Lateral Striatum

The current study revealed that excitotoxic lesions of the medial or Lateral Striatum significantly impaired acquisition, as measured by errors and latency, on this task without disruption of motor function.  

Following 5- and 10-minute MCA occlusions, 9 of 32 animals (28%) had microinfarcts mostly in dorsal Lateral Striatum.  

DHX-stimulated c-fos induction in AC5-/- mice was blunted in the dorso-Lateral Striatum, but it was overactivated in the dorso-medial striatum and NAc.  

The preservation of ICMS forelimb movement representations (the forelimb map) in rats with cell-specific CPu lesions suggests motor impairments following lesions of the Lateral Striatum are not due to the disruption of the motor map.  

We used pathway-tracing techniques to compare directly the targets of Area X and MSt with those of the Lateral Striatum (LSt) and globus pallidus (GP).  

Based on its striatal output, it has been subdivided in a caudomedial part which targets the ventromedial striatum, and a lateral part which targets the ventroLateral Striatum [ Ikemoto S (2007) Dopamine reward circuitry: two projection systems from the ventral midbrain to the nucleus accumbens-olfactory tubercle complex. This anatomical arrangement conceivably permits the ventromedial striatum to influence the activity of the Lateral Striatum.  

Following quinolinic acid lesions of the medial or Lateral Striatum, the lesioned rats showed significantly reduced accuracy and increased latencies in responding to both S1 and S2, although (contrary to initial hypothesis) the benefits of predictability of S2 were retained.  

Spike trains in tetrode recordings from the dorso-Lateral Striatum were used for computing MI as rats learnt a T-maze procedural task.  

Then all animals of groups 1 and 2 were lesioned unilaterally with 8 mug 6-OHDA into the Lateral Striatum on 8(th) day.  

Instead, an increase in ChAT ir neurons was detected in Lateral Striatum.  

Results from a control procedure showed that rats with either dorso-Lateral Striatum damage or dorsal hippocampal lesions were impaired on a tactile/spatial discrimination.  

In the two adult songbirds, there were a great number of labeled precursors in the ventricular zone (VZ) of the medial striatum and Lateral Striatum and forming proliferation 'the first hot spots'; in the top of LVZ and forming proliferation 'the second hot spots'. In Melanocorypha mongolica,there were a lot of labeled precursors in the tail of VZ in Lateral Striatum and forming proliferation 'the third hot spots'.  

Only E was able to prevent loss of DAT binding in the Lateral Striatum and to attenuate the MA-induced increase in striatal PPE mRNA levels (at 1 or 40 microg).  

The donor cells were transplanted into the ischemic Lateral Striatum at 24 h after the start of reperfusion.  

Mice at 3 ages (neonatal, 10-day-old, and young adult) received autologous blood (15, 25, and 50 microl respectively), thrombin (3, 5, and 10 units respectively), plasminogen (0.03, 0.05, and 0.1 units respectively) (the doses expected in same volume blood), or saline injection into Lateral Striatum.  

Both the single-site and widespread grafts reduced pregraft dyskinesias and normalized FosB/DeltaFosB in the dorsal two-thirds of the Lateral Striatum. However, single-site DA graft recipients developed a robust, novel forelimb-facial stereotypy and upregulated FosB/DeltaFosB expression in the ventroLateral Striatum, an area associated with movements of tongue and forelimbs.  

The same dose of METH induced depletion of DA transporter sites up to 61, 56, 71, and 69% in dorsal-medial, ventral-medial, dorsal-lateral, and ventral-Lateral Striatum, respectively, relative to vehicle-injected controls.  

Thus, Ei, but not Ex, makes a reciprocal connection with a distinct nucleus in the ventrolateral mesopallium and is a major source of projections to the Lateral Striatum.  

Film autoradiograms showed intense GAD65 labeling in many structures of the basal telencephalon, such as the medial and Lateral Striatum, the septum, the olfactory tubercle, the lateral bed nucleus of the stria terminalis, and the intrapeduncular nucleus, while the pallial telencephalon showed only a low level of labeling.  

Subsequent repeated L-DOPA treatment led to a sensitization of L-DOPA-induced rotational response and produced a second surge of NT induction, this time limited to DYN-positive cells and preferentially restricted to the Lateral Striatum.  

METH treatment produced a 38.5% (+/-5.6) and 46.7% (+/-6.7) dopamine (DA) depletion in the medial and Lateral Striatum, respectively. Serotonin (5-HT) was depleted 15.6% (+/-10.4) and 21.1% (+/-8.2) in the medial and Lateral Striatum, respectively.  

Lesions of the lateral part of the dorsal striatum disrupt this process, and rats with lesions to the Lateral Striatum showed selective sensitivity to devaluation of the instrumental outcome (Yin et al., 2004), indicating that this area is necessary for habit formation.  

Precursors from three postnatal actively neurogenic regions and three postneurogenic regions (cerebral cortex, Lateral Striatum, and optic nerve) were assayed at postnatal day 1, day 10, and adulthood, and compared to well-characterized ventricular subependymal neural stem cells.  

The expression of the mutant HD transgene led progressively to decreased steady-state levels of CB1 mRNA in neurons of the Lateral Striatum, which was dependent on the size of the CAG repeat and relative expression of the gene encoding mutant huntingtin (HD). The cell-specific conditions that allow for increased transcription of CB1 in the Lateral Striatum compared to other forebrain regions from all transcription start sites were affected by the expression of mutant huntingtin in a time-dependent manner..  

Group I was unilaterally sham-lesioned in medial, central, and Lateral Striatum. Group II was injected quinolinic acid (QA) 20 nM in medial, central, and Lateral Striatum.  

