Search PubMed⌕ Search

Biomedical subjects

J Glowinski

Publications and source records attributed to J Glowinski.

At least 343 records · Page 19Linked to original sources
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

Involvement of lateral habenula-dorsal raphe neurons in the differential regulation of striatal and nigral serotonergic transmission cats.

The importance of the lateral habenula-dorsal raphe pathway in the control of in vivo [3H]serotonin release in the cat basal ganglia was examined using the push-pull cannula technique and an isotopic method for the estimation of [3H]serotonin continuously formed from [3H]tryptophan. [3H]Serotonin was measured in both caudate nuclei and substantiae nigra and, in some cases, in the dorsal raphe. Electrical stimulation of the lateral habenula decreased [3H]serotonin release in all structures studied. Blockade of the GABA inhibitory pathway to the lateral habenula by the local application of picrotoxin reduced [3H]serotonin release in both substantiae nigra and increased release of the 3H-amine in the dorsal raphe but was without effect on [3H]serotonin release in either caudate nucleus. This inhibition of nigral [3H]serotonin release was antagonized by simultaneous application of picrotoxin to the dorsal raphe. Substance P delivery to the dorsal raphe produced the same effects on [3H]serotonin release as described for picrotoxin application to the lateral habenula except that inhibition of nigral [3H]serotonin release was not prevented by local co-administration of picrotoxin. These results suggest that the lateral habenula can control serotonergic transmission in the basal ganglia and that this regulation may be different for those serotonergic neurons innervating the caudate nucleus versus those projecting to the substantia nigra.

Animals↗
PubMed1982

Specific binding of an immunoreactive and biologically active 125I-labeled substance P derivative to mouse mesencephalic cells in primary culture.

Binding characteristics of 125I-labeled Bolton-Hunter substance P ([125I]BHSP), a radioactive analogue of substance P, were studied with mesencephalic primary cultures prepared from embryonic mouse brain. Nonspecific binding represented no more than 20% of the total binding observed on the cells. In contrast, significant specific binding--saturable, reversible, and temperature-dependent--was demonstrated. Scatchard analysis of concentration-dependent binding saturation indicates a single population of noninteracting sites with a high affinity (Kd = 169 pM). Substance P and different substance P analogues were tested for their competitive potencies with regard to [125I]BHSP binding. BHSP itself, substance P, (Tyr8)-substance P, and (nor-Leu11)-substance P strongly inhibited the binding. Good inhibition was also obtained with physalaemin and eledoisin, two peptides structurally related to substance P. When substance P C-terminal fragments were tested for their ability to compete with [125I]BHSP binding, a good relationship was found between competitive activity and peptide length. Regional distribution of [125I]BHSP binding sites was found using primary cultures obtained from different regions of embryonic mouse brain. Mesencephalic, hypothalamic, and striatal cultures had the highest [125I]BHSP binding capacities, whereas cortical, hippocampal, and cerebellar cells shared only little binding activity. Finally, when mesencephalic cells were grown under conditions impairing glial development, [125I]BHSP binding was not affected, demonstrating that binding sites are located on neuronal cells.

Animals↗
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↗
PubMed1981

Involvement of the thalamus in the asymmetric effects of unilateral sensory stimuli on the two nigrostriatal dopaminergic pathways in the cat.

The effects of unilateral sensory stimuli on dopamine (DA) release from nerve terminals and dendrites of the two nigrostriatal dopaminergic pathways were estimated in halothane-anaesthetized cats without or with sagittal transections. In control animals, the electrical stimulation of the right forelimb enhanced DA release in the right caudate nucleus (CN) and decreased DA release in the right substantia nigra (SN). Opposite effects were observed in the contralateral structures. Sagittal transections of the corpus callosum and commissura anterior, or of the mesencephalic decussations or of the thalamic massa intermedia were made to investigate mechanisms involved in the reciprocal regulation of the two dopaminergic pathways. These sections were without effect on the spontaneous release of DA from nerve terminals and dendrites. The transection of the thalamic massa intermedia was the only one which interrupted the asymmetric changes in DA release induced by unilateral sensory stimuli; an increased dendritic release of DA was only seen in the left SN but it was significantly less pronounced than that observed in control cats. The other transections did not prevent the asymmetric changes in DA release evoked by the sensory stimulation. However, the mesencephalic sagittal transection significantly reduced the stimulatory effect on DA release induced in the left SN. These results suggest that the thalamus is involved in the transfer of information implicated in the reciprocal regulation of the two dopaminergic pathways. In the light of electrophysiological data, the role of nigrothalamic neurones in this phenomenon is discussed.

