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Biomedical subjects

M F Chesselet

Publications and source records attributed to M F Chesselet.

At least 91 records · Page 5Linked to original sources
PubMed1989

Heterogeneous distribution of polysialylated neuronal-cell adhesion molecule during post-natal development and in the adult: an immunohistochemical study in the rat brain.

A monoclonal antibody raised against the capsular polysaccharides of meningococcus B was used for immunohistochemical studies in the rat brain, with particular focus on the substantia nigra. This antibody recognizes polysialic acid residues specifically associated with the neuronal-cell adhesion molecule, and reacts with the highly sialylated embryonic neuronal-cell adhesion molecule, but not with the weakly sialylated adult form of the molecule. Immunoreactivity to this monoclonal antibody was intense and widespread in the brain of 1-10-day-old hooded rats. Immunolabeling was associated with cell membranes and present in the intersomata space. In sections from 16- and 25-day-old rats, marked heterogeneity in the level of immunostaining appeared among individual brain nuclei. Areas devoid of labeling with the anti-meningococcus antibody still expressed immunoreactivity to a polyclonal anti-neuronal-cell adhesion molecule antibody. This suggests that the loss of immunostaining with the monoclonal antibody did not correspond to a loss of expression of neuronal-cell adhesion molecule, but to a maturation from the embryonic to the adult form of the molecule, occurring at different rates in various brain regions. In 2-month-old rats, immunolabeling with the monoclonal antibody was still present in discrete brain areas, including the substantia nigra, suggesting that the presence of highly sialylated neuronal-cell adhesion molecule outlasts post-natal development in those brain regions. It is proposed that neuronal-cell adhesion molecule associated polysialic residues may play a role in neuronal plasticity in restricted areas of the adult brain.

Aging↗
PubMed1988

In situ hybridization of mRNA for beta-preprotachykinin and preprosomatostatin in adult rat dorsal root ganglia: comparison with immunocytochemical localization.

In situ hybridization histochemistry was used to identify neurons in rat dorsal root ganglia that contained mRNAs encoding beta-preprotachykinin and preprosomatostatin. The distribution of these neurons was compared with the distribution of neurons containing tachykinins or somatostatin, identified using immunocytochemical techniques. Neurons labelled for beta-preprotachykinin mRNA constituted 20% of the total neuronal population and belonged to the small cell class. Neurons labelled for preprosomatostatin mRNA with either RNA or DNA hybridization probes constituted approximately 10% of the total cells and comprised a small cell group that differed in average size from the beta-preprotachykinin labelled population. The distribution of cells containing tachykinin- or somatostatin-like immunoreactive material was identical to the distribution of cells containing the respective mRNAs and, in addition, individual somata in adjacent sections contained both the mRNA precursor and the peptide. These results suggest that for these neuropeptides the sensitivity of the two methods is equivalent and the respective mRNAs and peptides are co-localized in the same neurons.

Animals↗
PubMed1988

Carboxypeptidase H-like immunoreactivity in the striatum of cats and monkeys.

The enzyme carboxypeptidase H was detected by immunohistochemistry in the striatum of adult cats and monkeys. Specific labelling was observed in the neuropil as well as in both medium-sized and large neuronal cell bodies. The distribution of neurons and neuropil expressing immunoreactivity to carboxypeptidase H was examined in relation to the pattern of immunoreactivity to the neuropeptides enkephalin and substance P. Carboxypeptidase H-like immunoreactivity was found both in zones rich and poor in immunostaining for the two peptides, but was usually denser in those striatal areas in which substance P-positive cell bodies are clustered (striosomes). The results further suggest a role for carboxypeptidase H in the metabolism of multiple neuropeptides in vivo.

Animals↗
PubMed1987

Comparative distribution of mRNAs for glutamic acid decarboxylase, tyrosine hydroxylase, and tachykinins in the basal ganglia: an in situ hybridization study in the rodent brain.

