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M F Chesselet

Publications and source records attributed to M F Chesselet.

At least 55 records · Page 3Linked to original sources
PubMed1994

GABA-ergic interneurons of the striatum express the Shaw-like potassium channel Kv3.1.

In addition to numerous GABA-ergic efferent neurons, the striatum contains a subpopulation of fast-firing GABA-ergic interneurons characterized by the presence of immunoreactivity for the calcium-binding protein, parvalbumin. Double-label in situ hybridization with digoxigenin- and radiolabelled cRNA probes was performed on striatal sections of adult rats to identify mRNAs expressed by striatal GABA-ergic interneurons. In the dorsolateral striatum, only parvalbumin mRNA-positive neurons expressed the mRNA encoding the potassium channel Kv3.1, a member of the Shaw family of potassium channels with rapid activation and inactivation kinetics, usually found in fast-firing neurons such as the basket cells of the hippocampus. Colocalization of the parvalbumin and Kv3.1 proteins was confirmed by double-label immunohistochemistry. Parvalbumin mRNA-positive neurons expressed very high levels of the mRNA encoding glutamic acid decarboxylase (Mr 67,000: GAD67) in the dorsolateral striatum. A smaller proportion of double-labelled neurons was found in the ventrolateral striatum. A small number of densely labelled neurons for GAD67 mRNA also expressed the mRNA encoding the dopamine D2 receptor, but none expressed detectable levels of the dopamine D1 receptor mRNA. This indicates major differences in the expression of dopamine receptor mRNA in a majority of GABA-ergic interneurons vs. GABA-ergic efferent neurons of the striatum. The results suggest that distinct molecular characteristics are associated with the distinct electrophysiological properties of striatal GABA-ergic neurons.

Animals↗
PubMed1994

Decreased opsin mRNA and immunoreactivity in progressive rod-cone degeneration (prcd): cytochemical studies of early disease and degeneration.

Opsin mRNA level and immunoreactivity were examined by in situ hybridization and immunocytochemistry in normal and progressive rod cone degeneration (prcd)-affected dogs. In situ hybridization used 35S- and/or 3H-labeled bovine opsin cRNA probes; immunocytochemistry used six monoclonal mouse anti-bovine opsin antibodies (MAb1) that are specific to different regions of the N-terminal, loop v-vi and the C-terminal domains. Optimal labeling and histological resolution at the single cell level were achieved with semi-thin sections of DGD wax-embedded tissues; it was possible to correlate the cytochemical observations with the disease staging in topographically defined regions that exhibited different disease severity. In early disease (stages 0-1), opsin mRNA levels and immunoreactivity were normal. During the transition from disease to degeneration (stage 2), however, opsin mRNA was reduced sharply; it then rapidly became undetectable in late stages of degeneration (stages 3, 4). Reduction of immunoreactivity was seen with all the MAbs in stages 2 and 3, but the degree of reduction varied remarkably in different regions of the protein molecule; immunoreactivity was reduced more in the cytoplasmic regions, particularly in the phosphorylation sites and the far end of the C-terminal domain. In contrast, the epitopes of the N-terminal domain that are located in the intradiscal compartment were better preserved. It is noteworthy that, in stages 2 and 3, many rod cells still survived despite the decrease in the mRNA level and immunoreactivity. The results indicate that early disease in prcd-affected rods is not initiated by a reduction of opsin mRNA or the protein quantity. However, opsin expression disappears in early degeneration and before cell death. The differences in immunoreactivity with disease may result either from alterations in the protein structure or configuration, or from selective loss of epitopes located in the cytoplasmic domains of the molecule.

Animals↗
PubMed1994

Dopaminergic stimulation of subthalamic nucleus elicits oral dyskinesia in rats.

