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At least 19 recordsLinked to original sources

Single K+ channels activated by D2 dopamine receptors in acutely dissociated neurons from rat corpus striatum.

Corpus striatum neurons acutely dissociated from the brains of young adult rats had membrane surfaces suitable for G omega-seal recording. Whole-cell current-clamp and voltage-clamp recordings indicated that the cells remained electrically excitable after dissociation. Cell-attached recordings frequently revealed single-channel openings in the presence of dopamine or of the D2 dopamine agonist quinpirole. Channel openings were rarely or never observed in the absence of drugs or in the presence of quinpirole plus the dopamine antagonist haloperidol. The D2 antagonist spiperone was more potent at blocking the appearance of the channel than was the D1 antagonist SCH-23390. The channel reversal potential varied with the extracellular K+ concentration as predicted by the Nernst equation. The channel current-voltage relationship was linear, with a conductance of approximately equal to 85 pS in the presence of 140 mM KCl. These results are consistent with the opening of single K+ channels following D2 dopamine receptor activation.

Action Potentials↗

A triggered hyperkinesia induced in rats by lesions of the corpus striatum.

The role of the corpus striatum (caudate, putamen, and globus pallidus) in movement control has been suggested to involve the modulation of sensory traffic to downstream motor mechanisms. We report that kainic acid lesions of the posterior corpus striatum, which preferentially spare fibers of passage while destroying striatopallidal neurons, produce a stimulus-sensitive movement pattern in rats that has a highly specific sensory trigger. The triggered choreic movement pattern is not a motor pathology per se, nor a response to diffuse states of arousal or stress, but rather is activated specifically in response to oral sensory stimulation. This sensory-specific hyperkinesia may be relevant to certain human sensorimotor pathologies.

Animals↗

The development and ultrastructure of previously dissociated embryonic chick corpus striatum cultured on feeder layers of liver cells.

Embryonic chick corpus striatum neurons were dissociated and maintained on liver feeder layers in culture. Although some large dark-cored vesicles were present in many nerve processes and presynaptic boutons they were substantially less numerous than chick spinal cord neurons grown under identical conditions. Paraformaldehyde-induced fluorescence, although observed in a few culture batches in aggregates of corpus striatum neurons, was otherwise absent and no decisive evidence was obtained to suggest that fluorescent corpus striatum neurons were commonly developed on liver feeder layers in culture. Microtubules filled most cell bodies and nerve processes, and extended well into synaptic boutons often approaching the active zones. They were much more abundant in cultures of corpus striatum than in comparable spinal cord preparations and formed the principal organelle of many nerve fibres. These differences between chick spinal cord and corpus striatum neurons are both interesting and difficult to interpret. It is possible that fewer appropriate cholinergic neurons are available for transformation into adrenergic neurons within the corpus striatum, and that excessive numbers of dark-cored vesicles indicate only a greatly increased rate of acetylcholine production and storage.

Acetylcholine↗

[Projection of afferent impulses from the brachial plexus and sciatic nerve to the corpus striatum in pigeons].

The corpus striatum were systematically explored by recording averaged potentials elicited by stimulation of the brachial plexus and sciatic nerve in 53 pigeons. It was found that the projection areas of brachial afferents were located within the neostriatum, the hyperstriatum and the ectostriatum. The sciatic projection areas overlap with the brachial projection areas in the neostriatum and a part of the hyperstriatum. Moreover, the brachial and sciatic projection are as in the striatum receive the inputs from both sides of the body. We suggest that the somatic projection areas of fore- and hindlimb are distributed diffusely in the striatum of the pigeon. That the projection area of forelimb is relatively larger is probably related with functional differentiation of the forelimb. Furthermore, the convergence of afferent impulses originating in the different regions of the body within the same brain area may be important for the integration of limb activities in pigeon.

Afferent Pathways↗

Stimulation-dependent phosphorylation of tyrosine hydroxylase in rat corpus striatum.

