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At least 19 recordsLinked to original sources

PubMed1999

Gender difference in dopamine concentration and postischemic neuronal damage in neostriatum after unilateral dopamine depletion.

Most neurons in the dorsal neostriatum die 1 day after 30 min of cerebral ischemia. Dopamine may play a role in the pathogenesis of neuronal injury in neostriatum following ischemia. It has been shown that the number of surviving neurons in the right neostriatum dramatically increased following ischemia after lesions were made in the right substantia nigra (SN), whereas no such protective effect was observed in the left neostriatum after left SN lesion. Using a voltammetric technique, the present study measured the dopamine concentration in neostriatum during ischemia after unilateral dopamine depletion and correlated it with the postischemic neuronal damage in neostriatum of male and female rats. In both genders, dopamine concentrations in the neostriatum of the intact side increased to 50-60 microM during ischemia while those of the lesion side were 15-30 microM. No difference in dopamine concentration was detected between animals with lesions in the left SN and those with lesions in right SN. In male rats, the number of surviving neurons in the right neostriatum (approximately 80% as control) was significantly greater than that in the left neostriatum (approximately 20%) after ipsilateral dopamine depletion, whereas in female animals, the number of surviving neurons in the right neostriatum (approximately 40%) was about the same as that in the left neostriatum (approximately 35%) after dopamine depletion. These results indicate that the asymmetry in ischemic outcome after unilateral dopamine depletion in male rats is not due to the difference in residual dopamine in neostriatum. The lateralization of D2 receptors in male rats may be responsible for the asymmetry of survivability of striatal neurons after transient forebrain ischemia.

Animals↗

PubMed2001

Differential expression of GABA(B)R1 and GABA(B)R2 receptor immunoreactivity in neurochemically identified neurons of the rat neostriatum.

Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the neostriatum. Functions of GABA are known to mediate GABA(A) and GABA(B) receptors. A functional GABA(B) receptor is known to compose of heteromeric subunits, namely the GABA(B)R1 and GABA(B)R2 subunits. Our previous report (Yung et al. [1999] Brain Res. 830:345-352) has demonstrated that all major subpopulations of striatal neurons express GABA(B)R1 immunoreactivity. The cellular localization of the second subunit of GABA(B) receptor protein, i.e., GABA(B)R2 immunoreactivity, in the rat neostriatum is not yet known. By using a new commercially available specific antibody against GABA(B)R2, immunofluorescence was performed to investigate the cellular expression of GABA(B)R2 in neurochemically identified subpopulations of neurons in the rat neostriatum. Immunoreactivity for GABA(B)R2 was primarily found in the neuropil of the rat neostriatum. Double labeling revealed that those perikarya that expressed immunoreactivity for parvalbumin, choline acetyltransferase, nitric oxide synthase, glutamate receptor two, N-methyl-D-aspartate receptor one, or GABA(A)alpha1 receptor, respectively, did not express GABA(B)R2 immunoreactivity. In addition, perikarya and most of the neuropilar elements in the neostriatum that expressed glutamic acid decarboxylase 67 immunoreactivity were found to be GABA(B)R2-negative. In contrast, immunoreactivity for GABA(B)R1 was found to be expressed by all of the above neuronal subpopulations. Moreover, a vast number of SV2-immunoreactive profiles and a number of tyrosine hydroxylase-immunoreactive profiles in the neuropil of the neostriatum were found to display GABA(B)R2 immunoreactivity. The present results indicate that there is a differential expression of GABA(B)R2 and GABA(B)R1 immunoreactivity in different subpopulations of striatal neurons that are identified by their specific neurochemical markers. Immunoreactivity for GABA(B)R2 is likely to localize in neuropilar elements of the neostriatum that may belong to non-GABAergic elements. These findings provide anatomical evidence of GABA(B)R2 receptor localization in the neostriatum that may have an important functional implication of the GABA(B)-mediated functions in neurons of the neostriatum.

Animals↗

PubMed1994

Evidence for volume transmission in the dopamine denervated neostriatum of the rat after a unilateral nigral 6-OHDA microinjection. Studies with systemic D-amphetamine treatment.

