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A Nieoullon

Publications and source records attributed to A Nieoullon.

At least 19 recordsLinked to original sources
PubMed1992

Behavioral effects of modulators of ATP-sensitive K+ channels in the rat dorsal pallidum.

The effects of the potent ATP-sensitive K+ channel blocker glipizide were measured on the locomotor activity of rats after bilateral intracerebral administration into the dorsal pallidum. Glipizide (10 pmol) was found to reduce spontaneous locomotor activity measured during the night cycle of the rats, whereas the ATP-sensitive K+ channel activator (-)-cromakalim (5 fmol) enhanced spontaneous locomotor activity. Glipizide (0.5, 2.5 and 10 pmol) was also found to depress noticeably d-amphetamine-induced locomotor activity (1 mg/kg s.c.). These results are in agreement with the idea that ATP-dependent potassium channels within the dorsal pallidum are involved in controlling motor activity in the rat.

Adenosine Triphosphate↗
PubMed1992

Cellular interactions in the striatum involving neuronal systems using "classical" neurotransmitters: possible functional implications.

The neostriatum contains a wide variety of neuroactive substances associated with several well-defined functional neuronal systems. This structure, which is the seat of numerous neurological pathological disorders, is commonly used as a model for studying the basic mechanisms of neurotransmitter interactions in the brain and their putative involvement in striatal functions. Increasing interest has been focusing lately on the cellular interactions that may occur between the corticostriatal putatively glutamatergic system and the nigrostriatal dopaminergic input. Current evidence suggests that the activatory corticostriatal glutamatergic input may play a more crucial role in regulating striatal functions than was formerly assumed in comparison with the dopaminergic input. The key role of cholinergic interneurons in the striatum may therefore be attributable to the fact that they modulate the glutamatergic transmission to GABA striatal efferent neurons. Likewise, dopamine may actually act indirectly in the striatum by "tuning down" the cortical excitation of striatal neurons. Consequently, an impairment of the dopaminergic transmission such as that occurring in Parkinsonism may lead to an increase in the corticostriatal glutamatergic transmission, which may further contribute towards reinforcing the "imbalance" between subsets of striatal neuronal systems controlling the output of the basal ganglia.

Animals↗
PubMed1992

Effects of lesion of the cholinergic basal forebrain nuclei on the activity of glutamatergic and GABAergic systems in the rat frontal cortex and hippocampus.

The effects of cholinergic basal forebrain lesions on the activity of the glutamatergic and GABAergic systems were investigated in the rat frontal cortex and hippocampus. Bilateral quisqualic acid injections in the nucleus basalis magnocellularis (NBM) at the origin of the main cholinergic innervation to the neocortex induced a cholinergic deficit in the cerebral cortex 15 days later, as shown by the marked selective decrease in cortical choline acetyltransferase (CAT) activity observed. Concurrent alterations in the kinetic parameters of high affinity glutamate uptake consisting mainly of a decrease in the Vmax were observed in the cerebral cortex. These changes presumably reflect a decreased glutamatergic transmission and provide support for the hypothesis that cortical glutamatergic neurons may undergo the influence of cholinergic projections from the NBM. Surprisingly, similar alterations in the glutamate uptake process were found to occur at hippocampal level in the absence of any significant change in the hippocampal cholinergic activity. These data indicate that the NBM may contribute to regulating hippocampal glutamatergic function without interfering with the hippocampal cholinergic innervation that mainly originates in the medial septal area-diagonal band (MSA-DB) complex. No change in parameters of GABAergic activity, namely the glutamic acid decarboxylase (GAD) activity and high affinity GABA uptake, were observed in any of the structures examined. In a second series of experiments involving bilateral intraventricular injections of AF64A, marked survival time-dependent decreases in CAT and high affinity choline uptake activities but no significant change in the high affinity glutamate uptake rate were observed in the hippocampus. No significant change in either parameters of cholinergic activity or in the glutamate uptake was concurrently observed in the cerebral cortex. The GABAergic activity was again unaffected whatever the survival time and the structure considered. Taken as a whole, these data suggest that basal forebrain projections originating in the NBM may play a major role in regulating glutamatergic but not GABAergic function in both the cerebral cortex and the hippocampus; whereas the glutamatergic and GABAergic activities in these two structures may not be primarily under the influence of the cholinergic projections from the MSA-DB complex.

Animals↗
PubMed1992

Early and widespread normalization of dopamine-neuropeptide Y interactions in the rat striatum after transplantation of fetal mesencephalon cells.