The effects of dopaminergic stimulation of the subthalamic nucleus (STh) on motor behavior were examined in conscious rats. Unilateral infusion of apomorphine (0.1 to 3.2 micrograms) into the STh induced a dose-dependent increase in abnormal, nondirected orofacial movements without altering turning, sniffing, grooming, or rearing behaviors. Orofacial movements elicited by local infusion of apomorphine (1.0 microgram) into the STh were blocked by peripheral administration of the D1 antagonist, SCH 23390 (0.1 mg/kg, sc), but not by the D2 antagonists haloperidol (1.0 mg/kg, sc) or sulpiride (50 mg/kg, sc). Furthermore, coinfusion of SCH 23390 (1.0 microgram), but not sulpiride (5.0 micrograms), with apomorphine (1.0 microgram) into the STh blocked oral dyskinesia. Oral movements could not be reelicited by an infusion of apomorphine into the STh after a kainic acid lesion of the STh. In addition, infusion of apomorphine (1.0 microgram) into sites proximal to but deliberately outside of the STh failed to elicit nondirected oral movements above baseline levels. The results indicate that stimulation of D1 dopaminergic receptors within the STh induces abnormal orofacial movements. This highlights the importance of the dopaminergic input to the STh in the regulation of motor function and suggests that D1 receptor antagonists could prove useful in the treatment of orofacial dyskinesia in humans.

Animals↗
PubMed1994

Pattern of expression of highly polysialylated neural cell adhesion molecule in the developing and adult rat striatum.

In rats, morphological and synaptic maturation of the striatum, a brain area involved in the control of movement and in cognitive behaviour, proceeds for several weeks postnatally. Little is known, however, about the molecular events associated with the final maturation of the striatum. In particular, there is little information on molecules playing a role in cell adhesion, a phenomenon of particular importance for neuronal development. We have examined the time course and topography of expression of the highly polysialylated form of the neural cell adhesion molecule in the rat striatum during postnatal development and in the adult, and compared it to growth-associated protein-43, a marker of axonal growth. As earlier during development [Aaron L. I. and Chesselet M.-F. (1989) Neuroscience 28, 701-710], immunolabelling for polysialylated neural cell adhesion molecule was very intense in the entire striatum at postnatal days 17-19. At postnatal days 21 and 22, loss of polysialylated neural cell adhesion molecule immunoreactivity in the caudal part of the striatum contrasted with the persistence of immunoreactivity at more rostral levels. Most of the striatum was devoid of polysialylated neural cell adhesion molecule immunoreactivity by postnatal day 25. At this age, as well as in the striatum of adult rats, immunolabelling was only observed along the ventricular edge of the striatum. In contrast to polysialylated neural cell adhesion molecule immunoreactivity, immunolabelling for growth-associated protein-43 had reached its adult pattern by postnatal day 17, indicating that polysialylated neural cell adhesion molecule persists beyond the period of major axonal growth. In the adult, an area of stronger growth associated protein-43 immunoreactivity overlapped with the region which retained immunoreactivity to polysialylated neural cell adhesion molecule. The results indicate that, in the developing rat striatum, the neural cell adhesion molecule remains highly sialylated not only during the ingrowth of cortical and nigral inputs but also during the formation of dendritic spine and synaptogenesis. Loss of polysialyated neural cell adhesion molecule occurs at the time of emerging spontaneous activity in cerebral cortex, and precedes the development of mature responses to cortical stimulation and adult membrane properties in a majority of striatal neurons.

Animals↗
PubMed1994

Regulation of mu-opioid receptor mRNA in rat globus pallidus: effects of enkephalin increases induced by short- and long-term haloperidol administration.

The mRNA encoding mu-opioid receptors is expressed in neurons of the globus pallidus, a region of the basal ganglia that receives a dense enkephalinergic innervation from the striatum. The regulation of the mRNAs encoding the opioid peptide enkephalin in the striatum and the mu-opioid receptor in the globus pallidus was examined with in situ hybridization histochemistry following short- or long-term haloperidol treatments, which alter striatal enkephalin mRNA levels. Animals were administered haloperidol daily for 3 or 7 days (1 mg/kg, s.c.) or continuously for 8 months (1 mg/kg, depot followed by oral). Enkephalin and mu-opioid receptor mRNA levels were unchanged after 3 days of haloperidol treatment. In contrast, the enkephalin mRNA level was increased in the striatum, and mu-opioid receptor mRNA levels were markedly decreased in the globus pallidus after 7 days of haloperidol administration. Similar effects were observed in rats treated with haloperidol for 8 months. The results provide the first evidence of regulation of mu-opioid receptor mRNA in vivo.

Animals↗
PubMed1993

Expression of GAD (M(r) 67,000) and its messenger RNA in basal ganglia and cerebral cortex after ischemic cortical lesions in rats.