In the present study the hypothesis has been tested if the dopamine releasing drug D-amphetamine via volume transmission can, at least partly, restore dopamine communication in the dopaminergically denervated neostriatum of rats. The experimental model used, has been a unilateral 6-hydroxydopamine-induced degeneration of the nigrostriatal dopamine neurons, based on nigral microinjections of this neurotoxin. Studies on c-fos like immunoreactivity after systemic D-amphetamine treatment demonstrated a wide-spread appearance of c-fos like immunoreactive neuronal nuclear profiles within the neostriatum on both the unlesioned and denervated side. In the unlesioned neostriatum a peak density of c-fos like immunoreactive profiles was found within the central part of the neostriatum, while on the denervated side the distribution pattern of c-fos like immunoreactive profiles peaked medially and gradually declined in a lateral direction. The microdialysis experiments demonstrated, after systemic d-amphetamine treatment, a marked and sustained increase of extracellular dopamine levels in the neostriatum on the unlesioned side, while no increases in the extracellular dopamine levels were observed on the dopaminergically denervated neostriatum. In the electrophysiological experiments, systemic D-amphetamine treatment produced an inhibition of the neuronal activity on the denervated side which showed a significant increase in basal discharge rate compared with the recordings obtained from the striata on the unlesioned side. The present immunocytochemical microdialysis and electrophysiological analysis provides evidence that in the unilaterally markedly dopamine depleted neostriatum with clearcut signs of dopamine receptor supersensitivity (rotational behaviour results), dopamine transmission may be partly restored via systemic D-amphetamine treatment through the release of dopamine, predominantly from the unlesioned neostriatum, which may diffuse into the cerebrospinal fluid to reach the contralateral dopaminergically denervated neostriatum.

Animals↗

PubMed2001

Modulation of the gene expression of N-methyl-D-aspartate receptor NR2B subunit in the rat neostriatum by a single dose of specific antisense oligodeoxynucleotide.

N-methyl-D-aspartate receptors (NRs) are a group of ionotropic glutamate receptors in the brain and they are composed of heteromeric subunits (NR1, NR2A-D and NR3). In the neostriatum, a brain region that is associated with movement in animals, NMDA channels are known to involve in the motor control. Our previous report (Lai et al., 2000, Neuroscience 98, 493-500) has shown that a single dose of antisense oligodeoxynucleotides that are specific to NR1 subunit results in blockage of the gene expression of NR1 as well as NR2A subunits in the neostriatum. In the present study, antisense oligodeoxynucleotides that are specific to NR2B (ANR2B) were then employed as molecular tools to further investigate the molecular interactions of NMDA receptor subunits in the neostriatum. A single dose of ANR2B was injected unilaterally into the rat neostriatum. After one day of injection, no modification of motor behavior was found in the ANR2B-injected rats. The mRNA level of NR2B in the ANR2B-injected neostriatum was found to be decreased (-20.4%) by reverse transcriptase polymerase chain reaction (RT-PCR). However, the mRNA levels of NR1, NR2A, NR2C and NR2D in the ANR2B-treated neostriatum were found to be unchanged. After two days of injection, NR2B immunoreactivity was found to decrease in the ANR2B-treated neostriatum by immunofluorescence (-35.1%). At higher magnification, NR2B immunoreactivity was found to decrease in presumed spiny neurons of the neostriatum (-23.4%). No change in NR1 immunoreactivity was observed. These results indicate that a single dose of ANR2B can successfully block the gene expression of NR2B in neurons of the neostriatum and there is less effect on NR1 and other NR2 subunits. The blockage of the gene expression of NR2B is therefore specific and the present results may provide important implications in applications of antisense in research and in clinical therapy of neurological diseases.

Animals↗

PubMed1998

The release of amino acids from rat neostriatum and substantia nigra in vivo: a dual microdialysis probe analysis.