Incubation of rat corpus striatal synaptosomes with 32PO4 led to a time-dependent incorporation of 32P into tyrosine hydroxylase. Depolarization of the synaptosomes with elevated [K+]o increased 32P incorporation into tyrosine hydroxylase. The depolarization-dependent increase in 32P incorporation into tyrosine hydroxylase occurred rapidly (less than 15 sec), persisted in the presence of elevated [K+]o (up to 120 sec), required the presence of [Ca++]o, and was associated with serine (but not threonine or tyrosine) residues. After limit tryptic digestion of the 32P-tyrosine hydroxylase, several phosphopeptides were separated by HPLC, and elevated [K+]o increased 32P incorporation into two of these phosphopeptides. Thus, depolarization of dopaminergic terminals from the rat corpus striatum increased the phosphorylation of tyrosine hydroxylase, and the increase in phosphorylation appeared to occur at multiple sites. Multiple-site phosphorylation of tyrosine hydroxylase has been previously shown in peripheral catecholaminergic tissues. However, substantial differences in the elution profiles of tyrosine hydroxylase phosphopeptides from striatal synaptosomes and from bovine adrenal chromaffin cells were observed. Thus, qualitative differences in the regulation of tyrosine hydroxylase may exist among the many catecholaminergic systems.

Animals↗

Cell cycle kinetics in the embryonic mouse corpus striatum.

Cells of the corpus striatum arise from the lateral ganglionic eminence of the telencephalic neuroepithelium. In mice, the length of the cell cycle and that of its component phases were estimated, and the interkinetic nuclear migratory pattern was characterized for lateral ganglionic progenitors on embryonic day 11 and 12 to gain insights into striatal cytogenetic process. An S-phase labeling paradigm using bromodeoxyuridine was employed. To assess regional variation in proliferative patterns, rostral, middle and caudal levels of the ganglionic neuroepithelium were examined separately. The pattern of interkinetic nuclear migration and the duration of G1-, G2-, and M-phases at the rostral and middle levels differed from those at the caudal level. The length of the cell cycle and that of the G1-phase increased during the interval embryonic day 11 to 12, especially at the rostral and middle levels. During the same interval, a sizable secondary proliferative population emerged at all three levels. Two principal conclusions are drawn: Progenitors at the different rostrocaudal levels are heterogeneous with regard to the pattern of cellular proliferation, and ganglionic progenitors are in advance of the cerebral cortical progenitors based on the relative size of the secondary proliferative population and the magnitude of cytokinetic parameters. Thus, proliferative behavior distinguishes progenitor populations at different rostrocaudal levels within the lateral ganglionic neuroepithelium and across the ganglionic and cerebral cortical domains of the telencephalic neuroepithelium.

Animals↗

Microsomal flavin-containing monooxygenase activity in rat corpus striatum.

Microsomal fractions isolated from rat corpus striatum catalyze the oxidation of thiobenzamide to the sulfoxide. The rate of thiobenzamide sulfoxidation is 6.9 +/- 4.8 nmol(min)-1 (mg microsomal protein)-1. The reaction is inhibited by an excess of sulfur- and nitrogen-containing substrates for the microsomal flavin-containing monooxygenase. These inhibitors of thiobenzamide sulfoxidation include methimazole, cysteamine, and trimethylamine. Enzyme activity is also destroyed by treatment of the microsomal preparation at 60 degrees for 1 min. In parallel experiments, rat liver microsomes exhibit similar inhibition characteristics. The data indicate the presence in corpus striatum of a microsomal monooxygenase with catalytic properties of the hepatic microsomal flavin-containing monooxygenase.

Animals↗

The role of the corpus striatum in neuroleptic- and narcotic-induced catalepsy.

Lesion experiments (in the rat) were designed to elucidate the function of the corpus striatum in neuroleptic- and narcotic-induced catalepsy, respectively. Bilateral lesions of the corpus striatum were observed to attenuate neuroleptic (CPZ)-induced catalepsy. However, analogous lesions of the corpus striatum potentiated narcotic (morphine)-induced catalepsy. These results suggests that (a) the corpus striatum may be a primary site of action of neuroleptic drugs (such as CPZ) in the production of catalepsy, and (b) narcotic (morphine)-induced catalepsy may not be exclusively mediated by the corpus striatum.