Glutamic acid decarboxylase (GAD) is present in most efferent neurons of the striatum and in interneurons both in the striatum and the cerebral cortex. We have examined the effects of unilateral lesions of the frontoparietal cortex by thermocoagulation of pial vessels in adult rats on GAD expression in the basal ganglia and in the contralateral cerebral cortex. Levels of GAD were measured in the striatum and its target areas (pallidum and substantia nigra) with radioimmunohistochemistry and an antibody specific for GAD (M(r) 67,000: GAD67); levels of the corresponding mRNA were measured at the single-cell level by in situ hybridization histochemistry with a [35S]RNA probe. Five days after surgery, GAD67 immunoreactivity was markedly increased in striatal target areas on the side of the lesion. In the striatum, increases in immunoreactivity were small at 5 days, larger at 3 weeks, and accompanied by an increase in mRNA levels lasting up to 3 months after surgery. In contrast, in the frontal cortex contralateral to the lesion, levels of labeling for GAD67 mRNA per neuron were decreased 3 weeks and 3 months after surgery. The results suggest that local ischemic lesions of cerebral cortex in adult rats lead to prolonged and opposite alterations in GAD67 synthesis in basal ganglia and contralateral cortex.

Animals↗
PubMed1993

Glutamic acid decarboxylase gene expression in thalamic reticular neurons transplanted as a cell suspension in the adult thalamus.

The goal of the present study was to determine whether alterations in neuronal morphology and connections in thalamic grafts were accompanied by changes in the expression of mRNA encoding glutamic acid decarboxylase (GAD), the key enzyme in the synthesis of GABA, the normal neurotransmitter of neurons of the thalamic reticular nucleus. Cell suspensions of rat fetal tissue containing both thalamic reticular nucleus and ventrobasal primordia were transplanted into the excitotoxically lesioned somatosensory thalamus of adult rats. Levels of messenger RNA (mRNA) encoding GAD (Mr 67,000; GAD67) were measured 7 days to 4 months following transplantation via quantitative in situ hybridization with 35S-radiolabeled antisense RNAs. Expression of GAD67 mRNA in the thalamic reticular nucleus was analyzed in parallel in rat pups between 0 and 30 days postnatally, and in adult animals. As already observed with immunohistochemistry, transplanted neurons of the thalamic reticular nucleus did not group in specific clusters but rather mingled with unlabeled (putatively ventrobasal) neurons. Levels of labelling for GAD67 mRNA per neuron increased over time and reached adult levels during the third week post-grafting, i.e. 2 weeks after the theoretical birthdate of the neurons (grafted at embryonic days 15-16). Similar values were observed and a plateau was reached at similar time points during normal ontogeny. The results suggest that, in contrast to morphology and size of the neuronal cell bodies, gene expression of GAD67 develops normally despite the ectopic location of neurons of the thalamic reticular nucleus in the somatosensory thalamus, the abnormal connectivity and the lack of segregation from non-GABAergic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Paradoxical increase in striatal neuropeptide gene expression following ischemic lesions of the cerebral cortex.

Ischemic lesions of the cerebral cortex occur frequently in humans as a result of stroke. One major consequence of the death of cortical neurons is the loss of excitatory cortical projections to subcortical regions. Little is known, however, about the transsynaptic effect of such lesions on neurotransmitter expression in subcortical structures. We have examined the effects of ischemic cortical lesions on the peptidergic neurotransmitters enkephalin and tachykinins in the striatum, a brain region massively innervated by glutamatergic cortical inputs. The levels of enkephalin and tachykinin mRNAs increased in the striatum of adult rats after thermocoagulation of pial vessels. The effects were more pronounced in the striatal region most heavily innervated by the lesioned cortex but were also observed in other striatal regions and on the contralateral side. Increased gene expression was accompanied by increased immunoreactivity for the two peptides. Elevated levels of enkephalin mRNA were observed up to 3 months after surgery in the ipsilateral striatum. Whereas results of previous studies of acute cortical ablations suggested that excitatory corticostriatal neurons were necessary to maintain normal peptide levels in striatal efferent neurons, the present data indicate that lesions of the same corticostriatal neurons secondary to local ischemia result in a paradoxical transsynaptic activation of neuropeptide synthesis in subcortical structures. This effect may play a role in the functional consequences of cortical strokes and progressive cortical atrophy in humans and may have critical bearing for their treatment and prognosis.

Animals↗
PubMed1992

Comparative distribution of messenger RNAs encoding glutamic acid decarboxylases (Mr 65,000 and Mr 67,000) in the basal ganglia of the rat.