It has previously been demonstrated, in dual probe microdialysis studies, that stimulation of the neostriatum with kainic acid causes the release of GABA both locally within the neostriatum and distally in the substantia nigra, observations that are consistent with the known anatomy of the basal ganglia. The object of the present study was to further examine the characteristics of GABA release and to determine whether taurine, which has been proposed to be present in striatonigral neurons, has similar characteristics of release, and to examine the release of excitatory amino acids under the same conditions. To this end, dual probe microdialysis studies were carried out on freely-moving rats. The application of kainic acid to neostriatum enhanced the release of GABA, taurine, aspartate and glutamate locally in the neostriatum and distally in the substantia nigra. The distal release of each amino acid in the substantia nigra was sensitive to the administration of 6,7-dinitroquinoxaline-2,3-dione and tetrodotoxin to the neostriatum. Similarly the local release of GABA, aspartate and glutamate but not taurine was sensitive to the intrastriatal application of 6,7-dinitroquinoxaline-2,3-dione or tetrodotoxin. It is concluded that the release of taurine from the substantia nigra has similar characteristics to that of GABA and may be released from the terminals of striatonigral neurons following the stimulation of their cell bodies in the neostriatum. The release of taurine in the neostriatum however, is likely to be mediated mainly by different mechanisms and not related to neuronal activity. The release of excitatory amino acids is likely to involve indirect effects in the neostriatum and polysynaptic pathways in the substantia nigra.

Animals↗

PubMed1981

Cell types of the auditory caudomedial neostriatum of the starling (Sturnus vulgaris).

Cell types of the auditory neostriatum in the starling forebrain are described. This area in the caudal neostriatum is defined neurophysiologically by the appearance of auditory neurons. Through use of the rapid Golgi technique, four types of neurons are identified, mainly on the basis of their processes: Neurons with long descending axons and thick dendrites rich in spines (type 1), neurons with long ascending axons and thin dendrites poor in spines (type 2), short-axon neurons (type 3), and microneurons (type 4). The axons of the long neurons pass outside the confines of the auditory neostriatum. Among neurons of type 1; some of the long descending axons directed toward the lower brain centers enter the capsula interna occipitalis (CIO). The descending axons give off many collaterals within the auditory neostriatum. With neurons of type 2; most of the ascending axons cross the lamina hyperstriatica, enter the hyperstriatum ventrale, and arborize near its periventricular region. Some of the long ascending axons reach the overlying hyperstriatum ventrale, pars caudale (HVc, the vocal control area). Among neurons of types 3 and 4; the axons of short-axon neurons and of microneurons end with fine branches within the auditory neostriatum. The dendrites of long-axon neurons are oriented in specific directions, whereas those of short-axon neurons and of microneurons do not show a definite pattern of orientation. In the region of the auditory neostriatum that lies immediately adjacent to the midline of the brain, the first three types of neurons are arranged around the central core known as field L, which is composed of the microneurons and the terminal ramifications of auditory afferents. Laterally the microneurons, along with the fibers of the input tract, undergo a rostral shift to occupy a more peripheral position within the auditory neostriatum. The neurons of the auditory neostriatum are compared with those of the mammalian auditory cortex, and a functional classification of nerve cells into projection neurons, association neurons, and interneurons is proposed.

Animals↗

PubMed1993

Amino acid levels and gamma-aminobutyric acidA receptors in rat neostriatum, cortex, and thalamus after neonatal 6-hydroxydopamine lesion.

The amino acid gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in brain, and GABAergic neurons have been proposed to play a major role in basal ganglia physiology. In the neostriatum (caudate putamen), medium-sized aspiny interneurons, as well as neostriatal output neurons that project to several brain regions, use GABA as their neurotransmitter. Dopamine fibers arising from the substantia nigra represent a major input to the neostriatum where, besides their classic neurotransmitter role, they are seemingly involved in the regulation of amino acid neurotransmitter release. To further characterize the nature of some of the amino acid/dopamine interactions, selective dopaminergic deafferentations were produced in neonatal rats (3 days postnatal) by intraventricular administration of the neurotoxin 6-hydroxydopamine (6-OHDA); the noradrenergic neurons were protected by prior administration of desmethylimipramine. After a 3-month survival, levels of catecholamines, indoleamines, and amino acids were determined in cingulate cortex, thalamus, and neostriatum. In addition, GABAA receptors were measured in membrane preparations from these three regions, using the specific agonist [3H]muscimol. In the 6-hydroxydopamine-lesioned rats, levels of dopamine and its metabolites homovanillic acid, 3,4-dihydroxyphenylacetic acid, and 3-methoxytyramine were decreased, as expected, in cortex and neostriatum, but remained unmodified in thalamus. In all three regions, serotonin content was increased; its metabolite, 5-hydroxyindole-3-acetic acid, was also elevated, but only in cortex and neostriatum. The levels of GABA were increased in neostriatum and thalamus, but remained unmodified in cortex. Glycine was increased in all three regions examined. There were also increases of phosphatidylethanolamine and serine in thalamus, and of aspartic acid and alanine in neostriatum. The density of GABAA binding sites was increased in neostriatum, but remained unchanged in cortex and thalamus. The changes in amino acid levels and [3H]muscimol binding sites induced by a neonatal 6-hydroxydopamine treatment differ from those found after similar lesions in adult animals, possibly because of the plastic and synaptic rearrangements that can still occur during early postnatal development. The present results also demonstrate that adaptations occur in response to a dopaminergic deafferentation at an early age and that these exhibit a regional specificity.