A multiple-channel, single unit recording method was used to record neuronal activity in the dorsal Lateral Striatum, the globus pallidus, the subthalamic nucleus, and the substantia nigra pars reticulata simultaneously during spontaneous movement and treadmill locomotion.  

In the present paper we tested the hypothesis that the amygdala incidentally acquires information during the acquisition of a task sensitive to damage to the dorso-Lateral Striatum.  

The results clearly show that Alix immunoreactivity is increased in the neuronal cell bodies of the Lateral Striatum, where degeneration is massive.  

Bilateral striatal infusions of the D1/D2 agonist apomorphine (10 microg/microl/side) into the ventral-Lateral Striatum (VLS) were previously shown to cause significant increases in SNr cell firing (to 133% of baseline) in normal rats.  

In the present study, the authors found that N-methyl-D-aspartate (NMDA) receptor antagonism in the central nucleus of the amygdala (CeA) and the posterior Lateral Striatum (PLS) impaired instrumental conditioning but had no effect in the anterior dorsal striatum.  

For example, the lobus parolfactorius and paleostriatum augmentatum were acknowledged to make up the dorsal subdivision of the striatal part of the basal ganglia and were renamed as the medial and Lateral Striatum.  

To investigate the role of basal ganglia in locomotion, a multiple-channel, single-unit recording technique was used to record neural activity simultaneously in the dorsal Lateral Striatum (STR), globus pallidus (GP), subthalamic nucleus (STN) and substantia nigra pars reticulata (SNr) during spontaneous and treadmill locomotion tasks in freely moving rats.  

The dopamine transporters, as determined by [ 3H]WIN35428 binding, were increased compared with wild-type mice in the ventral mesencephalic dopaminergic nuclei and in the Lateral Striatum, motor cortex and septum.  

Rats with neurotoxic damage to the dorso-Lateral Striatum were severely impaired on the acquisition of the S-R habit task but showed a conditioned-cue preference for the stimulus reinforced during S-R habit training.  

This latter projection arises predominantly from medial parts of the entopallium, which also receives a reciprocal projection from MVL, and projects to the Lateral Striatum. These findings suggest that the entopallium can be divided into medial and lateral parts having different functions, one of which is to provide for an extratelencephalic outflow from the medial part, via the Lateral Striatum.  

After labeled with 5-bromo-2'-deoxyuridine (BrdU), the NSCs were transplanted into the uni- or bi-Lateral Striatum of PD mouse.  

This suggests that NR2B-containing NMDA receptors are involved in mediating most of the NMDA-dependent c-Fos expression in the medial striatum, but only responsible for mediating part of this induction in the Lateral Striatum.  

They displayed a loose topography, with the more medial parafascicular neurons projecting to the medial frontal and cingulate cortex and medial striatum, and the more lateral neurons projecting to the lateral frontal cortex and Lateral Striatum.  

But increased 5-HT(2A) receptor densities were seen in the Lateral Striatum (+86%) compared to control mice.  

Caffeine modestly increased dopamine release in the intact dorsa-Lateral Striatum and no significant difference between the first (+38%) and the last (+51%) injection was observed.  

Our results show that the expression of the D2-R mRNA in the Lateral Striatum varies during the oestrous cycle, with the highest expression measured during DOE2.  

Histopathologically, there were discrete lesions of the dorsoLateral Striatum in 62.5% of mice together with a 32% reduction (P<0.0001) of the striatal volume, reduced caldbindin-D28K immunoreactivity in the Lateral Striatum, and met-enkephalin and substance P in the striatal output pathways.  

Intrastriatal injections of the mGluR1 antagonist, (RS) AIDA (7.5-15 microg/0.5 microl), but not of the agonist of group II mGluRs, 2R,4R-APDC (7.5-15 microg/0.5 microl), inhibited the muscle rigidity induced by haloperidol.In order to search for an influence of mGluRs on the striopallidal pathway, the effect of MPEP or of the agonist of group II mGluRs, DCG-IV, on the proenkephalin (PENK) mRNA expression in the dorso-Lateral Striatum was examined by an in situ hybridization.  

We found that the occurrence of striatal lesions was accompanied by (1) strong transcriptional alterations within the degenerative Lateral Striatum, (2) receptor upregulations within the preserved medial striatum, and (3) transcriptional increases within the unaltered cerebral cortex.  

Firing during sensorimotor exam was used to categorize single neurons in the Lateral Striatum of awake, unrestrained rats.  

In order to assess the role of striatal dopamine (DA) afferents in L-DOPA-induced dyskinesia, we have studied a large series of rats sustaining 2, 3, or 4 unilateral injections of 6-hydroxydopamine (6-OHDA) in the Lateral Striatum.  

The second group received 900,000 cells in both the medial and Lateral Striatum simultaneously (1.8 million total; n = 8). The final group received a second graft of 900,000 cells in the Lateral Striatum 6 weeks following initial transplantation of a medial graft (n = 6).  

The Lateral Striatum projects to globus pallidus and to three cellular groups associated to the lateral forebrain bundle: the anterior entopeduncular nucleus, the suprapeduncular nucleus, and the ventromedial thalamic nucleus. Nucleus rotundus is the origin of a prominent projection to the Lateral Striatum among other forebrain areas.  

Bilateral infusions of d-amphetamine into the rat ventral-Lateral Striatum (VLS) were previously shown to cause a robust behavioral activation that was correlated temporally with a net increase in firing of substantia nigra pars reticulata (SNpr) neurons, a response opposite predictions of the basal ganglia model.  

To determine if CCK modulates the effects of antipsychotic drugs through CCK-A receptors, we measured the haloperidol-induced zif268 mRNA response in the nucleus accumbens (NA) shell, NA core, and dorsal Lateral Striatum (DLS) in Otsuka Long Evans Tokushima Fatty (OLETF) rats that lack CCK-A receptors due to a spontaneous mutation.  