Glutamic acid decarboxylase, the enzyme required for GABA synthesis, exists as distinct isoforms, which have recently been found to be encoded by different genes. The relative expression of messenger RNAs encoding two isoforms of glutamic acid decarboxylase (Mr 67,000 and Mr 65,000) was measured at the single-cell level in neurons of the rat basal ganglia with in situ hybridization histochemistry. Both messenger RNAs were expressed in neurons of the striatum, pallidum, and substantia nigra pars reticulata, but marked differences in the relative level of labelling were observed with the two probes. In striatum, efferent neurons were more densely labelled for the messenger RNA encoding glutamic acid decarboxylase (Mr 65,000) than for the messenger RNA encoding glutamic acid decarboxylase (Mr 67,000), whereas the reverse was observed for GABA-ergic interneurons. Neurons of the entopeduncular nucleus were much more densely labelled for messenger RNA encoding glutamic acid decarboxylase (Mr 65,000) than for messenger RNA encoding glutamic acid decarboxylase (Mr 67,000). In addition, labelling for messenger RNA encoding glutamic acid decarboxylase (Mr 65,000) was higher in the entopeduncular nucleus (internal pallidum) than in the globus pallidus (external pallidum), a structure which expressed similar levels of both mRNAs. In contrast to neurons of the internal pallidum, efferent neurons of the substantia nigra pars reticulata expressed slightly more messenger RNA encoding glutamic acid decarboxylase (Mr 67,000) than that encoding the other isoform of the enzyme. The results suggest a differential expression of the messenger RNAs encoding the two isoforms of glutamic acid decarboxylase in subpopulations of basal ganglia neurons in rats.

Animals↗
PubMed1992

Messenger RNAs encoding glutamate-decarboxylases are differentially affected by nigrostriatal lesions in subpopulations of striatal neurons.

Dopaminergic nigrostriatal neurons constitute one of the major inputs to the striatum, and play a role in the regulation of gamma-aminobutyric acid (GABA) and glutamic acid decarboxylase (GAD), the GABA-synthesizing enzyme, in striatal neurons. The effect of nigrostriatal lesions on the level of expression of messenger RNAs encoding two distinct isoforms of glutamate decarboxylase was examined at the single cell level with in situ hybridization histochemistry. Rats received a unilateral injection of the neurotoxin 6-hydroxydopamine in the substantia nigra and were sacrificed 2 or 3 weeks later. Sections of the striatum were processed for in situ hybridization histochemistry with radiolabeled RNA probes selective for mRNAs encoding glutamate decarboxylase with molecular weights of 65,000 and 67,000, respectively. In addition, immunohistochemistry with a monospecific antibody for the latter glutamate decarboxylase isoform was performed. In agreement with previous reports, we observed increased labeling for the messenger RNA encoding glutamate decarboxylase (M(r) 67,000) in a population of medium-sized striatal efferent neurons normally expressing low levels of this messenger RNA. We now show that this effect occurred in two striatal compartments, the striosomes and the extrastriosomal matrix, and was accompanied by increased immunostaining for the corresponding protein with a monospecific antibody. In contrast, labeling for messenger RNA encoding GAD (M(r) 67,000) was decreased in a population of medium-sized neurons normally expressing high levels of this messenger RNA and corresponding to GABAergic interneurons. Labeling for messenger RNA encoding glutamate decarboxylase (M(r) 65,000) was not modified in the dopamine-depleted striatum. The results show that dopamine depletion differentially affects gene expression for different isoforms of glutamate decarboxylase in distinct subpopulations of striatal neurons in rat.

Animals↗
PubMed1992

Clozapine decreases enkephalin mRNA in rat striatum.

Typical antipsychotic drugs (i.e. haloperidol) induce extrapyramidal movement disorders while 'atypical' antipsychotics (i.e. clozapine) do not. In situ hybridization histochemistry followed by film autoradiography showed that clozapine treatment (20 mg/kg i.p. daily for 28 days) decreased the level of labelling for preproenkephalin mRNA in the striatum of the rat while haloperidol treatment (1 mg/kg i.p. daily for 28 days) resulted in no change compared with controls. The results suggest that these typical and atypical antipsychotic drugs exert differential effects on the enkephalin-containing striatal projection to the globus pallidus, a pathway critical for the expression of extrapyramidal movement disorders.