Amino Acids↗

PubMed1996

Modulation of neurotransmitter release by cholecystokinin in the neostriatum and substantia nigra of the rat: regional and receptor specificity.

The effect of cholecystokinin peptides on the release of dynorphin B, aspartate, glutamate, dopamine and GABA in the neostriatum and substantia nigra of the rat was investigated using in vivo microdialysis. Sulphated cholecystokinin-8S in the dialysis perfusate (1-100 microM) induced a concentration-dependent increase in extracellular dynorphin B and aspartate levels, both in the neostriatum and substantia nigra. Striatal dopamine levels were only increased by 100 microM of cholecystokinin-8S, while in the substantia nigra they were increased by 10-100 microM of cholecystokinin-8S. Extracellular GABA and glutamate levels were increased following 100 microM of cholecystokinin-8S only. Striatal cholecystokinin-8S administration also produced a significant increase in nigral dynorphin B levels. Local cholecystokinin-4 (100 microM) produced a moderate, but significant, increase of extracellular dynorphin B and aspartate levels in the neostriatum and substantia nigra. No effect was observed on the other neurotransmitters investigated. A 6-hydroxydopamine lesion of the nigrostriatal dopamine pathway did not affect the increases in dynorphin B and aspartate levels produced by local administration of cholecystokinin-8S. Basal extracellular GABA levels were increased significantly in both the neostriatum and substantia nigra ipsilateral to the lesion. Nigral glutamate and aspartate levels were also increased in the lesioned substantia nigra, but in the lesioned neostriatum aspartate levels were decreased. The cholecystokinin-B antagonist L-365,260 (20 mg/kg, s.c.), but not the cholecystokinin-A antagonist L-364,718 (devazepide; 20 mg/kg, s.c.), significantly inhibited the effect of cholecystokinin-8S on striatal dynorphin B and aspartate levels. In the substantia nigra, however, the effect of cholecystokinin-8S on dynorphin B and aspartate levels was inhibited to a similar extent by both L-365,260 and L-364,718. Pretreatment with L-364,718, but not with L-365.260, prevented the increase in nigral dopamine levels produced by nigral cholecystokinin-8S administration. Taken together, these results suggest that cholecystokinin-8S modulates dynorphin B and aspartate release in the neostriatum and substantia nigra of the rat via different receptor mechanisms. In the neostriatum, the effect of cholecystokinin-8S on dynorphin B and aspartate release is mediated via the cholecystokinin-B receptor subtype, while in the substantia nigra, cholecystokinin-8S modulates dynorphin B and aspartate release via both cholecystokinin-A and cholecystokinin-B receptor subtypes. Cholecystokinin-8S modulates dopamine release mainly in the substantia nigra, via the cholecystokinin-A receptor subtype.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2001

Differential changes of synaptic transmission in spiny neurons of rat neostriatum following transient forebrain ischemia.