Graft-to-host interactions were examined at cellular level, by measuring changes in the immunoreactivity of striatal interneurons expressing neuropeptide Y after dopamine denervation and transplantation of fetal mesencephalon neurons into the striatum of adult rats. Mesencephalic cell suspensions were implanted unilaterally into the dorsal part of the striatum in rats two weeks after intranigral injection of 6-hydroxydopamine. One month and three to four months later, rats showing abolition of amphetamine-induced turning were perfused. Serial brain sections containing intrastriatal grafts were treated for tyrosine hydroxylase and neuropeptide Y immunocytochemistry, and neuropeptide Y-immunoreactive neurons were quantified in various parts of the striatal surface and compared with the striatum of controls and age-matched rats with lesions. Biochemical analyses of dopamine and dihydroxyphenyl acetic acid tissue levels and [3H]dopamine uptake were also performed on striatal samples from similar groups of normal, lesioned and transplanted rats. As early as one month post-grafting, a complete reversal of the increase in the number of neuropeptide Y-immunoreactive neurons occurring after 6-hydroxydopamine lesion was observed in dopamine-grafted animals, although a partial restoration of the tyrosine hydroxylase immunostaining and a recovery of 8% dopamine tissue level were observed in the striata of grafted as compared to normal rats. This effect on the host immunoreactivity was found to be specific to dopamine grafts, since no reversal was observed in sham-spinal cord-transplanted rats. Moreover, similar degrees of normalization were recorded either in the total striatum, or in the area immediately adjacent to the graft, or even in the zone most sensitive to dopamine denervation in terms of neuropeptide Y immunoreactivity. No more pronounced functional effects were observed three to four months after transplantation. These data suggest that grafted dopamine neurons are able to induce rapid and extensive host responsiveness, possibly by means of mechanisms involving synaptic and diffuse release of dopamine and adaptive changes in the host brain. These data may provide a cellular basis for interpreting larger behavioural recoveries than those expected to occur with dopamine grafts in view of the partial restoration of the dopaminergic innervation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Ultrastructural relationships between choline acetyltransferase- and neuropeptide y-containing neurons in the rat striatum.

The relationships between cholinergic and neuropeptide Y-containing neuronal systems in the rat striatum were examined using a dual immunoperoxidase labelling method. These neurons were identified by their immunoreactivity to choline acetyltransferase and neuropeptide Y, respectively, and were visualized on the same sections using 3,3'-diaminobenzidine and benzidine dihydrochloride as distinct chromogens under two conditions: (i) neuropeptide Y detection by the 3,3'-diaminobenzidine diffuse brown reaction product and choline acetyltransferase detection by the benzidine dihydrochloride blue, granular reaction product; (ii) choline acetyltransferase detection by 3,3'-diaminobenzidine and neuropeptide Y detection by benzidine dihydrochloride. Although both neuropeptide Y- and choline acetyltransferase-immunoreactive cell bodies were simultaneously detected and were easily distinguishable whatever the conditions used, neuropeptide Y- and choline acetyltransferase-immunoreactive dendrites and axons could not be visualized on the same sections, since only the diaminobenzidine-labelled processes were detectable. Light microscopic observations on sections dual labelled with either method confirmed that choline acetyltransferase and neuropeptide Y immunoreactivities were localized in morphologically different populations of striatal neurons scattered throughout the striatum, choline acetyltransferase immunoreactivity being associated with large neurons and neuropeptide Y immunoreactivity with medium-sized neurons. In addition, the choline acetyltransferase-immunoreactive neurons were found to be more numerous than the neuropeptide Y-immunoreactive neurons and to be prevalent in the dorsolateral areas of the striatum, whereas neuropeptide Y-immunoreactive neurons were preferentially found in the ventromedial areas of this structure. Electron microscopic observations on sections processed under either condition revealed that choline acetyltransferase-positive terminals form synaptic contacts of the symmetrical type with neuropeptide Y-positive somata and proximal dendrites and that choline acetyltransferase-positive neurons are contacted by neuropeptide Y-positive terminals. These data show that the striatal neuropeptide Y- and choline acetyltransferase-containing neuronal systems have reciprocal synaptic interactions and provide morphological support for the hypothesis that striatal cholinergic and neuropeptide Y interneuron activities may be functionally linked.