Unilateral injections of amphetamine (20 microg/microl) into either the dorsal-rostral, central, or ventral-Lateral Striatum failed to appreciably alter behavior and, in parallel electrophysiological studies, failed to consistently or significantly alter the activities of SNpr neurons in either chloral hydrate-anesthetized rats or awake locally anesthetized rats. However, when amphetamine was infused bilaterally into the ventral-Lateral Striatum (VLS; 20 microg/microl per side), a robust behavioral activation ensued (increased locomotor activity, oral movements, and sniffing) with an onset ranging from immediate to 20 min post-infusion and persisting for at least 40 min.  

Six months later, histological analyses showed severe neurodegeneration within the Lateral Striatum accompanied by apparent cell loss in the ventral pallidum and entopedoncular nucleus.  

These data suggest that the medial and Lateral Striatum have contrasting roles in the control of instrumental responding related to the primary sources of their cortical innervation..  

Though 3 of 7 animals subjected to 2.5 minutes of ischemia showed decreased myelin-associated glycoprotein (MAG) immunostaining and increased numbers of adenomatous polyposis coli-stained oligodendrocytes in Lateral Striatum, this did not explain the microglia/macrophage proliferation.  

The numbers of Isl-1-positive cells were decreased from the medial to the lateral regions, so that there were only a few Isl-1-positive cells scattered in the Lateral Striatum.  

Pretreatment with either scopolamine or quinpirole increased staining in the Lateral Striatum, but the combination of the two drugs was no more effective than was quinpirole alone.  

YAC72 mice develop selective degeneration of medium spiny projection neurons in the Lateral Striatum, similar to what is observed in Huntington disease.  

YAC72 mice display a hyperkinetic movement disorder by 7 months of age, and have evidence for selective and specific degeneration of medium spiny neurons in the Lateral Striatum by 12 months of age.  

We have previously demonstrated that NMDA receptor antagonists block gene expression induced by a high dose of eticlopride in medial and central but not Lateral Striatum. Less PKA activation by the low dose of eticlopride might explain why the expression was more sensitive in the Lateral Striatum to NMDA receptor blockade than in our previous study.  

Labeling for D1A receptor mRNA was intense in the medial and Lateral Striatum, and moderately abundant in the pallial regions termed the archistriatum and the neostriatum, in the hypothalamic paraventricular nucleus region, and in the superficial gray layer of optic tectum of the midbrain. D1B receptor mRNA was abundant in the medial and Lateral Striatum, and in the pallial region termed the hyperstriatum ventrale, and moderately abundant in the intralaminar dorsal and posterior thalamus and in the superficial gray of the optic tectum. At the cellular level, about 75% of neurons in the medial striatum and 59% of neurons in the Lateral Striatum were labeled for D1A receptor mRNA, whereas about 39% of the neurons in the medial striatum and 21% in the Lateral Striatum were labeled for D1B receptor mRNA.  

Levels of the GluR2 subunit of the AMPA receptor were up-regulated in the medial prefrontal cortex and the nucleus accumbens and down-regulation was observed in the dorso-Lateral Striatum.  

By contrast, treatment with a full D(1)/D(5) receptor agonist up-regulates striatal c-fos messenger RNA homogenously and in similar proportions of D(1) and D(2) receptor messenger RNA-containing projection neurons in both medial and Lateral Striatum, but has only minor effects on c-fos messenger RNA expression in cholinergic interneurons.These results provide a neuroanatomical/neurochemical correlate to the well-known behavioral interaction between dopamine D(1)/D(5) agonists and dopamine D(2) agonists.  

At six, seven, eight and 10 weeks of age, however, the Huntington's disease mice exhibit reduced levels of cannabinoid receptor messenger RNA in the Lateral Striatum compared to age-matched controls.  

Concentric microdialysis probes were stereotaxically implanted in the Lateral Striatum of rats of both age groups and microdialysis was begun 24 h later.  

METHODS: Using a three vessel occlusion model of focal cerebral ischemia combined with bilateral microdialysis, hydroxylation of 4-hydroxybenzoate (4HB) was continuously monitored in both hemispheres in either the Lateral Striatum or frontoparietal cortex. RESULTS: Induction of ischemia resulted in a 30-fold increase in dopamine release in the Lateral Striatum. Compared to the nonischemic striatum, the ratio of the hydroxylation product 3,4-dihydroxybenzoate (34DHB) to 4HB (trapping agent) in the ipsiLateral Striatum increased significantly 30 min after ischemia induction. CONCLUSION: The increase in the 34DHB/4HB ratio in the Lateral Striatum coincides with the increased dopamine release suggesting a role for dopamine oxidation in the increased production of hydroxyl radicals.  

The DA-induced lesions produce significant bilateral reductions in the expression of GluR1 and NMDAR1 subunit mRNA in the medio-Lateral Striatum, whereas the expression of striatal GluR2 receptors was not changed.  

In contrast, COX-2 mRNA was not induced in the ischemic core (Lateral Striatum) but only in the penumbral area (MCA cortex).  

In both the medial and the Lateral Striatum a near-total overlap was found between strongly FosB-like immunoreactive cell groups and areas showing pronounced dynorphin expression.  

The immunoreactivity for TRX was enhanced in hippocampal CA3, dentate gyrus and Lateral Striatum, but not detected in hippocampal CA1 subfield after 3-NP intoxication.  

In contrast, repeated dosage twice daily for 10 days and ascending from 10 to 50 mg/kg resulted in a sharply delineated morphine-induced c-fos synthesis in the dorsomedial and Lateral Striatum, lateral septum, medial mammillary nuclei, anterior thalamus and, in part masked by a high background due to injection stress, in the cingulate cortex.  