Spiny neurons in neostriatum are vulnerable to cerebral ischemia. To reveal the mechanisms underlying the postischemic neuronal damage, the spontaneous activities, evoked postsynaptic potentials and membrane properties of spiny neurons in rat neostriatum were compared before and after transient forebrain ischemia using intracellular recording and staining techniques in vivo. In control animals the membrane properties of spiny neurons were about the same between the left and right neostriatum but the inhibitory synaptic transmission was stronger in the left striatum. After severe ischemia, the spontaneous firing and membrane potential fluctuation of spiny neurons dramatically reduced. The cortically evoked initial excitatory postsynaptic potentials were suppressed after ischemia indicated by the increase of stimulus threshold and the rise time of these components. The paired-pulse facilitation test indicated that such suppression might involve presynaptic mechanisms. The inhibitory postsynaptic potentials in spiny neurons were completely abolished after ischemia and never returned to the control levels. A late depolarizing postsynaptic potential that was elicited from approximately 5% of the control neurons by cortical stimulation could be evoked from approximately 30% of the neurons in the left striatum and approximately 50% in the right striatum after ischemia. The late depolarizing postsynaptic potential could not be induced after acute thalamic transection. The intrinsic excitability of spiny neurons was suppressed after ischemia evidenced by the significant increase of spike threshold and rheobase as well as the decrease of repetitive firing rate following ischemia. The membrane input resistance and time constant increased within 6 h following ischemia and the amplitude of fast afterhyperpolarization significantly increased after ischemia. These results indicate the depression of excitatory monosynaptic transmission, inhibitory synaptic transmission and excitability of spiny neurons after transient forebrain ischemia whereas the excitatory polysynaptic transmission in neostriatum was potentiated. The facilitation of excitatory polysynaptic transmission is stronger in the right neostriatum than in the left neostriatum after ischemia. The suppression of inhibitory component and the facilitation of excitatory polysynaptic transmission may contribute to the pathogenesis of neuronal injury in neostriatum after transient cerebral ischemia.

Action Potentials↗

PubMed1976

The rodent neostriatum: a Golgi analysis.

In the adult rodent, coronal sections of Golgi impregnations of the neostriatum display a compact segregation of axon fascicles, neuronal clusters, and dendritic bundles thus forming an areolar configuration. Isolated neurons are rarely seen. The dorsomedial region of the neostriatum appears free of axon fascicles and dendritic bundles. Horizontal and sagittal sections of the neostriatum show clusters of cells parallel to axon fascicles. The neurons exhibit spine-laden dendrites with an initial spine-free segment. Neonatal impregnations exhibit a different configuration. Neonatally, cells tend to cluster but there is no bundling of dendrites. Neurons are spine-free or have protospines on the soma and the dendrites, including the initial segment. Transition from neonate to adult configuration is discernible at about 15 days after birth. The neostriatum of carnivores exhibits a different structure from the rodent neostriatum. This difference is associated with a developed anterior limb of the internal capsule in the carnivore. The axon fascicle-free portion of the carnivore neostriatum lacks dendritic bundles and pallisades. Portions near the capsule with axon fascicles appear similar to the rodent neostriatum with dendritic bundlings and pallisading. Such findings emphasize the importance of total neuronal configuration (neuronal-architectonics) in morphologic analyses.

Animals↗

PubMed1987

The organization of the nucleus basalis-neostriatum complex of the mallard (Anas platyrhynchos L.) and its connections with the archistriatum and the paleostriatum complex.

The pattern of connections between the nucleus basalis, neostriatum, hyperstriatum ventrale, paleostriatum complex and archistriatum in the mallard has been analysed using Nissl material and a combination of neuroanatomical tracing procedures (autoradiography, horseradish peroxidase and horseradish peroxidase-wheat germ agglutinin histochemistry, lesion/degeneration technique). The frontal part of the mallard's telencephalon is characterized by its multilayered organization and the predominantly vertical arrangement of the connecting fiber systems. The nucleus basalis, endstation of the ascending sensory trigeminal system, is a large laminar cell area with a dorsal and a ventral layer. The overlying neostriatum frontale can be subdivided into a medial, a dorsal and a ventral intermediate, and a lateral area. The nucleus basalis has distinct connections with the ventral layer and sparse connections with the dorsal layer of the intermediate neostriatum, and abundant reciprocal connections with the ventral layer of the hyperstriatum ventrale. The ventral intermediate neostriatum also has reciprocal connections with the hyperstriatum ventrale; its projections overlap partly with those from the nucleus basalis. The ventral layer of the intermediate neostriatum frontale has a distinct projection upon the paleostriatum augmentatum. The dorsal layer sends fibers to the lateral neostriatum, to the rostral "sensorimotor" part of the archistriatum and to the lateral zone of the lobus parolfactorius. Another source of archistriatal afferents is the paleostriatum ventrale, an area that may also send fibers to the brainstem. Figure 21 summarizes the connections described in this paper. The functional significance of this organization is discussed in relation to its possible role in the guidance of pecking and other feeding behaviors in the mallard. Differences in the organization of the systems in pigeon and mallard are related to the differing degrees of visual and tactile (trigeminal) contributions to feeding in the two birds. It is suggested that the pattern of reciprocal connections between the hyperstriatum ventrale and the nucleus basalis and ventral intermediate neostriatum frontale forms the neuroanatomical substrate for a "comparator-system".