3,3'-Diaminobenzidine↗
PubMed1992

Intracerebroventricular administration of neuropeptide Y affects parameters of dopamine, glutamate and GABA activities in the rat striatum.

The effects of intracerebroventricular (ICV) injection of neuropeptide Y (NPY) on parameters of dopamine (DA), glutamate (Glu) and gamma-aminobutyric acid (GABA) activities were investigated in the rat striatum. NPY (1.17-4.70 nmol) induced a dose-dependent increase in the striatal endogenous DA release monitored in freely moving animals by means of a voltammetric method. Maximal increase was observed about one hour after the peptide injection. This result is consistent with the hypothesis that NPY may influence striatal DA turnover in a facilitatory manner by activating DA release. DA, DOPAC, Glu and GABA endogenous contents as well as 3H-Glu and 3H-GABA synaptosomal high affinity uptakes were examined one hour after NPY ICV administration at the same dose range in chloral hydrate-anesthetized animals. Depending on the NPY dose injected, opposite changes in Glu uptake were observed, suggesting that NPY has a bimodal influence on glutamatergic transmission. The Glu uptake rate increased markedly at 1.17 nmol NPY and decreased at 4.70 nmol, which may reflect an activation and an inhibition of the striatal Glu transmission, respectively. In parallel, the GABA uptake was found to decrease slightly at the higher doses of NPY tested, whereas no significant alteration of the striatal concentrations of either DA, DOPAC, Glu or GABA was observed. These results indicate that NPY may be involved in regulating the activity of nigral dopaminergic and cortical glutamatergic afferent pathways and that of intrinsic GABA neurons in the rat striatum.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Effects of riluzole (2-amino-6-trifluoromethoxy benzothiazole) on striatal neurochemical markers in the rat, with special reference to the dopamine, choline, GABA and glutamate synaptosomal high affinity uptake systems.

Riluzole, a new compound with anticonvulsant properties, was found to induce a dose-dependent decrease in the uptake of 3H-dopamine, 3H-GABA and 3H-glutamate into striatal synaptosomes when added to the incubation medium or after in vivo administration, whereas an inhibition of 3H-choline uptake was detected only in the in vitro experiments. Interestingly, riluzole affected 3H-dopamine and 3H-glutamate uptake differentially since 3H-dopamine uptake was found to be more sensitive to the compound. Moreover, riluzole inhibited 3H-dopamine uptake competitively and 3H-glutamate uptake non-competitively, which further suggests that the action of the compound is selective. After in vivo injection, riluzole did not affect the striatal dopamine, DOPAC, serotonin, 5HIAA, glutamate, aspartate or GABA contents. Since this compound was previously reported to induce a decrease in the spontaneous release of glutamate, serotonin, dopamine and possibly acetylcholine, the hypothesis is put forward that riluzole may, at least at high concentrations, have general effects on the striatal nerve terminals affecting both the uptake and release processes. This action may be correlated with the recently identified blocking properties of the compound on the sodium channels, as previously shown for local anaesthetics.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

[Neurobiochemistry of experimental lesions of the basal nucleus of Meynert].

Lesions of the nucleus basalis magnocellularis (of Meynert) in rats induce severe cognitive impairments, in both mnesic and attentional functions. During the last 10 years, many studies tended to establish some relationships between the behavioral and biochemical effects of such lesions. Recent data show that the activity of some peptidergic and glutamaterigic neurons in target areas is modified by cholinergic deafferentation. A new physiological interpretation may be proposed for the associated cognitive deficits.

Alzheimer Disease↗
PubMed1991

Neglect of contralateral visual stimuli in monkeys with unilateral striatal dopamine depletion.

Unilateral lesions of the nigrostriatal dopaminergic system were induced by injecting 6-hydroxydopamine into the substantia nigra of three monkeys trained to initiate arm movements in response to stimuli randomly presented at various locations in their immediate visual space. This procedure resulted in partial reduction of dopamine content, as compared to intact side, in both the putamen and caudate nucleus, with the exception of the putamen in one monkey. A concomitant reduction in the level of dihydroxyphenylacetic acid was observed, but less systematically than the dopamine decrease in the same striatal regions. All monkeys displayed a predominant contralateral arm hypokinesia consisting of a slowness in initiating movements, little or not affected by the hemispace of presentation of the trigger stimulus. Conversely, when the monkeys responded with the arm ipsilateral to the lesion, the movement was initiated more slowly when the trigger stimulus was presented to the hemispace contralateral to the striatal dopaminergic depletion as compared to the ipsilateral hemispace. The results suggest that the visual neglect is more conspicuous when monkeys performed with the arm ipsilateral to the damaged nigrostriatal system. This neglect may be described as a disorder in the ease with which stimuli presented to the side contralateral to the impaired dopaminergic transmission are able to elicit behavioral responses, possibly as the result of a lack of selective attention or defective movement initiation.