By 12 months of age, YAC72 mice have a selective degeneration of medium spiny neurons in the Lateral Striatum associated with the translocation of N-terminal htt fragments to the nucleus.  

It is suggested that the Lateral Striatum mediates the selection of responses, and the medial striatum acts to influence inhibitory control over responding.  

Autoradiographic labeling of these receptors by the selective antagonist [ 3H]MDL 100,907 and saturation experiments with cortical membranes revealed: (1) a new localization of these receptors in the external field of striatum (possibly in striosomes); (2) regional variations in adaptive changes in the density of 5-HT2A receptors in 5-HT(-/-) mutants (-30-40% in the claustrum, cerebral cortex and Lateral Striatum; no significant change in the striatum core) as compared to wild-type mice..  

ChAT-containing neurons were detectable at birth in the Lateral Striatum.  

To gain insight into the role of striatal dopamine in basal ganglia functioning, dopaminergic drugs alone and in combination with the glutamate receptor agonist kainic acid were infused in the Lateral Striatum via a microdialysis probe, while single-unit recordings of substantia nigra reticulata neurons were made in chloral hydrate-anaesthetized rats.  

T2 was increased in the dorsal-Lateral Striatum 1 and 3 days post-ischemia, and in the hippocampus 3 days post-ischemia. T2 was normal 10 days post-ischemia, and decreased in the hippocampus and dorsal-Lateral Striatum 30 days post-ischemia. Neuronal counts in the dorsal-Lateral Striatum and CA1 hippocampal region were uniformly decreased 30 days post-ischemia.  

Although there was a trend toward suppression of the gene induction in Lateral Striatum, it did not reach statistical significance and was not typically dose dependent.  

Concentric microdialysis probes were stereotaxically implanted in the Lateral Striatum of rats, and microdialysis was commenced 24 h after surgery.  

The somatotopic organization of the Lateral Striatum has been demonstrated by anatomical studies of corticostriatal projections from somatosensory and motor cortices and by single-cell recordings in awake animals. Electrode tracks through Lateral Striatum of anesthetized rats (pentobarbital or ketamine) revealed spontaneously discharging neurons but no discharges evoked by somatosensory examination (passive manipulation and cutaneous stimulation of 14 body parts).  

More pronounced deficits were obtained in animals where the same total dose of 6-OHDA was distributed over three or four sites along the rostro-caudal extent of the Lateral Striatum or where the injections were made close to the junction of the globus pallidus. The results show that a 60-70% reduction in tyrosine hydroxylase (TH)-positive fiber density in the Lateral Striatum, accompanied by a 50-60% reduction in TH-positive cells in substantia nigra (SN), is sufficient for the induction of significant impairment in initiation of stepping. Impaired skilled paw-use, on the other hand, was obtained only with a four-site (4 x 7 microgram) lesion, which induced 80-95% reduction in TH fiber density throughout the rostrocaudal extent of the Lateral Striatum and a 75% loss of TH-positive neurons in SN.  

The number of NMDA receptors, as determined by [ 3H]MK-801 binding in the presence of a saturating concentration of L-glutamate, was reduced in the inner frontal cortex, entorhinal cortex and the Lateral Striatum in aged rats when compared with young adults.  

In females only, MK-801 pretreatment resulted in a dramatic increase in the number of Fos-immunoreactive cells in Lateral Striatum.  

Withdrawal after treatment to a maximum dose of 120 mg/kg of morphine did not alter dopamine concentrations in the substantia nigra, ventral tegmental area, striatum, or nucleus accumbens; but did decrease concentrations of DOPAC and the ratio of DOPAC to dopamine in the Lateral Striatum and nucleus accumbens.  

The effects of intracerebroventricularly (i.c.v.) administered CRF on microdialysate concentrations of 5-HT in the Lateral Striatum of freely moving rats were determined.  

In the forebrain of 56-day-old rats, histochemical studies revealed that the subcutaneous injection of a psychotomimetic phencyclidine (PCP; 1 and 10 mg/kg) induced a dose-related and dense nuclear c-Fos-like immunoreactivity in the pyriform cortex, layers IV-VI of the neocortex and septum, but a sparse c-Fos immunostaining in the olfactory tubercle and mid-Lateral Striatum. However, a similar expression pattern of PCP-induced c-Fos was observed in the pyriform cortex, mid-Lateral Striatum, olfactory tubercle and septum between the infant and adult periods.  

It rapidly decreased and nearly disappeared at 4 and 16 hours after MCA occlusion in the Lateral Striatum and frontoparietal cortex, respectively. In hybridization experiments, TRX mRNA decreased and nearly disappeared 4 hours after MCA occlusion in the Lateral Striatum.  

Microdialysis, a powerful in vivo technique to monitor the extracellular levels of neurotransmitters, was used to monitor the baseline changes in the levels of serotonin in rat brain anterior Lateral Striatum post paroxetine administration, which is a measure of the neuropharmacodynamic effect of the drug. Paroxetine caused a statistically significant increase in the extracellular levels of serotonin in the anterior Lateral Striatum sampled by microdialysis.  

Pretreatment with the D2-like agonist quinpirole (3 mg/kg) potentiated staining in the Lateral Striatum, but actually decreased the number of immunoreactive cells observed in the medial portion of the rostral striatum.  

Subacute 3-nitropropionic acid treatment (15 mg/kg per day intraperitoneally for 10 days) produced dramatic motor symptoms associated with extensive neuronal loss and gliosis in the Lateral Striatum as well as severe hippocampal degeneration in 50% of the cases. In contrast, chronic 3-nitropropionic acid treatment (10 mg/kg per day subcutaneously for one month) led to more subtle excitotoxic-like lesions, selective for the dorsoLateral Striatum and more closely resembling Huntington's disease striatal pathology.  