Animals↗
PubMed1992

Relative sparing of GABAergic interneurons in the striatum of gerbils with ischemia-induced lesions.

Striatal gamma-aminobutyric acid (GABA)ergic interneurons express intense immunoreactivity to glutamic acid decarboxylase (GAD), GABA and parvalbumin. The distribution of these cells in the striatum of gerbils was examined 2-90 days after transient occlusion of the common carotid, a procedure which results in a zone of profound neuronal loss in the dorso-lateral sector of the head of the caudate-putamen (striatum), with relative sparing of somatostatinergic and cholinergic interneurons. Despite a marked decrease in GAD immunoreactivity corresponding to the loss of striatal efferent neurons in this area, isolated neurons expressing intense immunoreactivity to GAD and parvalbumin were still observed in the lesioned area, suggesting that striatal GABAergic interneurons are also relatively spared by ischemic insult in the adult gerbil.

Animals↗
PubMed1992

Effects of nigrostriatal lesions on the levels of messenger RNAs encoding two isoforms of glutamate decarboxylase in the globus pallidus and entopeduncular nucleus of the rat.

The neurotransmitter gamma-aminobutyric acid (GABA) is present in efferent neurons of the striatum and of the pallidum, one of the main striatal target areas. Dopaminergic nigrostriatal neurons play a critical role in the regulation of GABAergic neurotransmission in the striatum. In the present study, we investigated their role in the regulation of glutamate-decarboxylase (GAD) mRNA expression in two divisions of the pallidum in rats: the globus pallidus and entopeduncular nucleus, equivalent to the external and internal pallidum, respectively, of primates. Dopaminergic neurons were lesioned by unilateral injections of 6-hydroxydopamine (6-OHDA) in the substantia nigra of adult rats. Two or 3 weeks after the lesion, frontal cryostat-cut sections of the brain were processed for in situ hybridization histochemistry with 35S-labeled RNA probes synthesized from cDNAs encoding two distinct isoforms of GAD of respective molecular weight 67,000 (GAD67) and 65,000 (GAD65). The number of labeled cells was determined, and intensity of labeling in individual cells was analyzed by computerized image analysis on emulsion radioautographs. In the globus pallidus, the number of labeled neurons and intensity of labeling per cell were increased on the side ipsilateral to the lesion as compared with control rats in sections hybridized with the GAD67 RNA probe. No changes were detected on the side contralateral to the lesion or in the levels of labeling for GAD65 mRNA. Confirming previous data, the level of labeling for GAD65 mRNA was much higher than for GAD67 mRNA in the entopeduncular nucleus of control rats. In rats with a 6-OHDA lesion, labeling for both GAD67 and GAD65 mRNAs was decreased on the side contralateral, but not ipsilateral, to the lesion, as compared with control rats. The results show that lesions of the nigrostriatal pathway in rats affect the levels of mRNAs encoding two distinct isoforms of GAD in neurons of the globus pallidus and entopeduncular nucleus differently. In addition, results in the entopeduncular nucleus further support a bilateral effect of unilateral dopaminergic lesions.

Animals↗
PubMed1992

Effects of quinolinic acid on messenger RNAs encoding somatostatin and glutamic acid decarboxylases in the striatum of adult rats.

The level of expression of mRNAs encoding somatostatin and two isoforms of glutamic acid decarboxylase (Mr 65,000, GAD65 and 67,000, GAD67) was examined by quantitative in situ hybridization histochemistry in the striatum of adult rats after local injections of quinolinic acid. After a 2-week survival period, Nissl strains showed a profound loss of neurons in the injected striata. With a dose of 120 nmol quinolinic acid, the lesioned area was completely devoid of somatostatin mRNA-positive neurons but contained cells expressing nicotinamide adenine dinucleotide-diaphorase activity (a marker of somatostatinergic interneurons in striatum). After 60 nmol of quinolinic acid, the number of neurons expressing somatostatin mRNA in the lesioned area was similar to controls but the level of labeling per neuron was increased. In the lesioned area, labeling for GAD65 mRNA was abolished and labeling for GAD67 mRNA markedly reduced. However, scattered neurons expressing GAD67 mRNA could still be detected. The majority of surviving GABA-ergic neurons expressed immunoreactivity to parvalbumin, a marker for striatal GABA-ergic interneurons. The results show that quinolinic acid induces dose-dependent alterations in the expression of striatal somatostatin mRNA and reveal a relative sparing of GABA-ergic interneurons in the quinolinic acid-lesioned rat striatum.