Animals↗
PubMed1990

Somatostatin-immunoreactive neurons in the rat striatum: effects of corticostriatal and nigrostriatal dopaminergic lesions.

The present study examined the effects of the impairment of corticostriatal and nigrostriatal dopaminergic transmission on the mean number and the topographical distribution of somatostatin-containing neurons in frontal sections of the rat rostral striatum. These neurons, visualized by an immunohistochemical method using a specific anti-somatostatin(28) antibody were shown to be unevenly distributed; the number of immunoreactive perikarya being consistently lower in the dorsolateral and higher in the middle areas of striatal sections than in the remaining parts of the structure. Such a distribution and number were not altered either by unilateral 6-hydroxydopamine (6-OHDA)-induced lesion of the nigrostriatal dopaminergic neurons after 2- to 3-week survival periods, or by alpha-methylparatyrosine-induced dopamine depletion. In animals with similar 6-OHDA-induced lesions, no change in the striatal concentration of somatostatin measured by radioimmunoassay was observed. These results suggest that somatostatin levels in striatal neurons are not under a dopaminergic influence in contrast to that previously described for neuropeptide Y, although both peptides are thought to coexist extensively in the same striatal neuron population. On the contrary, extensive unilateral frontoparietal ablation of the cerebral cortex elicited, 2-3 weeks later, a significant increase in the mean number of somatostatin-immunoreactive cells per section in the ipsilateral striatum preferentially localized to the dorsolateral zone of the structure with no change in the contralateral side. Data from immunohistochemical studies were further discussed in comparison with results obtained by radioimmunoassay showing that similar cortical lesion induced no change in somatostatin endogenous levels in the ipsilateral striatum and a 30% decreased concentration of the peptide in the contralateral striatum. These data suggest that the corticostriatal pathway influences the expression of somatostatin at either a translational, processing or metabolic level in a topographically restricted population of striatal somatostatin-containing neurons.

Animals↗
PubMed1990

Expression of neuropeptide Y immunoreactivity in the rat nucleus accumbens is under the influence of the dopaminergic mesencephalic pathway.

The density of neuropeptide Y (NPY) immunostained neurons examined in the rat nucleus accumbens (NAcc) was shown to be constant across the anteroposterior extent of the nucleus and did not present any right-left hemispheric difference. Selective unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigral dopaminergic neurons induced, 15 to 21 days later, a bilateral decrease in the NPY neuron density which was, interestingly, more marked in the contralateral than in the ipsilateral NAcc. Dopamine depletion induced by alpha-methylparatyrosine treatment elicited a decrease in NPY neuronal density similar in amplitude to that induced by the 6-OHDA lesion in the ipsilateral NAcc suggesting that similar mechanisms underly both NPY responses. In both experimental conditions, changes in NPY immunostaining were quite homogeneous in the two antero-posterior NAcc portions arbitrarily considered. Apomorphine treatment in animals with 6-OHDA injury completely reversed the ipsilateral lesion effect in the anterior part of the NAcc but only partially the contralateral one. In contrast, no significant effect of apomorphine was observed in either side of the NAcc posterior portion. This data suggests the involvement of at least 2 components in the NPY neuron responses to the lesion. The component reversed by apomorphine treatment was presumed to be directly linked to the DA depletion, while the second component not antagonized by apomorphine was considered independent on DA transmission. These data therefore provide morphological evidence for the occurrence of complex functional interactions between dopaminergic afferents and NPY-containing neurons within the NAcc.

Animals↗
PubMed1990

Changes in striatal cholinergic, gabaergic, dopaminergic and serotoninergic biochemical markers after kainic acid-induced thalamic lesions in the rat.