Animals↗

Corpus striatum and traumatic brain injury.

The possibility of a 'subcortical' syndrome differentially affecting memory in traumatic brain injury (TBI) subjects was examined. Magnetic resonance imaging scans of 46 traumatic brain injured male patients were compared with those of 34 male control subjects. Surface area measurements of the corpus striatum were calculated for both groups. Results demonstrated no significant differences in corpus striatum surface area measurements. Additionally, TBI patients were grouped according to severity of injury, as well as degree of corpus striatum atrophy, and neuropsychological outcome was examined. There were modest (r = 0.35) but significant correlations between corpus striatum degeneration and the delayed recall trial and total score of the Rey Auditory Verbal Learning Test, but no other correlations between neuropsychological and corpus striatal surface area were significant. Because subcortical pathology may have a differential effect on memory, recognition and recall memory were further analysed, but no significant differences were found. TBI subjects with the smallest corpus striatum values did not test significantly different from TBI patients with normal corpus striatum values or differences in cortical atrophy, as determined by a ventricle-to-brain ratio. These findings suggest that there is not a unique pattern of subcortical pathology involving the corpus striatum in TBI.

Adolescent↗

A short echo 1H spectroscopy and volumetric MRI study of the corpus striatum in patients with obsessive-compulsive disorder and comparison subjects.

OBJECTIVE: It is likely that the corpus striatum is involved in obsessive-compulsive disorder (OCD). Prior studies have inconsistently found alterations in caudate volumes in patients with OCD. This study was undertaken in the hope that N-acetylaspartate and volumetric measures together would elucidate the presence and nature of corpus striatum volumetric abnormalities in OCD. METHOD: Thirteen patients meeting the DSM-IV criteria for OCD, who had been medication free for a minimum of 6 weeks, and 13 psychiatrically normal matched comparison subjects participated in the study. Short echo 1H magnetic resonance spectroscopy (1H-MRS) was used to measure levels of N-acetylaspartate and several other cerebral metabolites from a 4.5-cm3 volume in the left corpus striatum of all 26 subjects. Metabolite levels were estimated by fitting the time domain spectroscopy data with a noninteractive computer program. Volumes of the left and right head of the caudate nucleus in each subject were determined by semiautomatic segmentation of the volumetric images. RESULTS: N-Acetylaspartate levels from the left corpus striatum were significantly lower in the patients with OCD than in the comparison subjects. There were no differences in either left or right caudate volume between the two groups. CONCLUSIONS: Despite the lack of differences in caudate volumes between the OCD patients and the comparison subjects, the lower level of N-acetylaspartate in the left corpus striatum of the patients suggests reduced neuronal density in this region. Inconsistent volumetric findings among prior studies may reflect a poorer sensitivity of magnetic resonance imaging morphometry for detecting neuronal loss compared with 1H-MRS measurement of N-acetylaspartate.

Adult↗

Some morphological studies on the corpus striatum of the cerebrum of the goat.

The corpus striatum of the cerebral hemisphere is carrying out automatic reflexes responsible for feeding, defence, and maintainance of pusture. Our studies were applied on 60 heads of goats from both sexes which were collected from Damanhour sloughter house and injected by 10% formalin through the common carotid artery and put in 10% formalin solution for 1 week. The corpus striatum consists of great basal nuclei and capsules, caudate nucleus, lentiform nucleus, claustrum, capsula interna, capsula externa, and amygdaloidea.

Animals↗

Localization of dopamine receptor subtypes in corpus striatum and nucleus accumbens septi of rat brain: comparison of D1-, D2-, and D4-like receptors.