CGS 21680 (5 mg/kg) stimulated c-fos expression also in the lateral septal nucleus and dorso-medial striatum, but not in the dorso-Lateral Striatum.  

In the cases where the biocytin injections had been made in the dorsal or Lateral Striatum, biocytin-labelled terminals made synaptic contact with cholinergic cells in the region between the main termination zones in the globus pallidus and the entopeduncular nucleus.  

Single unit recordings in awake, unrestrained rats confirmed and extended previous findings regarding the functional organization of the Lateral Striatum. Oral representation was most ventral of all body parts and extended to the ventral boundary of the Lateral Striatum. These data provide a more complete description of the dorsal-ventral somatotopy in the Lateral Striatum of the rat, which as shown previously, extends throughout the medial-lateral, and much of the anterior-posterior dimensions of the Lateral Striatum..  

To further study the opioid system in this animal model of cholestasis, we studied the release of endogenous opioid peptides into the extracellular fluid of the dorso-Lateral Striatum by the technique of in-vivo microdialysis.  

These results are consistent with a requirement of dopamine terminals (presynaptic kappa receptors) for the inhibitory action of dynorphin in the dorsal/Lateral Striatum, but not in the ventral striatum.  

Haloperidol and buspirone administration resulted in a significant quantitative increase in the number of Fos-immunoreactive neurons in the Lateral Striatum and a presumable qualitative increase in the nucleus accumbens.  

One hour following a single dose of 2 or 15 Gy the expression of c-fos and zif-268 but not of c-jun mRNAs was induced in a scattered cell population in the Lateral Striatum, whereas in the piriform cortex the expression of zif-268 mRNA was decreased.  

Both treatment methods resulted in a decrease of [ 3H]GBR 12935 binding in dorsal Lateral Striatum of cocaine-exposed offspring on PND 10. Thus, prenatal cocaine exposure by either daily injection from GD 8-21 or continuous infusion from GD 18-21 resulted in a transient decrease in DA transporter binding in the dorsal Lateral Striatum that was apparent on PND 10..  

A fourth neuron type (oval neurons with dendrites oriented in bipolar fashion) was found in the Lateral Striatum.  

Extracellular dopamine levels in Lateral Striatum were not affected by either manipulation.  

No clear differences were observed between TH+ and DA+ terminals within medial striatum (whose neurons project to the nigra in birds) or between TH+ and DA+ terminals within Lateral Striatum (whose neurons project to the pallidum in birds).  

Neuronal injury assessed histopathologically 7 days post-ischemia was significantly reduced in the CA1 region of the hippocampus, the dorsal Lateral Striatum, and the neocortex, in rats treated with 100 mg/kg NaDCA, but not in rats treated with 10 mg/kg NaDCA..  

However, unlike competitive antagonists, local infusion of 1 mM MK-801 potentiated D1-mediated increases in c-fos and zif268 mRNAs in Lateral Striatum.  

the nucleus accumbens (NAC), the medial prefrontal cortex (MPC) and the Lateral Striatum (STR).  

However, STEP was also expressed within a subset of calbindin-positive neurons in the Lateral Striatum, but not with these neurons elsewhere in the striatum.  

The alpha 1 and alpha 3 subunits are about 35% more abundant in the dorsal than in the ventral striatum, while the beta 2/3 and gamma 2 subunits are about 40% more abundant in the medial than in the Lateral Striatum.  

Late in pregnancy females had significantly 18-27% lower levels of binding to D1 dopamine receptors in the Lateral Striatum, the medial striatum, and the nucleus accumbens when compared to all other groups. Late in pregnancy, females had also significantly 11-25% lower levels of binding to D2 dopamine receptors in the Lateral Striatum, the anterior striatum, the nucleus accumbens and the olfactory tubercle compared to all other experimental groups.  

Rats in Group D showed significantly higher rCBF (41-400%, p < 0.05) in the ischemic cortical and subcortical areas, and a significant reduction (66%, p < 0.01) in the total volume of ischemic damage and reduction of PDBu binding (p < 0.05) in the Lateral Striatum of the ischemic hemisphere, as compared to the rats in Groups A-C.  

Cortical electrical stimulation has been shown to induce dense and widespread Fos expression throughout the ipsilateral and contraLateral Striatum. Preadministration of the D1-selective dopamine antagonist SCH-23390 alone or in combination with the D2-selective dopamine antagonist eticlopride led to a reduction in the stimulation-induced density of Fos-positive nuclei of about 60-65% in the Lateral Striatum, but no significant change in the medial region. These results indicate that both dopamine and NMDA glutamate receptors are involved in the induction of Fos by cortical stimulation, and support the hypothesis that cortex-dopamine interactions in the Lateral Striatum may be functionally different from those in the medial striatum..  

However, [ 125I]RTI-55 binding was significantly higher than [ 3H]WIN 35,428 binding in the substantia nigra zona compacta, ventral tegmental area, subthalamic nucleus and a number of other subcortical nuclear groups while [ 3H]WIN 35,428 binding was higher in Lateral Striatum and in olfactory tubercle.  

Haloperidol, chlorpromazine, raclopride and risperidone all significantly increased Fos expression in the medial and Lateral Striatum. Distinguishing it from the other neuroleptics, clozapine did not increase Fos expression in the Lateral Striatum, but induced a significant increase in Fos expression in the prefrontal cortex.  