Kinetic parameters of 3H-choline, 3H-GABA and 3H-dopamine (DA) uptakes in striatal homogenates containing nerve endings were determined 2 to 3 weeks after kainic acid injection into the ipsilateral "centre médian"-parafascicular complex area of the thalamus in the rat. Results showed a marked decrease in 3H-choline uptake concomitant with a selective decrease in Vmax. Data also showed a large decrease in 3H-GABA uptake resulting from a decreased affinity of uptake sites for their substrate. These data were associated with the previously described decrease in choline acetyltransferase and increase in glutamic acid decarboxylase apparent activity, respectively. An apparent marked increase in 3H-DA uptake was likewise measured, mainly related to an increase in Vmax. Determination of serotonin (5HT) and 5-hydroxyindole acetic acid (5HIAA) endogenous contents showed in the deafferented striatum a decrease in 5HT concentrations associated with an increase in 5HIAA levels. Taken together, all these changes in neurotransmitter markers suggest that, directly through the thalamostriatal pathway or indirectly, the thalamus can exert a complex influence on striatal cholinergic and GABAergic neuronal functions as well as on the activity of dopaminergic and serotoninergic striatal afferent fibers.

Animals↗
PubMed1990

Pyridostigmine-induced inhibition of blood acetylcholinesterase (AChE) and resulting effects on manual ocular tracking performance in the trained baboon.

A method was developed to determine the effects of pyridostigmine on sensory-motor control in baboons trained to perform visuo-oculo-manual tracking tasks. The performance was evaluated in terms of accuracy, maximum smooth pursuit velocity, and gain. Administration of pyridostigmine (0.4-0.7 mg/kg intramuscularly) induced a dose-related decrease in smooth pursuit performance which appeared 10 to 30 min after injection and lasted about 1 h. If the animal was allowed to track the target with its hand or to move the target itself, the smooth pursuit performance increased significantly, returning to near normal values. The movement of the hand was not altered. The effect of intramuscular injections of pyridostigmine (0.5 mg/kg) was studied on blood acetylcholinesterase activity in alert baboons. Maximum inhibition of about 60% of baseline activity was observed 10 min after pyridostigmine injection. Subsequently the activity slowly tended to return to control level. Three hours after drug administration, acetylcholinesterase activity inhibition was still 34.1% of control value. In the baboon, the time-course of acetylcholinesterase activity recovery after injection is similar to that recorded in human. The similarity of the time-course of blood acetylcholinesterase activity and changes in smooth pursuit performance suggests a causal relationship between the two factors. A further experiment showed that pyridostigmine administered per os at a dose normally used as a prophylactic against organophosphates does not significantly alter sensorimotor performance as evaluated at the oculomanual tracking system level. When compared to the literature, our results suggest that the baboon can be used as a human experimental analog for pharmacological studies such as the action of acetylcholinesterase inhibitors.

Acetylcholine↗
PubMed1990

Motor impairments and neurochemical changes after unilateral 6-hydroxydopamine lesion of the nigrostriatal dopaminergic system in monkeys.

Unilateral lesions of the nigrostriatal dopaminergic system were induced in five monkeys by intranigral injections of the neurotoxin 6-hydroxydopamine. Following the lesion, all monkeys showed a transient reluctance in using the contralateral forelimb, accompanied, in two monkeys by semi-flexed posture of the disabled forelimb. Three of the monkeys that had been conditioned to perform a visually triggered goal-directed arm movement, showed an increase in latency and duration of contralateral arm movements. Task performance recovered spontaneously to preoperative levels within four months in two monkeys despite significant reductions of endogenous dopamine and dihydroxyphenylacetic acid contents in the caudate nucleus, putamen and globus pallidus ipsilateral to the neurotoxic nigral injection. The third monkey exhibited a persistent increase in movement latency associated with a near complete loss of dopamine in both the putamen and the caudate nucleus. In all cases, an increase the dihydroxyphenyl-acetic acid to dopamine ratio was detected in the striatum and pallidum suggesting a compensatory increase in dopamine turnover in remaining intact dopaminergic nerve terminals. The level of serotonin was changed in all monkeys consisting of either a decrease or an increase, depending on the striatopallidal regions studied. Changes in choline acetyltransferase and glutamic acid decarboxylase activities in the same regions were only seen in some cases. The present results show that 6-hydroxydopamine-induced partial unilateral lesion of nigral dopaminergic neurons produced predominantly contralateral hypokinesia, accompanied by reductions of dopamine content in the ipsilateral striatum and pallidum. The use of this locally applied neurotoxin appears to be a suitable method for investigating neurophysiological mechanisms underlying hypokinesia since deficits in both initiating and executing movements can be expressed independently of other behavioral symptoms. The results show more persistent deficits in starting movements than in their execution and thus suggest that motor initiation is more dependent upon the functional integrity of the nigrostriatal dopamine system than movement completion.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Localization of N-methyl-D-aspartate receptors in the rat striatum: effects of specific lesions on the [3H]3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid binding.