Neurotransmitter-related messenger RNAs were detected by in situ hybridization in sections of rat and mouse brains by using 35S-radiolabelled RNA probes transcribed from cDNAs cloned in SP6 promoter-containing vectors. The distribution of messenger RNAs for glutamic acid decarboxylase, tachykinins (substance P and K), and tyrosine hydroxylase was examined in the striatum, pallidum, and substantia nigra. Dense clusters of silver grains were observed with the RNA probe complementary of the cellular messenger RNA for glutamic acid decarboxylase (antisense RNA) over most large neurons in the substantia nigra pars reticulata and medium-sized to large neurons in all pallidal subdivisions. A few very densely and numerous lightly labelled medium-sized neurons were present in the striatum. Among the areas examined, only the striatum contained neurons labelled with the antisense tachykinin RNA. Most of these neurons were of medium size, and a few were large. With the antisense tyrosine hydroxylase RNA, silver grains were found over neurons of the substantia nigra pars compacta and adjacent A10 and A8 dopaminergic cell groups. No signal was observed with RNAs identical to the cellular messenger RNA for glutamic acid decarboxylase or tachykinin (sense RNA). These results show a good correlation with immunohistochemical studies, suggesting that documented differences in the distribution and the level of glutamic acid decarboxylase, tyrosine hydroxylase, and substance P immunoreactivities in neurons of the basal ganglia are related to differences in the level of expression of the corresponding genes rather than to translation accessibility, stability, or transport of the gene products.

Animals↗
PubMed1987

Different effects of electrical stimulation of the mesencephalic and pontine reticular formation on the release of dopamine and acetylcholine in the cat caudate nucleus.

The effects of unilateral electrical stimulation of the pontine (PRF) and mesencephalic (MRF) reticular formation on the release of acetylcholine (ACh) and of [3H]dopamine continuously synthesised from [3H]tyrosine were examined in both caudate nuclei of halothane-anaesthetised cats implanted with push-pull cannulae. Stimulation of PRF led to a prolonged bilateral increase in the release of [3H]dopamine, whereas a significant reduction in [3H]amine release was observed in the ipsilateral caudate nucleus following stimulation of the MRF. Changes in ACh release were also seen, but they seemed to be independent from those in dopamine release: the release of ACh was enhanced markedly in both caudate nuclei following stimulation of the MRF, whereas a more moderate increase in the release of ACh occurred ipsilaterally following stimulation of the PRF. These data indicate that both the MRF and the PRF are involved in the control of dopaminergic and cholinergic transmission in the basal ganglia.

Acetylcholine↗
PubMed1987

Preprotachykinin messenger RNA detected by in situ hybridization in striatal neurons of the human brain.

Sections from postmortem human brain were processed for in situ hybridization histochemistry using a 35S-labelled RNA probe transcribed from a cDNA coding for the human preprotachykinin which contains both substance P and K. Labelled neurons were observed in the caudate nucleus and the putamen but not the cerebellum. The labelled cells were of medium size and their distribution and morphology were compatible with previous data on substance P-like immunoreactivity in the human brain. The results confirm the presence of preprotachykinin mRNA in a subpopulation of striatal neurons in the human and show that in situ hybridization can be used to detect specific neurotransmitter-related mRNAs in postmortem tissue from normal and diseased humans.

Aged↗
PubMed1986

A new enzyme marker for striatal compartmentalization: NADPH diaphorase activity in the caudate nucleus and putamen of the cat.

The distribution of dihydronicotinamide adenine dinucleotide phosphate diaphorase (NADPH diaphorase) was studied by enzyme histochemistry in the striatum of the adult cat. Neurons and neuropil expressing NADPH diaphorase activity were found throughout the striatum. The diaphorase-positive neurons formed a sparse population of medium-sized cells. In the caudate nucleus they were recognized by antisera against somatostatin 14, somatostatin 28(1-12), neuropeptide Y and avian pancreatic polypeptide. The diaphorase activity of the striatal neuropil was characterized by a modular organization that was particularly distinct in the caudate nucleus. This organization was analyzed by comparing the patterns of diaphorase staining with the distribution of acetylcholinesterase activity in adjacent sections. The NADPH diaphorase activity was found to be dense in the acetylcholinesterase-rich matrix of the caudate nucleus, but weak in the acetylcholinesterase-poor compartments known as striosomes. Because of the colocalization of perikaryal NADPH diaphorase activity and somatostatinlike immunoreactivity, a comparison was also made between the distribution of diaphorase staining and immunostaining for somatostatinlike peptide in the striatal neuropil. Both observed striosomal ordering, so that the acetylcholinesterase-poor zones detected in adjoining sections corresponded to regions of low somatostatinlike immunoreactivity as well as low NADPH diaphorase staining. In some regions striosomes were more clearly delineated in the stains for diaphorase and somatostatinlike suggest that NADPH diaphorase may be a sensitive marker for the somatostatinergic neuropil as well as the somatostatinergic perikarya of the striatum, and that this enzyme could prove valuable in attempts to differentiate the processes of intrinsic somatostatin-containing fibers from any extrinsic somatostatin afferents that may exist.

Acetylcholinesterase↗
PubMed1986

Striatal neurons expressing somatostatin-like immunoreactivity: evidence for a peptidergic interneuronal system in the cat.