Animals↗

PubMed1993

Changes of D1 and D2 receptors in adult rat neostriatum after neonatal dopamine denervation: quantitative data from ligand binding, in situ hybridization and iontophoresis.

The specific binding of [3H]SCH23390 to D1 and of [3H]raclopride to D2 dopamine receptors was measured by autoradiography in the rostral and caudal halves of neostriatum and in the substantia nigra of adult rats subjected to near total destruction of nigrostriatal dopamine neurons by intraventricular 6-hydroxydopamine soon after birth. Three months after this lesion, [3H]SCH23390 binding (D1 receptors) was slightly but significantly decreased in the rostral neostriatum (22%), but unchanged in its caudal half and in the substantia nigra. In contrast, [3H]raclopride binding (D2 receptors) was considerably increased throughout the neostriatum (10-40%), while markedly decreased in the substantia nigra (80%). In the rostral neostriatum, there were no parallel changes in D2 receptor messenger RNA levels, as measured by in situ hybridization on adjacent sections. Caudally, however, slight but significant increases in D2 messenger RNA could be observed (10-20%). As assessed by quantitative iontophoresis, there was a marked enhancement (63%) of the inhibitory responsiveness of spontaneously firing units in the rostral neostriatum to dopamine and the D1 agonist, SKF38393, in neonatally lesioned compared to control rats. On the other hand, responsiveness to PPHT, a potent D2 agonist, appeared to be unchanged. Such opposite changes in the number of D1 and D2 binding sites, dissociated from the expression of D2 receptor messenger RNA and from the sensitivity to dopamine and D1 and D2 agonists, suggested independent adaptations of these various parameters following the neonatal dopamine denervation of neostriatum. They also provided further evidence for mechanisms other than the dopamine innervation in the control of the expression of neostriatal D2 receptor messenger RNA during ontogenesis, and emphasized that the effects of dopamine and its D1 and D2 agonists in neostriatum do not depend strictly on the number of D1 and D2 primary ligand recognition sites.

Animals↗

PubMed1990

Comparison of transmitter amino acid levels in rat globus pallidus and neostriatum during hypoglycemia or after treatment with methionine sulfoximine or gamma-vinyl gamma-aminobutyric acid.

The levels of amino acids in globus pallidus, a structure heavily innervated with gamma-aminobutyric acid (GABA)-ergic terminals but few glutamergic terminals, were compared with the levels in neostriatum, a structure richly innervated with glutamergic terminals but intermediate in GABAergic terminals. The level of glutamate in neostriatum was twice as high as in globus pallidus whereas the level of GABA in globus pallidus was three times higher than in neostriatum. The level of aspartate was similar in both regions whereas the level of glutamine was correlated with the level of glutamate. Methionine sulfoximine, a glutamine synthetase inhibitor, reduced the level of glutamine to 10-20% of control in both structures. This reduction was accompanied by the largest decrease in the level of glutamate in neostriatum, indicating that transmitter glutamate turns over more rapidly than other glutamate pools. Likewise, insulin decreased the levels of glutamate and glutamine more in neostriatum than in globus pallidus. gamma-Vinyl GABA increased the level of GABA in globus pallidus more than in neostriatum although the percent increase was largest in neostriatum. Treatment with gamma-vinyl GABA was accompanied by a large reduction in the level of GABA, indicating that a substantial proportion of the glutamine pool is linked to GABA metabolism.

Amino Acids↗

PubMed1981

Prenatal formation of cortical input and development of cytoarchitectonic compartments in the neostriatum of the rhesus monkey.