Microautoradiography analysis demonstrated different increases in the preproenkephalin A mRNA level in different parts of the striatum: +124 +/- 22% in the dorso-median striatum, +131 +/- 19% in the dorso-Lateral Striatum, +119 +/- 8% in the ventro-Lateral Striatum and +75 +/- 6% in the ventro-median striatum.  

In addition, there were activation regions in Lateral Striatum where body region representations may overlap.  

Somata positive for VIP were not seen throughout cortical regions such as the neostriatum and hyperstriatum but were abundant in the Lateral Striatum (paleostriatum augmentatum, PA) and may contribute to a dense field of terminal labeling seen in the globus pallidus.  

However, the administration of vinconate inhibited a significant elevation in the spirodecanone binding in the Lateral Striatum and the stratum radiatum of hippocampal CA1 sector 7 days after ischemia. Pentobarbital also prevented a significant elevation only in the Lateral Striatum. A histological study revealed that cerebral ischemia caused severe neuronal damage in the Lateral Striatum and hippocampal CA1 and CA3 sectors.  

In contrast, the cellular expression of PPE mRNA remained up-regulated in the Lateral Striatum, which receives more sparse innervation from the frontal cortical pole.  

D2R sites were increased over control in Lateral Striatum by day 6, and remained elevated through postnatal day 35. Total D2R mRNA was increased over control in both medial and Lateral Striatum at 7 and 14 days but was equal to control at 35 days.  

The T2 high-signal-intensity areas representing ischemic edema were observed in the Lateral Striatum and/or the cerebral cortex by day 1 in all rats with 1- to 5-hour ischemia, and the areas were larger and detected earlier with longer durations of ischemia. In three of six rats with 15-minute ischemia and five of six rats with 30-minute ischemia, the T2 high-signal-intensity areas appeared transiently on day 1 in the dorsoLateral Striatum where loss of neurons expressing calcineurin immunoreactivity and associated gliosis were found.  

With caffeine treatment, about 73% of neuron-like cells were c-fos labelled in the Lateral Striatum, but labelling was much less pronounced in the medial part or in the accumbens.  

A very strong IgG infiltration with clear-cut borders was detected at one to 3 days in ischemic core areas (Lateral Striatum and adjacent cortex) that fell into porencephaly later.  

The [ 3H]IP3 binding also decreased in the Lateral Striatum after three 2-min ischemic insults but not after 6 min of ischemia.  

This study examined the relationship of single-neuron activity (n = 739), recorded from the Lateral Striatum of freely moving rats, to oral movements involved in licking single drops of liquid. Lick-related neurons were located in the Lateral Striatum, throughout the entire anterior-posterior range studied (from +1.5 to -1.5 mm anterior-posterior, A-P, bregma = 0).  

Quantitative analysis of the sections indicated that immunoreactive cells were more numerous in the medial than the Lateral Striatum and, within these regions, appeared to be randomly distributed. When combined with the highest dose of A-77636, which produced substantial staining by itself, quinpirole produced an increase in the number of immunoreactive cells seen in the Lateral Striatum but actually decreased the number present in the medial striatum.  

We could demonstrate the appearance of collapsed neurons in the Lateral Striatum and adjacent cortex where the dark neuron groups gave columnar patterns.  

Neuroleptic drugs such as haloperidol (H) induce a rapid increase in neurotensin/neuromedin N (NT/N) gene expression in the dorsoLateral Striatum (DLSt) and nucleus accumbens (NA) in young adult rats. In addition to the blunted NT/N mRNA response, significant decreases in D2 receptor mRNA were observed in the Lateral Striatum of another group of young, middle-aged, and aged rats.  

Occlusion of the middle cerebral artery (MCA) for one hour induced ischemic infarcts mainly in the Lateral Striatum, as detected by magnetic resonance imaging (MRI) and histology.  

In the Lateral Striatum of aged rats, dopamine D-2 receptor density is reduced and glutamate tissue content is elevated.  

CPP inhibited [ 3H]MK-801 binding in outer cortex (OC) and medial cortex (MC) with apparent Ki values of 0.32-0.48 microM, whereas in the medial striatum (MS), Lateral Striatum (LS), CA1, and dentate gyrus (DG) of hippocampus, apparent Ki values were 1.1-1.6 microM.  

Chronic estradiol treatment of ovariectomized rats (10 micrograms, twice each day, for 2 weeks) increased Lateral Striatum total receptor density and left unchanged the proportion and affinity of the agonist high- and low-affinity states of this receptor in the striatum.  

HSP70 protein was induced in endothelial cells in infarcted neocortex following 60-90 min of MCA occlusion, and HSP70 was induced in endothelial cells in infarcted regions of Lateral Striatum following 30-90 min of MCA occlusion.  

Intraluminal occlusion of the middle cerebral artery (MCA) for 1 h induced ischemic infarcts in the Lateral Striatum and the adjacent cortex.  

In the striatal body the characteristic lateral to medial gradient of binding site density is apparent by day 5, and development is more rapid in the Lateral Striatum.  

Acc.) and the antero-medial striatum but not in the dorso-Lateral Striatum or the medial prefrontal cortex (mPFC).  

Third, a scattered population of calbindin-positive cells with morphologies different from the common medium-sized calbindin-immunoreactive neurons of the striatum appeared in the dorsal and Lateral Striatum from about E20 to P15.  

[ 35S]TBPS binding sites in the Lateral Striatum decreased 47% 4 days after occlusion.  

Kainate binding was higher in the Lateral Striatum but there was no medial-lateral striatal gradient for other binding sites.  

Seven regions were examined, including the magnocellular preoptic/substantia innominata region, frontal cortex, medial septal region, hippocampus, diagnoal band, and medial and Lateral Striatum.  