Neurons expressing immunoreactivity to antisera against somatostatin 14 and other somatostatin-related peptides were identified in the striatum of cats and nonhuman primates. In each species, immunoreactive neurons were distributed singly and in small groups in the caudate nucleus, putamen and ventral striatum. A detailed study was made of somatostatin-positive neurons and neuropil in the caudate nucleus of the cat. First, the mean diameters and surface areas of neurons expressing immunoreactivity to somatostatin 14 were made from peroxidase-antiperoxidase stained material. Second, fluorescence immunohistochemistry was combined with retrograde labeling of striatal neurons to determine whether such somatostatin 14-positive neurons emit axons projecting out of the striatum. Third, the distributions of neurons and neuropil expressing immunoreactivity to somatostatin 14 or somatostatin 28 (1-12) were plotted in relation to the locations of acetylcholinesterase-poor zones ("striosomes") visible in adjoining sections. The morphometric analysis suggested that somatostatin 14-positive neurons in the caudate nucleus form a single population of medium to medium-large neurons having mean diameters of 20 micron and mean surface areas of 154 micron2. The retrograde tracer study suggested that these somatostatin 14-positive neurons are interneurons. Injections of fast blue into all of the known targets of striatofugal fiber projections failed to label somatostatin 14-positive neurons save in a few instances (less than 0.3% of more than 4000 neurons) in each of which labeling was equivocal. Analysis of the distribution of somatostatin-positive neurons and neuropil in the striatum demonstrated that both observe striosomal ordering. Somatostatin immunoreactive neuropil was dense outside and weak inside identified striosomes, and most immunoreactive neurons lay outside. Often somatostatin-positive neurons lay beside, and sometimes striosomes partly rimmed them. The processes of such neurons tended to run along the borders of the striosomes without crossing them, but occasionally single processes and rarely entire dendritic trees crossed from one compartment to the other. These results suggest that, in the striatum of the cat, somatostatin is present: (1) in fibers organized according to the compartmental distribution already recognized for other neurochemical compounds in the striatum as well as for its afferent and efferent systems, and (2) in interneurons, mostly present in the extrastriosomal matrix, but also located near striosomes, where they could serve as interfaces between the striosomes and extrastriosomal matrix.

Animals↗
PubMed1984

Compartmental distribution of striatal cell bodies expressing [Met]enkephalin-like immunoreactivity.

Striatal cell bodies and fibers expressing [Met]enkephalin [( Met]Enk)-like immunoreactivity were studied with two variants of the peroxidase-antiperoxidase method in normal primates and cats and in cats pretreated with colchicine. Strikingly different patterns of [Met]Enk-like immunoreactivity were observed, both in fiber and cell body immunostaining, depending on the technical protocols followed; no single histochemical protocol fully revealed the compartmentalization present. In the dorsal striatum, patches of [Met]Enk-positive neuropil, known to line up with the acetylcholinesterase-poor striatal zones called striosomes, appeared in sections treated by protocols favoring fiber immunostaining. In sections stained by procedures favoring perikaryal staining, the striosomes appeared as Enk-poor patches in a field of immunoreactive cells and neuropil. When cell-body staining was enhanced by pretreatment with colchicine, cells expressing [Met]Enk-like immunoreactivity appeared both in and out of striosomes, and the striosomal neuropil appeared Enk-rich. These results suggest that there are subtypes of Enk-positive neurons in the striatum, including a "colchicine-dependent subtype" in dorsal striosomes, and suggest that the Enk-positive striatal neuropil is also made up of different components. Immunospecificity of this dorsal striosomal system was further demonstrated by the finding that neurons expressing intense immunoreactivity to substance P and to dynorphin B were largely confined to striosomes.

Acetylcholinesterase↗
PubMed1983

Local and distal effects induced by unilateral striatal application of opiates in the absence or in the presence of naloxone on the release of dopamine in both caudate nuclei and substantiae nigrae of the cat.