The timing, hemispheric laterality, and mode of termination of input from the prefrontal association cortex to the neostriatum were studied in fetal and neonatal rhesus monkeys using autoradiography for tracing connections. In addition, the cytological maturation of the neostriatum was examined in Nissl-stained sections from the same and other monkeys of selected prenatal and postnatal ages. A small contingent of corticostriatal axons reaches both the caudate nucleus and the putamen by the 69th embryonic day (E69) of the 165-day gestation period in this species and steadily expands over the next 3 fetal months. Throughout this period, ipsilateral perfrontostriatal connections predominate, and only a small and variable amount of label is detectable over the contralateral neostriatum. A major feature of the developing corticostriatal projection is a transfiguration in the distribution of its terminals: from E69 to E95, cortical terminals are distributed uniformly among neostriatal neurons; beginning around E105, areas of higher and lower grain density begin to emerge until finally, by E133, 250- to 500-micrometers-wide circular and elliptically shaped label-free cores perforate a field of densely labeled cortical terminals as in the neostriatum of the adult monkey (Goldman, P. S., and W. J. H. Nauta (1977) J. Comp. Neurol. 171: 369-386). The cytoarchitectonic composition of the neostriatum also changes during gestation: from E69 through E95, the small postmitotic neurons of the immature neostriatum are packed densely and, for the most part, are distributed homogeneously; by E105, they become segregated into cellular islands consisting of densely packed neurons that are encapsulated by fiber-rich annuli and embedded in a matrix of less densely arrayed neurons. The shape and size of the islands in Nissl-stained sections correspond to label-free cores in autoradiograms of fetuses with cortical injections, while the surrounding annuli and adjacent matrix cells correspond to areas of dense accumulation of label. Thus, the formation of the corticostriatal projection in primates involves a transformation in the distribution of ingrowing terminals synchronized with changes in cellular organization of the neostriatum.

Adrenal Cortex Hormones↗

PubMed1995

Developmental expression of KG-CAM in the rat neostriatum.

The present study examines the developmentally regulated expression pattern of an Ig superfamily member, KG-CAM, in the neostriatum of the rat. KG-CAM is a 90-kDa glycoprotein that is related to the DM-GRASP/Neurolin family of adhesion molecules. In the embryonic and early postnatal neostriatum, the distribution of KG-CAM correlates with the distribution of dopaminergic terminals. Early in neostriatal development, KG-CAM is found in the tyrosine hydroxylase-positive patches. In the maturing neostriatum, the levels of KG-CAM remain high within the patches, and KG-CAM upregulates in the matrix compartment. As the neostriatum is reaching its adult morphology, 5 weeks postnatal, the expression of KG-CAM in the matrix is approximately equal to that of the patches. When the distribution of KG-CAM is examined at the ultrastructural level, the immunoreactivity is localized to the external surface of neuronal and glial profiles in the neuropil. KG-CAM does not appear to be associated with the guidance of dopaminergic axons from the substantia nigra to the striatum, for this pathway is not immunopositive for this member of the Ig superfamily. The present study identifies an Ig superfamily member, KG-CAM, that appears to play a major role in the development of the neostriatum. Furthermore, the high levels of KG-CAM in the adult neostriatum suggest that this Ig superfamily member may be involved in maintaining the integrity of this structure in the adult rat.

Activated-Leukocyte Cell Adhesion Molecule↗

PubMed1998

Increased levels of extracellular dopamine in neostriatum and nucleus accumbens after histamine H1 receptor blockade.