Changes in D1-, D2- and D4-like dopamine receptor binding in rat brain were examined by quantitative autoradiography following: (i) unilateral surgical ablation of frontal cerebral cortex to remove descending projections to corpus striatum and nucleus accumbens, (ii) unilateral injections of kainic acid into corpus striatum or nucleus accumbens to degenerate local intrinsic neurons, (iii) unilateral injections of 6-hydroxydopamine into substantia nigra to degenerate ascending dopamine projections. Rats were killed one week after lesioning, with contralateral tissue controls. Radioligands were: [3H]SCH-23390 for D1-like (D1/D5) receptors, [3H]nemonapride alone for D2-like (D2/D3/D4) receptors, and [3H]nemonapride with 300 nM S[-]-raclopride and other masking agents for D4-like receptors (identified by blockade with D4 selective L-745,870). Frontal cerebral cortex ablation did not alter D1- or D2-like receptor density, but D4-like binding decreased significantly in both corpus striatum (18%) and nucleus accumbens (23%). Kainic acid markedly reduced D1-like (75% and 84%) and D2-like binding (44% and 52%), with smaller D4-like losses (28% and 27%) in corpus striatum and nucleus accumbens, respectively. Nigral 6-hydroxydopamine lesions (verified by autoradiographic loss of dopamine transporters labelled with [3H]GBR-12935) did not significantly change D1-, D2-, or D4-like binding in the corpus striatum. These results suggest that the majority of D1-, and D2-like, and a smaller portion of D4-like receptors in corpus striatum and nucleus accumbens arise on intrinsic postsynaptic neurons, and that some D4-like, but neither D1- nor D2-like, receptors are found on presynaptic corticostriatal afferents.

Animals↗

Characteristics and displaceability of neurotensin binding sites in the rat cerebral cortex and corpus striatum.

1. Neurotensin binding to synaptosomes isolated from the rat cerebral cortex and corpus striatum reached saturation after 4 min of incubation. 2. The rates of binding were found to be higher in the corpus striatum than in the cerebral cortex. 3. Concentration study revealed the presence of two different and independent classes of neurotensin binding sites with a negative cooperative interaction within each class of binding sites. 4. At saturation levels, the low affinity binding component was found to have a flat regional difference, while the high affinity binding component showed regional differences in terms of maximal binding capacity, suggesting a higher number of high affinity binding sites in the striatum than in the cortex. 5. In the competition related experiments, dopamine was found to displace around 70% of neurotensin binding sites in the corpus striatum and the cerebral cortex. 5. Substance P displaced around 50% of [3H]neurotensin in the cerebral cortex. Whereas, 50% and 70% displacement were observed in the striatum at high and low affinity binding sites, respectively. 6. These results show the overlap in the binding sites of neurotensin, dopamine and substance P.

Animals↗

Ontogeny of dopaminergic function in the rat midbrain tegmentum, corpus striatum and frontal cortex.

Ontogenic development of the dopaminergic system in rat brain was investigated. This was accomplished by monitoring changes in postsynaptic dopamine receptor formation and presynaptic dopamine content in the midbrain tegmentum, frontal cortex and corpus striatum from the 18th day of gestation through adulthood. The dopamine antagonist spiperone was used as the binding ligand to quantitate receptor number while dopamine content was measured chromatographically. [3H]Spiperone binding kinetics in adult animals revealed that the maximum number of receptor sites (Bmax) was 160, 900 and 597 fmol/mg protein in midbrain tegmentum, frontal cortex and corpus striatum, respectively, while the corresponding equilibrium constant (Kd) values were 0.15, 0.52 and 0.15 nM. During the course of development, the affinity for spiperone binding in corpus striatum and frontal cortex did not change significantly, while in midbrain tegmentum the binding affinity in younger animals was significantly lower. Results from competitive inhibition experiments using various serotonergic and dopaminergic antagonists suggested that at all ages dopamine D2-receptors were responsible for spiperone binding in corpus striatum and midbrain tegmentum. In frontal cortex, binding properties consistent with D2-receptors were observed in non-adult animals; by the time adulthood was reached, however, spiperone binding characteristics were altered and appeared to correspond to serotonin sites. The developmental patterns of the dopaminergic markers were different in all 3 tissues. Adult receptor levels were achieved very early in midbrain tegmentum, while increases in receptor number continued in corpus striatum and frontal cortex, at different rates, throughout the postnatal period. A marked increase in dopamine in corpus striatum occurred during the second and third postnatal weeks and the transmitter content remained relatively constant after this time. Transient fluctuations in endogenous dopamine during the postnatal period were observed in midbrain tegmentum and frontal cortex. A general feature of the ontogenic pattern in all tissues appeared to be increases in dopamine receptor preceding increases in dopamine synthesis. A hypothesis on the developmental regulation of dopamine neurons was derived.

