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Biomedical subjects

J Glowinski

Publications and source records attributed to J Glowinski.

At least 325 records · Page 18Linked to original sources
PubMed1983

Evoked release of proteins from central neurons in vivo.

Push-pull cannulae were implanted in both substantiae nigrae and caudate nuclei of the halothane-anesthetized cat. The release of total protein, acetylcholinesterase, and nonspecific cholinesterases was examined. Following direct application of potassium to one substantia nigra, changes occurred in the local release of total protein and acetylcholinesterase, but not nonspecific cholinesterases; changes also were observed in both caudate nuclei and the contralateral substantia nigra. The local evoked release of acetylcholinesterase and of total protein differed in the extent to which they were calcium-dependent. Control studies suggest that release of these compounds, both spontaneous and evoked, is related, at least in part, to neuronal activity. The significance of the neuronal release of proteins is discussed.

Acetylcholinesterase↗
PubMed1983

Chlordiazepoxide reduces in vivo serotonin release in the basal ganglia of encéphale isolé but not anesthetized cats: evidence for a dorsal raphe site of action.

By using a push-pull cannula technique and an isotopic method for the estimation of [3H]serotonin continuously synthetized from [3H]tryptophan, the effects of a benzodiazepine, chlordiazepoxide, were investigated on the in vivo release of [3H]serotonin in the cat basal ganglia. Chlordiazepoxide injection (10 mg/kg i.p.) decreased striatal and nigral [3H]serotonin release and enhanced the [3H]amine release in the dorsal raphe. These changes were blocked by the continuous superfusion of the dorsal raphe with Ro 15-1788 (10(-5) M), a benzodiazepine receptor antagonist. Chlordiazepoxide (10(-5) M) applied to the dorsal raphe reduced nigral [3H]serotonin release while decreasing [3H]serotonin release locally in the dorsal raphe. Furthermore, the superfusion of serotonergic nerve terminals of the substantia nigra or the caudate nucleus with chlordiazepoxide (10(-5) M) never altered the local release of [3H]serotonin. These data strongly suggest that the (inhibitory) influences exerted by chlordiazepoxide on serotonergic transmission more likely involved cell bodies and/or dendrites rather than terminals of serotonergic neurons. Chlordiazepoxide-induced changes in [3H]serotonin release were only observed in "encéphale isolé" and not in halothane-anesthetized cats. Further experiments revealed that GABAergic neurons of the dorsal raphe could participate to such a differential reactivity of serotonergic cells to chlordiazepoxide. For instance, [3H]gamma-aminobutyric acid release in the dorsal raphe was enhanced by halothane anesthesia. These findings further suggest the possibility that the influence exerted by benzodiazepines on serotonergic transmission, perhaps through a gamma-aminobutyric acid-dependent process, can significantly be involved in the pharmacological actions of these drugs.

Anesthesia↗
PubMed1983

Specific influence of striatal target neurons on the in vitro outgrowth of mesencephalic dopaminergic neurites: a morphological quantitative study.

In previous studies, we have shown that dissociated dopaminergic neurons from embryonic mouse in co-culture with striatal target neurons take up and synthesize dopamine to a greater extent. We now report that striatal target cells influence the morphology of dopaminergic neurons as well. In co-culture, the total length of neuritic arborization visualized by autoradiography is reduced when compared to cultures of mesencephalic neurons alone or to co-cultures with cerebellar cells. Experiments performed in the presence of striatal glial cells at the same density as striatal neurons or with media conditioned with striatal glia or neurons suggest that striatal neurons regulate dopaminergic afferent growth in vitro through specific neuro-neuronal interactions.

Animals↗
PubMed1982

In vivo modulations by GABA-related drugs of met-enkephalin release in basal ganglia of the cat brain.

The influence of the intrapallidal application of GABA-related compounds on the release of Met-enkephalin in the globus pallidus and the caudate nucleus in the two hemispheres was investigated in vivo in the cat. For this purpose, the 4 structures were continuously superfused with an artificial CSF through implanted push-pull cannulae and Met-enkephalin released in superfusates was determined using a specific radioimmunoassay. GABA (10-500 microM) reduced the local release of Met-enkephalin during its application but once the amino acid was removed from the superfusing fluid, an increase in the peptide release was observed. Diazepam (10 microM) induced only an inhibitory effect whereas muscimol (1 microM) stimulated Met-enkephalin release. Opposite changes in Met-enkephalin release were also seen with the GABA antagonists, bicuculline methiodide (1 microM) and picrotoxin (10 microM), suggesting that the local regulation of Met-enkephalin release by GABA related compounds may be mediated by at least two types of GABA receptors. In several cases, the unilateral pallidal application of GABA agonists and antagonists induced significant changes in Met-enkephalin release at distant structures. The most striking effect was observed with diazepam which markedly reduced the peptide release in both caudate nuclei and pallida. These data suggest that GABAergic systems can contribute to some bilateral regulation of striato-pallidal enkephalinergic neurones.