The dopaminergic system plays a central role in the processing of reward or reinforcement since drugs that have reinforcing properties all share the ability to elevate dopamine (DA) levels in the nucleus accumbens or neostriatum. Histamine H1 receptor antagonists are known to have reinforcing effects in humans and laboratory rats. Here, we examined the effect of systemic (i.p.) treatment with two H1 antagonists, chlorpheniramine and pyrilamine, on the extracellular levels of DA and its metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the neostriatum and nucleus accumbens of urethane-anesthetized rats. Dopamine and metabolites were measured using in vivo microdialysis and HPLC with electrochemical detection. Saline injections did not produce significant effects on DA, DOPAC, or HVA levels in the neostriatum or nucleus accumbens. In the neostriatum, chlorpheniramine administration (5 and 20 mg/kg) produced a sustained increase in DA to approximately 140 and 180% of pre-injection baseline levels, respectively. In the nucleus accumbens, chlorpheniramine (20 mg/kg) produced a transient increase in DA levels to about 300% of baseline. In both the neostriatum and nucleus accumbens, DOPAC and HVA decreased after chlorpheniramine treatment. Pyrilamine administration (10 and 20 mg/kg) produced a sustained increase in neostriatal DA levels to 140 and 165%, respectively, and accumbens DA increased transiently to 230% after a dose of 20 mg/kg. Levels of neostriatal and accumbens DOPAC and HVA decreased after pyrilamine treatment. These results show that H1 antagonists can potently enhance DA levels in the neostriatum and nucleus accumbens of urethane-anesthetized rats. The neurochemical effects on DA and its metabolites seen here (increased DA, decreased DOPAC and HVA) are similar to those commonly observed with drugs of abuse (e.g. psychostimulants). The interaction of H1 antagonists with dopaminergic transmission may explain the reinforcing effects and abuse potential associated with these compounds.

Animals↗

PubMed2000

Ubiquitin-immunoreactive skein-like inclusions in the neostriatum are not restricted to amyotrophic lateral sclerosis, but are rather aging-related structures.

We examined the presence of ubiquitin-immunoreactive skein-like inclusions (SLI) in the neostriatum and spinal cord in normal individuals and patients with different neurodegenerative diseases. Ubiquitin-immunoreactive SLI in the neostriatum were observed both in the normal individuals and in the patients with a variety of neurodegenerative diseases. In particular, SLI were frequently seen in normal aged subjects and certain neurodegenerative diseases, such as progressive supranuclear palsy and myotonic dystrophy. In contrast, the occurrence rate of SLI in cases with Pick's disease and multiple system atrophy tended to decrease. On the other hand, SLI in the spinal anterior horn were detected in cases of amyotrophic lateral sclerosis, but not in any cases with other neurodegenerative diseases. SLI in the neostriatum were also identifiable using phosphotungstic acid-hematoxylin and Gomori trichrome staining. Ubiquitin immunoelectron microscopy demonstrated that the SLI in the neostriatum corresponded to bundles of filaments. These features of SLI in the neostriatum were quite similar to those of intracytoplasmic rod-like inclusions (RLI) in the large neurons of caudate nucleus, which were first described by Kojima and Ogawa in 1974. Our findings indicate that SLI in the neostriatum are ubiquitin-related structures whose occurrence increases by aging, and less frequently accompany several neurodegenerative diseases, and are identical to at least some RLI.

Aging↗

PubMed2000

Depletion of glutamate GluR2 receptor-containing neurons in the rat neostriatum by specific immunotoxin.

In the present study, a novel GluR2 receptor-specific immunotoxin was produced. The immunotoxin was produced by conjugation of molecules of trichosanthin, a ribosome inactivating protein, with goat anti-mouse immunoglobulin molecules. The secondary antibody was then combined with a commercially available GluR2 specific primary antibody to form an immunotoxin. The immunotoxins were unilaterally injected either into the neostriatum or into the lateral ventricle of rats. After one week, ipsilateral turning movements were observed after apomorphine treatments in those animals injected by the striatal route. In perfuse-fixed sections of the neostriatum, immunoreactivity for GluR2 was found to decrease in the striatal-lesioned animals. Most of the GluR2-immunoreactive perikarya in the neostriatum, the presumed medium spiny neurons, were depleted. In addition, immunoreactivity for GluR2/3, GluR5/6/7 and NMDAR1 was found to decrease to a different extent in the lesioned neostriatum. The number of GluR1-immunoreactive perikarya in the neostriatum, a group of striatal interneurons, was not affected by the GluR2 lesion. Ventricular administration of the GluR2 immunotoxin however, was found to be less potent. These results demonstrate for the first time that an indirect immunotoxin is useful for immunolesioning. A difference in potency was also observed in different routes of administration. The depletion of GluR2-containing medium spiny neurons in the neostriatum may upset the balance of the output systems of the basal ganglia and has a profound effect in movement control of the animals.

Animals↗