and changes in the amygdala and putamen were similar in both groups.  

RESULTS: Binding potential of [ (11)C]doxepin in female subjects was significantly higher than that in male subjects at the following brain sites: amygdala, Hippocampus, medial prefrontal cortex, orbitofrontal cortex, and temporal cortex.  

From E12.5 to E16.5, p57Kip2 expression was detected mainly in ventricular zone (VZ) and/or mantle zone of Hippocampus, septum, basal ganglia, thalamus, hypothalamus, midbrain, and spinal cord.  

RESULTS AND DISCUSSION: In WT mice, LY341495 induced widespread c-Fos expression in 68 out of 92 brain areas, including limbic areas such as the amygdala, septum, prefrontal cortex, and Hippocampus.  

Using infusions of protein synthesis inhibitors, antisense oligonucleotide targeting brain-derived neurotrophic factor (BDNF) mRNA or tPA-STOP (an inhibitor of the proteolysis of BDNF protein) into the Hippocampus of the awake rat, we show that acquisition and extinction of contextual fear memory depended on the increased and decreased proteolysis of proBDNF (precursor BDNF) in the Hippocampus, respectively.  

Grid cells in the medial entorhinal cortex and place cells in the Hippocampus are thought to participate in the formation of a dynamic representation of the animal's current location, and these cells are presumably critical for storing the representation in memory. To traverse the environment, animals must be able to translate coordinate information from spatial maps in the entorhinal cortex and Hippocampus into body-centered representations that can be used to direct locomotion.  

No abnormalities were observed in the gross morphology and synapses of the Hippocampus.  

GAD revealed a significant increase in complexity during ictal cingulate activity and a consistent pattern of subsequent complexity changes in the Hippocampus 30 seconds later.  

Using positron emission tomography and [ (11)C]diprenorphine (DPN) in healthy volunteers, we found significantly reduced DPN binding to opioid receptor in the Hippocampus during positive mood induction compared to neutral mood.  

Our results showed that muscarinic receptor activation significantly increased the expression of phosphorylated p70S6K, eIF4E and ERK without modification of mTOR activity in neuroblastoma cells and in cerebral cortex and Hippocampus of mice, suggesting a stimulation of protein synthesis.  

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