Animals↗
PubMed1982

Long-term local and distal increases in tryptophan hydroxylase activity following intracerebral kainic acid injections in the rat.

The administration of kainic acid (1--2 micrograms) into the right striatum of adult rats resulted in a marked local increase in tryptophan hydroxylase activity (+ 54--106%). This change was significant as soon as on the second day after the treatment and persisted for at least 12 days. In addition, long-lasting elevations of tryptophan hydroxylase activity were also observed in the anterior raphe area, septum and ipsilateral hippocampus and cerebral cortex. In contrast, the intrahippocampal injection of kainic acid (1 microgram) induced a long-term increase in tryptophan hydroxylase activity only in the injected structure. In all cases, the changes in tryptophan hydroxylase activity were associated with significant increases in the Vmax of the enzyme with no alteration of its apparent affinities for tryptophan and the pterin cofactor. Studies of the sensitivity of tryptophan hydroxylase from control and from kainic acid-treated rats to in vitro activating conditions (Ca2+-dependent phosphorylation, partial trypsinization, exposure to sodium dodecyl sulfate) suggest that the intrastriatal injection of the neurotoxin induced a long-lasting activation of the enzyme. These findings indicate that intracerebral injections of kainic acid may be a valuable approach to explore further the mechanisms controlling tryptophan hydroxylase activity in vivo.

Animals↗
PubMed1982

Bilateral asymmetrical changes in the nigral release of [3H]GABA induced by unilateral application of acetylcholine in the cat caudate nucleus.

In halothane anaesthetized cats, a push-pull cannula was implanted into the right caudate nucleus (CN) and in each substantia nigra (SN). The release of [3H]GABA continuously formed from [3H]glutamine was estimated in each structure. Acetylcholine (ACh, 5 x 10(-5) M) added in presence of eserine (5 x 10(-5) M) for 50 min in the right caudate nucleus 2 h after the onset of superfusion with [3H]glutamine, stimulated the [3H]GABA release locally. The effect was biphasic when ACh application was made in the median two-thirds of the structure and it was monophasic and transient when the ACh application was restricted to the lateral part. ACh application in the right caudate nucleus also induced changes in [3H]GABA released in the anterior (pars reticulata) and posterior (pars compacta) parts of both SN. While [3H]GABA release was enhanced in the ipsilateral anterior SN, it was reduced in the contralateral anterior SN. Respective opposite effects were observed in the posterior parts of the ipsi- and contralateral SN. These bilateral asymmetrical changes in [3H]GABA release were not dependent on the site of ACh application in the right caudate nucleus. These results indicate that the facilitation of cholinergic transmission in one caudate nucleus influences in an opposite way the striato-nigral GABA neurones on both sides of the brain.

Acetylcholine↗
PubMed1982

Reduction of dopamine utilization in the prefrontal cortex but not in the nucleus accumbens after selective destruction of noradrenergic fibers innervating the ventral tegmental area in the rat.

The present study was made to determine the role of the noradrenergic (NA) neurons which innervate the ventral tegmental area (VTA) in the regulation of VTA dopaminergic (DA) neurons projecting to the prefrontal cortex and the nucleus accumbens. For this purpose, a 6-hydroxydopamine lesion was made in benztropine pretreated rats medially just above the decussatio of the pedunculus cerebellaris superior in order to specifically destroy the NA fibers innervating the VTA without affecting those projecting to the prefrontal cortex. Seven days later the ratio of DOPAC and DA levels was estimated in the prefrontal cortex and the nucleus accumbens and used as an index of DA utilization. In the lesioned rats the DOPAC/DA ratio was significantly decreased in the prefrontal cortex but not in the nucleus accumbens. These results suggest that the NA neurons which innervate the VTA exert a specific tonic excitatory influence on the mesocortico-prefrontal DA neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Application of L-glutamic acid and substance P to the substantia nigra modulates in vivo [3H]serotonin release in the basal ganglia of the cat.

L-Glutamic acid or substance P were applied to the caudate nucleus (CN) or substantia nigra (SN) and their effects on local, spontaneous, in vivo [3H]serotonin ([3H]5-HT) release as well as [3H]5-HT release in the contralateral CN and SN were studied using cats implanted with push-pull cannulae. L-Glutamic acid (5 x 10(-5) M), when applied to the CN or SN inhibited the local release of [3H]5-HT but did not affect release in the contralateral CN and SN. In the SN, the L-glutamic acid effect was blocked by L-glutamic acid diethylester. Substance P (10(-7) M) applied to the SN induced an increase in [3H]5-HT release that was delayed in onset. Furthermore, [3H]5-HT release was elevated in the contralateral CN immediately upon the application of substance P to the SN. These results suggest that L-glutamic acid and substance P may control 5-HT transmission in the basal ganglia.

Animals↗
PubMed1982

Sensory stimuli differentially affect in vivo nigral and striatal [3H]serotonin release in the cat.