Aging↗

Investigation of possible interactions between substance P and transmitter mechanisms in the substantia nigra and corpus striatum of the rat.

The effect of substnace P (SP) on the uptake and release of radiolabelled dopamine (3H-DA), 5-hydroxytryptamine (3H-5-HT) and y-aminobutyric acid (3H-GABA) was studied in slices of rat substantia nigra and corpus triatum. SP, 10(-9) to 10(-5) m, failed to modify the uptakes of these compounds during incubations (10-90 min) with slices of either brain region. SP, 10(-6)M, had no apparent effect on the spontaneous output of any of these compounds in either substantia nigra or corpus striatum. In the corpus striatum, SP seemed to potentiate the potassium-stimulated outflow of 3H-DA and 3H-5-HT, but not 3H-GABA, while the realeases from substantia nigra were unaffected. Morphine (10(-3)M), but not met-enkephalin (5 X 10(-6)M), weakly antagonized K+- EVOKED RELEASE OF 3/-DA in the corpus striatum. These results are discussed with reference to the possible interaction of SP with transmitter mechanisms at presynaptic sites in the central nervous system.

Animals↗

Interaction of age and thyroid hormone status on beta-endorphin content in rat corpus striatum and hypothalamus.

These studies investigated the effect of aging on thyroid hormone regulation of beta-endorphin in rat corpus striatum and hypothalamus. In both brain areas, basal levels of beta-endorphin declined with age. In addition, age modified the response of beta-endorphin to thyroid hormone status. Hypothyroid rats aged 6 months (mature) exhibited a 67% mean decline in the level of beta-endorphin in the corpus striatum. Hypothyroid rats aged 20-24 months (senescent) exhibited no change in the level of beta-endorphin in the corpus striatum. Hypothyroid rats aged 6 months had a 28% mean decline in the level of hypothalamic beta-endorphin. There was no change in hypothalamic beta-endorphin content in hypothyroid senescent rats. Hyperthyroidism resulted in elevations of beta-endorphin in both the corpus striatum and hypothalamus in senescent, but not mature rats. Changes in beta-endorphin seen with age are at least in part thyroid hormone dependent. In addition, age is capable of modifying the response of brain tissue to thyroid hormone.

Aging↗

The effect of long-term penfluridol treatment on the sensitivity of the dopamine receptors in the nucleus accumbens and in the corpus striatum.

The effect of local application of dopamine to the nucleus accumbens or corpus striatum on locomotor activity was studied in rats 4 days after withdrawal from a 6 weeks term of penfluridol medication. The bilateral application of dopamine into the nucleus accumbens of penfluridol-treated rats produced a very marked increase in coordinated locomotor activity which was 3-5 times higher than that of rats not treated with penfluridol. This effect of dopamine in both penfluridol-treated and control rats was antagonized by intraperitoneally administered haloperidol. The bilateral application of dopamine into the corpus striatum of penfluridol-treated animals produced a marked stereotyped behavioural syndrome in all rats studied, whereas no signs of stereotyped behaviour were observed in any of the rats not treated with penfluridol. The results indicate that long-term treatment of rats with the dopamine receptor blocking agent penfluridol produces an increase in the sensitivity of the dopamine receptors in the nucleus accumbens and corpus striatum and that the nucleus accumbens may play a role in locomotor activity.

Animals↗