The binding of [3H]3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid ([3H]CPP), a rigid analogue of 2-amino-7-phosphonoheptanoic acid (AP7) and reported to be a selective N-methyl-D-aspartate (NMDA) antagonist, was studied in rat striatal membranes using a centrifugation procedure to separate bound and free radioligand. [3H]CPP bound with high affinity (KD = 272 nM) in a saturable, reversible, and protein concentration-dependent manner. Specific binding was suggested to involve a single class of noninteracting binding sites. The most potent [3H]CPP binding inhibitors tested were CPP, L-glutamate, 2-amino-5-phosphonovalerate, and AP7. NMDA, L-aspartate, and alpha-aminoadipate were also shown to be efficient in inhibiting the binding, whereas quisqualate, D,L-2-amino-4-phosphonobutyrate, kainate, L-glutamate diethylester, and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid were found to be essentially inactive. These data are therefore consistent with the view that [3H]CPP selectively binds to NMDA receptors in the rat striatum. Lesions of intrastriatal neurons using local injections of kainic acid revealed a marked decrease in [3H]CPP binding, suggesting an almost exclusively postsynaptic location of binding sites in the striatum. Conversely, bilateral lesion of corticostriatal glutamatergic fibers resulted in an increased number of [3H]CPP striatal binding sites, providing evidence for a putative supersensitivity response to this striatal deafferentation. Interestingly, lesion of the nigrostriatal dopaminergic neurons using intranigral 6-hydroxydopamine injections resulted, 2-3 weeks later, in a similar increase in the number of [3H]CPP striatal binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1989

Ultrastructural correlates of functional relationships between nigral dopaminergic or cortical afferent fibers and neuropeptide Y-containing neurons in the rat striatum.

This study examines the ultrastructural relationships established by the nigrostriatal dopaminergic and the corticostriatal afferent fibers with neuropeptide Y (NPY)-containing neurons in the rat striatum. By means of dual immunolabeling procedures using peroxidase conjugated F(ab) fragments and 125I-labeled protein A, direct appositions and morphologically defined synaptic contacts of the symmetrical type were visualized between tyrosine hydroxylase-labeled nerve terminals and NPY-labeled neurons. After deafferentation of the striatum from its cortical input direct appositions and asymmetrical synaptic contacts were evidenced between characteristic degenerative boutons and NPY-positive neurons in the striatum. These results suggest that striatal NPY interneurons undergo direct influence from both nigrostriatal dopaminergic and corticostriatal neuronal systems.

Animals↗
PubMed1989

Ultrastructural features of NPY-containing neurons in the rat striatum.

In the present study, we examined the ultrastructure of striatal neurons containing neuropeptide Y (NPY) which were labeled by an immunohistochemical method using peroxidase-conjugated F(ab) fragments in the rat. Each of the 26 neurons identified had a deeply indented oval nucleus. The cytoplasm, which was mainly concentrated at the emergence of the dendrites, contained an abundant Golgi apparatus and a well-developed granular endoplasmic reticulum. Dendrites were poorly branched and rarely exhibited varicosities or dendritic spines. NPY-immunoreactive (Ir) axons were small in diameter and unmyelinated. These features corresponded to a subpopulation of striatal neurons classified as aspiny type IV in previous Golgi studies. Axon terminals forming symmetrical synapses were numerous on the NPY-Ir perikarya and proximal dendrites. On distal NPY-Ir dendrites, synaptic contacts were mainly of the asymmetrical type, suggesting that NPY neurons are contacted by at least 2 categories of afferent fibers. Several NPY-Ir axonal processes and boutons were found to form symmetrical synapses with dendrites, dendritic spines and perikarya belonging to spiny type neurons. These data were consistent with the view that NPY may act as a neurotransmitter of striatal interneurons. Moreover, the frequent observation of NPY axonal processes in the close vicinity of striatal vessels suggested that NPY might also play a role in the control of cerebral vasomotricity. Thirty hours after intranigral injection of 6-hydroxydopamine to induce a degeneration of nigrostriatal dopamine terminals, some characteristic degenerative boutons were observed in close apposition to NPY-Ir cell bodies, suggesting that NPY neurons are under a direct nigrostriatal dopaminergic influence.

Animals↗