The effect of auditory, visual and peripheral nerve stimulation on in vivo [3H]serotonin release in both caudate nuclei and substantiae nigrae was studied in either awake 'encéphale isolé' or halothane-anesthetized cats. Release of endogenously synthesized [3H]serotonin was estimated in each brain structure, using push--pull cannulae, continuously superfused with [3H]tryptophan. Bilateral and simultaneous application of click noises and light flashes to awake 'encéphale isolé' cats enhanced [3H]serotonin release in both substantiae nigrae but was without effect on striatal [3H]serotonin release. Unilateral, low intensity electrical stimulation of the forepaw of halothane-anesthetized cats diminished [3H]serotonin release in both caudate nuclei and the ipsilateral substantia nigra. No effect was observed in the contralateral substantia nigra. In contrast, high-intensity electrical stimulation of one forepaw increased [3H]serotonin release in the ipsilateral substantia nigra but was without significant effect on release in the other brain areas examined. The results are discussed in light of previously known anatomical data concerning serotoninergic pathways and electrophysiological evidence of the effect of sensory stimuli on serotoninergic neurons. Our findings suggest that serotonin neurons may serve an important function in the integration of sensory information.

Acoustic Stimulation↗
PubMed1982

The striatonigral substance P pathway and dopaminergic mechanisms.

The biosynthesis of 35S-labelled substance P (SP) has been shown in the rat striatum after continuous delivery of [35S]methionine through a push-pull cannula. In vitro and in vivo studies of SP release have demonstrated that release of the peptide depends on nerve activity and is regulated by presynaptic influences. When the 125I-labelled Bolton and Hunter SP derivative was used, specific binding was observed on mesencephalic cells of the mouse embryo in primary cultures and various characteristics of SP receptors could be determined. Finally, the effects of facilitation or prevention of SP transmission in the substantia nigra on the activity of nigrostriatal dopaminergic neurons have been studied in vivo in the cat by measuring dopamine released from nerve terminals and dendrites. The results obtained indicate that the striatonigral SP neurons exert a tonic facilitatory influence on the dopaminergic neurons.

Animals↗
PubMed1982

Long-term development of mesencephalic dopaminergic neurons of mouse embryos in dissociated primary cultures: morphological and histochemical characteristics.

In 13 and 15 day-old mouse embryos mesencephalic dopaminergic neurons could already be visualized at the level of the mesencephalic flexure by tyrosine hydroxylase immunocytochemistry at day 13. At this time, noradrenergic cells in the locus coeruleus area were not detectable. In most in vitro experiments, dissociated mesencephalic cells of 13 day-old embryos were grown in presence of serum. Four approaches were used to identify the dopaminergic neurons in vitro: fluorescence histochemistry of newly taken up exogenous norepinephrine, radioautography after labelling with (3H) dopamine, tyrosine hydroxylase-like immunoreactivity and fluorescence histochemistry of endogenous stores of catecholamines. Control experiments performed at various times in vitro with selective inhibitors of amine transport into dopaminergic, noradrenergic and serotoninergic neurons indicated that only dopaminergic neurons were detected by these various approaches, noradrenergic neurons being virtually absent from the cultures. The uptake of exogenous norepinephrine was detected already 24 h after plating and preceded the appearance of tyrosine hydroxylase-like immunoreactivity (48 h). The number of neurons revealed by these two techniques increased up to 4 and 10 days, respectively. Endogenous stores of dopamine were only seen after three weeks in vitro by fluorescence histochemistry. At this time, the same number of neurons was revealed whatever the method used. The presence of striatal target cells (co-cultures) affected neither the sequential appearance of the markers nor the number of dopaminergic cells. The two main types of dopaminergic neurons (fusiform and multipolar) described in vivo both in the substantia nigra (A9) and the ventral tegmental area (A10) of adult animals were identified in vitro and their development into well-differentiated neurons can be followed for up to six weeks. This in vitro system seems, therefore, to be particularly suitable for biochemical and electrophysiological studies of these dopaminergic neurons.

Animals↗
PubMed1982

In vivo biosynthesis of 35S-substance P from [35S]methionine in the rat striatum and its transport to the substantia nigra.

Rats with a push-pull cannula implanted in the right striatum were used to study the biosynthesis of 35S-substance P (SP) from [35S]methionine and its transport to the ipsilateral substantia nigra. [35S]Methionine was delivered for 2, 3 or 5 h to the push-pull cannula. 35S-SP in striatal and nigral tissues was estimated after immunoadsorption and HPLC. Higher levels of 35S-SP in striatal homogenates were found after a 5-h labelling period. 35S-P biosynthesis was inhibited when cycloheximide was superfused together with [35S]methionine. The identity of 35S-SP was further checked by its conversion into 35S-SP sulphoxide. After a 5-h labelling period, 35S-SP was also recovered in the substantia nigra. This was not the case after hemisection of striato-nigral fibers. When rats were killed 15 or 24 h after the 5-h labelling period, 35S-SP levels in the substantia nigra were higher than those found just after 5-h labelling period, while the reverse was observed in the striatum.

Animals↗