Halothane-anesthetized cats implanted with push-pull cannulae in both caudate nuclei (CN) and substantiae nigrae (SN) were used to study the effects of naloxone and various opiates when applied into the left CN on the release of newly synthetized tritiated dopamine (DA) from nerve terminals and dendrites of the two nigro-striatal dopaminergic pathways. In all cases, the drugs (naloxone, opiates alone or in the presence of naloxone) were applied for 30 min into the left CN. When applied alone, naloxone (10(-6) M) induced a delayed reduction in tritiated DA release both in the ipsilateral and contralateral CN. These effects were seen after removal of the drug from the superfusion fluid. Complementary experiments made with tritiated naloxone (10(-6) M) revealed that the contralateral effect on DA release was not due to a diffusion of the opiate antagonist from its application site. Locally, D-Ala2, Met-enkephalinamide (D-Ala2, Met-Enk, 10(-6) M) and the potent delta agonist Tyr-D-Ser-Gly-Phe-Leu-Thr (DSThr, 5 X 10(-8) M) induced a biphasic increase in tritiated DA release. The local changes in tritiated DA release evoked by morphine (10(-6) M) and mu agonists such as Tyr-D-Ala-Gly-NH-C6H13 (10(-8) M) and fentanyl (10(-8) M) differed from those of delta agonists and furthermore differed from each other. For instance, morphine induced a delayed increase in tritiated DA release whereas a biphasic increase followed by a delayed inhibition occurred with fentanyl. Among all the opiates tested D-Ala2-Met-Enk was the only one which elicited a distal effect, that is a reduction of tritiated DA release in the ipsilateral SN. Marked differences in these opiates' effects on tritiated DA release occurred both locally and in distal structures when opiates were applied simultaneously with naloxone (10(-6) M). Locally, the changes induced by mu agonists were particularly altered since during morphine's application with naloxone a reduction of tritiated DA release occurred. In addition, the opiate antagonist prevented the second increase and the delayed inhibition of tritiated DA release evoked by fentanyl (10(-8) M). Interestingly, the combined application of naloxone with either D-Ala2, Met-Enk (10(-6) M), DSThr (5 X 10(-8) M) or morphine (10(-6) M) resulted in the appearance of changes in tritiated DA release in contralateral structures. The most striking effect was seen with D-Ala2, Met-Enk which enhanced tritiated DA release in the contralateral CN and SN. These results are discussed in the light of the involvement of several types of opiate receptors and of the polysynaptic pathways responsible for the distal changes in dopaminergic transmission.

Animals↗
PubMed1983

GABA in the thalamic motor nuclei modulates dopamine release from the two dopaminergic nigrostriatal pathways in the cat.

Halothane anesthetized cats were implanted with five push-pull cannulae and the release of (3H)dopamine (3H-DA), newly synthetized from (3H)tyrosine, was measured in both caudate nuclei (CN) and substantiae nigrae (SN). GABA was applied by means of one of the cannula in the ventralis medialis (VM) and the adjacent part of the ventralis lateralis (VL) nuclei of the thalamus. Autoradiographic studies performed with (14C)-GABA showed that the diffusion of the amino-acid in our experimental conditions was restricted to a 4.2 mm3 sphere at the tip of the push-pull cannula. Multi-unit activity was recorded both at the site of GABA injection and in the contralateral VM or VL nucleus. During and after a 30-min application of GABA (10(-5) M) in the VM-VL nuclei, neuronal firing was markedly enhanced locally and decreased in the homologous structures, while (3H)DA release increased in both CN and the contralateral SN. No effect was observed in the ipsilateral SN. These results show that thalamic motor nuclei could play a role in the regulation of the activity of the two dopaminergic nigrostriatal pathways and will be discussed in the light of previous data indicating a role of the thalamus in the bilateral regulation of dopaminergic transmission in the basal ganglia.

Animals↗
PubMed1983

Effects of unilateral electrical stimulation of various thalamic nuclei on the release of dopamine from dendrites and nerve terminals of neurons of the two nigrostriatal dopaminergic pathways.

The role of several motor and intralaminar thalamic nuclei in the regulation of dopamine release from terminals and dendrites of the nigrostriatal dopaminergic neurons was investigated in halothane-anaesthetized cats. For this purpose, the effects of the unilateral electrical stimulation of various thalamic nuclei on the release of newly synthesized [3H]dopamine were simultaneously determined in both substantiae nigrae and caudate nuclei using the push-pull cannula method. The electrical stimulation of the motor nuclei was the only one to induce asymmetric changes in the four structures since [3H]dopamine release was enhanced in the ipsilateral caudate nucleus and reduced in the contralateral structure while opposite responses were observed in the corresponding substantiae nigrae. A reduction of [3H]dopamine release occurred in the four structures or only in the contralateral substantia nigra and caudate nucleus following the stimulation of the parafascicularis nucleus and the adjacent posterior part of the nucleus centrum medianum or of the nucleus centralis lateralis and the adjacent paralaminar part of the nucleus medialis dorsalis, respectively. The stimulation of the anterior part of the nucleus centrum medianum, which in contrast to other thalamic nuclei examined, receives few nigral inputs, selectively enhanced [3H]dopamine release in the contralateral substantia nigra. No significant changes in [3H]dopamine release were seen either in the substantiae nigrae or in the caudate nuclei following the stimulation of midline thalamic nuclei. These results indicate that the motor and intralaminar thalamic nuclei exert multiple and selective influences on the release of dopamine from terminals and/or dendrites of the dopaminergic neurons. They also further support a role of thalamic nuclei in the transfer of information from one substantia nigra to the contralateral dopaminergic neurons. The possible involvement of connections between paired thalamic nuclei was underlined by the observations of evoked potentials in contralateral homologous nuclei following unilateral stimulation of motor, or some intralaminar, nuclei. The present report provides new insights on the mechanisms contributing to the reciprocal and/or bilateral regulations of nigrostriatal dopaminergic pathways.