Acetylcholinesterase↗
PubMed1992

Acute and repeated administration of fluphenazine-N-mustard alters levels of tyrosine hydroxylase mRNA in subsets of mesencephalic dopaminergic neurons.

Changes in striatal dopamine turnover and levels of tyrosine hydroxylase messenger RNA were examined in mice injected with D2 selective doses of fluphenazine-N-mustard, an irreversible blocker of dopaminergic receptors. The animals were killed at different times after acute and repeated injections of the drug and dopamine turnover was assessed by measuring dopamine and its metabolite, dihydroxyphenylalanine, in the striatum. Tyrosine hydroxylase mRNA was measured at the single-cell level in neurons of the substantia nigra pars compacta and the ventral tegmental area with quantitative in situ hybridization histochemistry. Acute treatment with fluphenazine-N-mustard induced an increase in both striatal dopamine turnover and the level of tyrosine hydroxylase mRNA in the substantia nigra but not the ventral tegmental area. After two days of repeated drug injections (twice daily), tyrosine hydroxylase mRNA was decreased in the substantia nigra despite the persistence of an elevated dopamine turnover in the striatum. The decrease in mRNA was still observed after four days of repeated treatment while, at that time, turnover values were not different from control. No changes were observed in the ventral tegmental area. The initial increase in tyrosine hydroxylase mRNA in substantia nigra pars compacta suggests that activation of nigrostriatal neurons triggers a very rapid increase in genomic expression of the enzyme. The following decrease in mRNA levels precedes desensitization to the effects of the drug on dopamine turnover, further illustrating a lack of correspondence between increased neurotransmission and levels of tyrosine hydroxylase mRNA in catecholaminergic neurons of the central nervous system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Clozapine and haloperidol have differential effects on glutamic acid decarboxylase mRNA in the pallidal nuclei of the rat.

The striatum, and one of its targets, the pallidum (globus pallidus and entopeduncular nucleus) are based ganglia nuclei involved in extrapyramidal movement control. Gamma-aminobutyric acid (GABA)ergic neurons of the pallidum may be important for the expression of the effects of agents which alter striatal neurotransmission. In this study, rats were treated once daily for 28 days with either haloperidol or clozapine, two drugs which respectively, do and do not, induce extrapyramidal movement disorders. In situ hybridization histochemistry was used to quantify the levels of labeling for the messenger ribonucleic acid encoding glutamic acid decarboxylase, the main synthesizing enzyme for GABA in neurons of the striatum, globus pallidus, and entopeduncular nucleus. Neither drug treatment altered levels of labeling in the striatum. Haloperidol treatment increased the level of labeling in the entopeduncular nucleus and clozapine treatment increased labeling in the globus pallidus suggesting that these drugs exert different regulatory effects on pallidal neurons.

Animals↗
PubMed1991

Subpopulations of mesencephalic dopaminergic neurons express different levels of tyrosine hydroxylase messenger RNA.

Subpopulations of mesencephalic dopamine containing neurons possess different electrophysiological, pharmacological, biochemical, and anatomical properties. In order to determine whether such differences are related to the regulation of tyrosine hydroxylase, the rate limiting enzyme in the synthesis of catecholamines, the regional distribution of tyrosine hydroxylase messenger RNA in these neurons was examined using in situ hybridization histochemistry. In the mouse, labelling for tyrosine hydroxylase messenger RNA associated with individual neurons was significantly less in the lateral substantia nigra pars compacta than in the medial substantia nigra pars compacta and the ventral tegmental area. A similar pattern of labelling was observed in the rat. Labelling for tyrosine hydroxylase messenger RNA was significantly less in the lateral substantia nigra pars compacta than in medial pars compacta (a densely cellular region), the area dorsal to the medial substantia nigra pars compacta (a less cell dense region), and the ventral tegmental area. Differences in levels of labelling for messenger RNA in mesencephalic dopamine neurons were not related to differences in cell size as measured in sections processed for tyrosine hydroxylase immunohistochemistry. The results suggest that tyrosine hydroxylase messenger RNA is differentially regulated in subpopulations of mesencephalic dopamine neurons, supporting the view that these neurons are physiologically distinct.

Afferent Pathways↗