The resulting increase in D2 receptors labeled with [ 3H]spiroperidol (27%) was most evident in the Lateral Striatum and topographically correlated with an increase in choline uptake sites labeled with [ 3H]hemicholinium-3 (20%). All doses of icv 6-OHDA produced a significant loss of DA and of [ 3H]mazindol binding as compared to vehicle injections that was more pronounced in the medial than in the Lateral Striatum. No increase in D1 receptors was observed with any dose of 6-OHDA and greater than 90% loss of DA and [ 3H]mazindol resulted in an increase in D2 receptors in the Lateral Striatum and a reduction in D1 receptors in the dorsal striatum.  

Literature indicating that the Lateral Striatum of the rat receives similar cortical inputs and subserves sensorimotor functions prompted a study of whether this subregion contains similar representations of the body. Neurons related to individual body parts were recorded throughout the entire anterior-posterior extent of the dorsoLateral Striatum (+1.60 to -2.12 mm A-P, from bregma), intermingled among each other in all 3 dimensions.  

Twenty-four hours after hypoglycemic coma, intense calcium staining was apparent in layer III of the cerebral cortex, the Lateral Striatum, and the crest of the dentate gyrus.  

Using Percoll density gradient centrifugation, free (nonsynaptosomal) mitochondria were isolated from the dorsal-Lateral Striatum and paramedian neocortex of rats during complete forebrain ischemia and reperfusion. By contrast, in mitochondria from the dorsal-Lateral Striatum (a region containing neurons susceptible to global ischemia), decreases in state 3 and uncoupled respiration rates (25 and 30% less than control values) were again observed after 6 h of recirculation. By 24 h of recirculation, respiratory activity with either pyruvate plus malate or succinate was greatly reduced in samples from the dorsal-Lateral Striatum, probably reflecting complete loss of function in some organelles. In contrast with these marked changes in free mitochondria, the respiratory properties of synaptosomal mitochondria, assessed from measurements in unfractionated homogenates, were unchanged from controls in the dorsal-Lateral Striatum at each of the time points studied, but showed reductions (19-22%) during ischemia and after 24 h of recirculation in the paramedian neocortex..  

During the first postnatal week, corresponding patches of DA afferents and substance P (SP)-immunoreactive neurons existed in the striatum of normal animals, and AChE-positive zones overlapped these patches in the Lateral Striatum.  

the Lateral Striatum and posterior striatal areas.  

Large reductions in apomorphine-induced rotations could result from small lesions of the dorso-Lateral Striatum.  

To examine the activity of single units in the Lateral Striatum of the awake rat with respect to sensorimotor function, 788 units were recorded during locomotion and passive testing. These results show that functional representations of individual limbs can be demonstrated in the Lateral Striatum of the rat, within a subregion containing terminals of projections from somatic sensorimotor cortex.(ABSTRACT TRUNCATED AT 400 WORDS).  

Dopamine receptors were assayed in the same animals by autoradiography; D2 receptors increased on the hormone-treated side relative to the untreated side after four days of treatment, only in the Lateral Striatum.  

Turning resulted in bilateral increases in DOPAC in Lateral Striatum as well as nucleus accumbens/medial striatum. During free drinking, dopamine release was significantly increased in Lateral Striatum but not in nucleus/medial striatum.  

Rats with ibotenate lesions of either the medial striatum or the Lateral Striatum were trained in a forelimb reaching task and in acquisition, retention and reversal of either turn (left-right) discrimination or brightness (black-white) discrimination in a cross-shape maze. The findings indicate a predominant role of the medial striatum in monitoring of directional responses, confirm the regionally specific role of the Lateral Striatum in reaching, and are interpreted to support the hypothesis of parallel motor and cognitive forebrain circuits comprising distinctive regions of the striatum..  

Tissue samples were taken from the cerebral cortex, Lateral Striatum, CA1 subfield of the hippocampus, thalamus, and cerebellum for measuring ornithine decarboxylase (ODC) activity and putrescine levels. In addition, 20-microns-thick coronal tissue sections were taken from the level of the striatum and stained with hematoxylin/eosin for evaluating the extent of ischemic neuronal necrosis in the Lateral Striatum. In control animals ODC activity and putrescine levels amounted, respectively, to 0.32 +/- 0.03 nmol/g/h and 10.2 +/- 0.5 nmol/g in the cerebral cortex; 0.34 +/- 0.02 nmol/g/h and 12.8 +/- 0.5 nmol/g in the Lateral Striatum; 0.58 +/- 0.05 nmol/g/h and 10.5 +/- 0.7 nmol/g in the hippocampal CA1 subfield; 0.35 +/- 0.01 nmol/g/h and 9.8 +/- 0.4 nmol/g in the thalamus; and 0.25 +/- 0.01 nmol/g/h and 8.3 +/- 0.6 nmol/g in the cerebellum.  

Chronic administration of haloperidol (1 mg/kg for 28 days) induced a significant decrease in the labeling for preprosomatostatin mRNA in neurons of the nucleus accumbens, frontal cortex, and medial but not Lateral Striatum.  

We have focused on the chronological changes of neuronal damage in the dorsoLateral Striatum and neocortex following various durations of transient middle cerebral artery occlusion, which does not cause cerebral infarction and is clinically designated "transient ischemic attack". In the rats subjected to 15 min middle cerebral artery occlusion, the neocortex and Lateral Striatum were rarely damaged, whereas the small to medium-sized neurons only in the narrow area restricted to the dorsal striatum showed slowly progressive neuronal damage. Prolongation of ischemic duration to 30 min accelerated the evolution of neuronal damage in the dorsoLateral Striatum and also extended the distribution of neuronal damage to the neocortex, especially to layer III and more superficial layers.  