Animals↗
PubMed1983

Somatostatin regulates dopamine release in rat striatal slices and cat caudate nuclei.

The effects of somatostatin on the release of tritiated dopamine (DA) formed continuously from tritiated tyrosine were studied in vitro in superfused striatal slices and in vivo in both caudate nuclei and both substantiae nigrae of halothane-anesthetized cats using a push-pull cannula technique. Somatostatin (3 X 10(-10) to 3 X 10(-7) M) increased the spontaneous tritiated dopamine release from rat striatal slices. This effect was dose dependent and was completely prevented by tetrodotoxin (5 X 10(-7) M). When applied for 30 min in one cat caudate nucleus, somatostatin (10(-7) M) immediately increased the local release of tritiated DA, while a gradual inhibition of the tritiated amine's efflux was observed in the contralateral caudate nucleus. No changes in tritiated dopamine were seen in either substantia nigra during or after the peptide's application in the caudate nucleus. These results suggest that somatostatin in the striatum may play a role in the local and the distal control of dopamine release from the terminals of dopaminergic nigrostriatal neurons.

Animals↗
PubMed1982

Striatal dopamine release in vitro: a beta-adrenoceptor-regulated response not mediated through cyclic AMP.

The effects of (-)isoproterenol (10(-6) M), dibutyryl cyclic AMP (10(-3) M), and the phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine (IBMX) (10(-4) M) on in vitro [3H]dopamine ([3H]DA) efflux and synthesis were studied in rat striatal slices continuously superfused with [3H]tyrosine. The beta-adrenoceptor agonist (-)isoproterenol induced an immediate and significant facilitation of [3H]DA efflux but did not alter [3H]DA synthesis as measured by [3H]H2O formation. In contrast, both dibutyryl cyclic AMP and IBMX enhanced [3H]DA synthesis as well as efflux. The presence of IBMX in the superfusing medium did not potentiate the augmentation of [3H]DA efflux caused by (-)isoproterenol. Additionally, the blockade of [3H]DA synthesis by alpha-methyl-p-tyrosine (10(-4) M) completely prevented the action of dibutyryl cyclic AMP on [3H]DA efflux. However, under similar conditions, (-)isoproterenol was still able to increase [3H]DA efflux. The results suggest that (-)isoproterenol can modify striatal DA release through a mechanism not involving cyclic AMP.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Modulation of dopamine release in rat striatal slices by delta opiate agonists.

The effects of various opiates on the spontaneous release of [3H]dopamine ([3H]DA) continuously formed from [3H]tyrosine has been studied in rat striatal slices. Morphine (5 x 10(-6) M), fentanyl (5 x 10(-8) M) and the tripeptide Tyr-D-Ala-Gly-NH-CH(CH3)CH2-CH(CH3)2 (10(-6) M) were without effect, whereas D-Ala2-Met-enkephalinamide (3 x 10(-7) to 10(-5) M), D-Ala2-D-Leu2-enkephalin (5 x 10(-9) M) and the hexapeptide Tyr-D-Ser-Gly-Phe-Leu-Thr (10(-7) M) enhanced [3H]DA release in vitro. The D-Ala2-Met-enkephalinamide stimulation of [3H]DA release was not accompanied by any increase in [3H]DA synthesis and persisted in the presence of tetrodotoxin (5 x 10(-7) M). Naloxone (5 x 10(-7) M) completely blocked the effect of Tyr-D-Ser-Gly-Phe-Leu-Thre (10(-7) M) on [3H]DA release. However, the opiate antagonist did not affect the action of the hexapeptide or of D-Ala2-Met-enkephalinamide when used at a concentration equal to or lower than the agonist. This suggests that both peptides act on opiate receptors having a low sensitivity to naloxone. According to these various results and to the pharmacological characteristics of the opiates tested as described in peripheral organs or in the brain, it is concluded that opiates acting on delta opiate receptors may presynaptically regulate the release of DA in the striatum.

Animals↗