The suppression of food intake and rate of feeding in 6-hydroxydopamine-treated rats was correlated with the depletion of dopamine in the Lateral Striatum, but not the medial striatum.  

Ischemic cell damage in the medial, lateral, and overall CA 1/2 hippocampus, inferior frontal cortex, and dorsal-Lateral Striatum was significantly (p less than 0.05) less severe in heated animals than in nonheated animals..  

No changes in KA binding were found until 1 week posthypoglycemia, when a significant reduction in binding was noted in the Lateral Striatum..  

Five days after EEDQ a slight difference in labeling density between the medial and Lateral Striatum was detected, whereas after 18 days a prominent lateromedial gradient in silver grain density was seen, resembling the gradient seen without EEDQ treatment. Five days after EEDQ treatment, clusters of silver grains in the Lateral Striatum were seen.  

Peroxidase extravasation was most dense within the territory of the occluded artery including neocortical areas and dorso-Lateral Striatum.  

These findings support the hypothesis of a motor somatotopy in the lateral region of the rat's rostral striatum and of a critical role of the Lateral Striatum in initiation, scaling, and coordination of reaching movements..  

The findings of this study indicate a critical and selective role of the rat's Lateral Striatum in performance of tongue and forelimb reaching. Lesions of the Lateral Striatum caused severe and chronic impairments of movement initiation, postural synergisms and amplitude of both tongue and forelimb reaches. These findings support the hypothesis of a selective role of the Lateral Striatum in the initiation and execution of reaching movements..  

Behavioral studies of rats with ibotenic acid-induced lesions of distinctive regions of the rostral striatum demonstrated clearcut motoric impairments after lesions of the Lateral Striatum, but not after lesions of the medial striatum. Neurotoxic lesions of the Lateral Striatum produced deficits of motor energizing analogous to those of human parkinsonism. These results support the hypothesis that neurodegenerative processes affecting the Lateral Striatum (putamen) in humans may specifically account for parkinsonian symptoms.  

Ten-micrometer-thick coronal cryostat sections were stained with cresyl violet to assess the extent of ischemic cell damage in the Lateral Striatum, the CA1-layer of the hippocampus, and the thalamus. In addition, tissue samples (about 4 mg each) were taken from the Lateral Striatum, CA1 layer of the hippocampus and the thalamus. Reversible cerebral ischemia produced a significant increase in putrescine in the Lateral Striatum (from 11.15 +/- 0.79 to 44.83 +/- 11.76 nmol/g, P less than or equal to 0.05), the CA1 subfield of the hippocampus (from 11.27 +/- 0.64 to 41.80 +/- 3.62 nmol/g, P less than or equal to 0.05) and less so in the thalamus (from 11.28 +/- 0.70 to 16.50 +/- 1.71 nmol/g)..  

Ischemia-sensitive regions which develop extensive neuronal loss during the recirculation period (dorsal-Lateral Striatum, CA1 hippocampus) were compared with ischemia-resistant areas (paramedian neocortex, CA3 plus CA4 hippocampus). After 3 h of recirculation, a significant decrease in respiratory activity (measured in the presence of ADP or uncoupling agent) was observed in the dorsal-Lateral Striatum which progressed to reductions of greater than 65% of the initial activity by 24 h.  

In contrast to the unanimous decrease of LCBF in the ipsilateral cortices and the Lateral Striatum, complexed changes in LCGU were found in not only the cortex and striatum but also in many other subcortical regions which were closely related to the distribution of the mesencephalic dopamine neurons, such as globus pallidus, substantia nigra, subthalamic nucleus, nucleus accumbens, olfactory tubercle and lateral habenular nucleus.  

Finally, whereas increased Type I cell activity in the Lateral Striatum was associated with the aphagia, adipsia, and akinesia induced by large DA-depleting brain lesions, increased Type II cell activity in the medial striatum was found to be associated with these impairments. Because accumulating evidence suggests that the functioning of the Lateral Striatum is more critical for these behaviors, however, it is proposed that the substrate of the behavioral dysfunctions resulting from DA depletion is the Type I cell population in Lateral Striatum..  

Results showed that the spontaneous activity of Type II neurons in either the medial or Lateral Striatum increased only when local DA depletions exceeded 90%; when local depletions were less than 90%, spontaneous firing rates of Type II neurons were equivalent to control values.  

In the Lateral Striatum, some medium-sized aspiny interneurons are also parvalbumin immunoreactive.  

Dopamine assays indicated that of the 5 striatal subregions analyzed, the Lateral Striatum at the level of the anterior commissure was most directly related to the behavioral deficit.  

Regional cerebral blood flow, measured autoradiographically, fell by 85-90% in the ischemic dorsolateral and lateral neocortex, hippocampus and Lateral Striatum, but remained at 71% of control or higher contralaterally. Metabolite assay revealed a gradient of energy depletion, with profound reductions in ATP and phosphocreatine and marked elevations of lactate in lateral neocortex, Lateral Striatum, hippocampus and lateral thalamus.  

Phosphocreatine, ATP, and glucose were severely depleted, and the lactate levels were increased in the paramedian neocortex, dorsal-Lateral Striatum, and CA1 zone of hippocampus of rats exposed to 30 min of forebrain ischemia.  

On the other hand, marked differences were found in a comparison of the medial and Lateral Striatum. Choline acetyltransferase, muscarinic receptor binding and high affinity choline uptake were more concentrated in the Lateral Striatum than the medial striatum, and the magnitude of this medio-lateral disparity increased from rostral to caudal regions of the nucleus. The Lateral Striatum exhibited no significant rostrocaudal variations in the cholinergic parameters; however, the medial portion of the striatum did exhibit differences along its rostrocaudal extent, with the rostral-most sections being enriched relative to the more caudal sections.  

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