Animals↗
PubMed1981

Activation by stress of the habenulo-interpeduncular substance P neurons in the rat.

Substance P levels were significantly decreased in the ventro-tegmental area and the interpeduncular nucleus of rats submitted for 20 min to electric foot-shocks. Substance P levels in the substantia nigra and in the prefrontal cortex were not affected. These results are discussed in light of the selective activation of the mesocortico-prefrontal dopaminergic neurons induced by this stress situation.

Animals↗
PubMed1981

Opposite changes in dopamine utilization in the nucleus accumbens and the frontal cortex after electrolytic lesion of the median raphe in the rat.

As revealed by the changes in dihydroxyphenylacetic acid (DOPAC) levels and in the DOPAC/Dopamine (DA) ratio, DA utilization was markedly enhanced in the nucleus accumbens and reduced in the prefrontal cortex of rats five days after the electrolytic lesions of the median raphe. These opposite effects were not seen any more seventeen days after the injection. These results suggest that neurones originating from the median raphe and projecting to the ventral tegmental area exert an opposite effect on the activity of DA cells innervating the nucleus accumbens and on those projecting to the prefrontal cortex.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Inhibitory effects of GABA, L-glutamic acid and nicotine on the potassium-evoked release of substance P in substantia nigra slices of the rat.

Rat substantia nigra slices were superfused with a physiological medium containing a diluted substance P (SP) antiserum, bacitracin and serum albumin to measure SP released in superfusates. As shown by measuring the degradation of a SP-labelled derivative incubated with cerebellar slices, this medium prevented the enzymatic inactivation of SP. Potassium (K+, 50 mM) and veratridine (5 X 10(-5) M) stimulated SP release and these effects were respectively prevented in absence of calcium and in presence of tetrodotoxin (5 X 10(-7) M). GABA (5 X 10(-5) M), nicotine (10(-6) M) and L-glutamic acid (5 X 10(-5) M) reduced the K+ (50 mM)-evoked release of SP. In contrast, glycine (5 X 10(-5) M), oxotremorine (5 X 10(-5) M), D-glutamic acid (5 X 10(-5) M) and serotonin (5 X 10(-5) M) were without effect. Pempidine (10(-5) M) prevented the inhibitory effect of nicotine (10(-6) M) on the K+-evoked release of SP. Glutamic acid diethyl ester (10(-4) M) completely abolished the L-glutamic acid-induced inhibition of the K+-evoked release of SP. Picrotoxin (5 X 10(-5) M) did not influence the L-glutamic acid inhibitory effect excluding the intervention of GABAergic mechanisms.

Animals↗
PubMed1981

In vivo evidence for GABAergic control of serotonin release in the cat substantia nigra.

Push-pull cannulae were used for estimating the release of endogenously synthesized [3H]serotonin in both substantia nigra and caudate nuclei of halothane-anaesthetized cats. The unilateral nigral application of GABA (10-5 M) reduced the local release of [3H]serotonin picrotoxin induced an opposite effect. Both treatments failed to modify [3H]serotonin release in the caudate nuclei or in the contralateral substantia nigra. These results suggest that GABAergic neurons innervating the substantia nigra may regulate nigral serotonin transmission. The possibility that such a regulation could be presynaptic (direct or through other nigral neurotransmitters) or related to a change in the activity of the nigro-raphe projection is discussed.

Animals↗
PubMed1981

Dendritic release of dopamine in the substantia nigra.

Dopamine can be released in the substantia nigra for the dendrites of nigrostriatal dopaminergic neurones, to be involved there in the self-regulation of the dopaminergic cells, to control the release of neurotransmitters from nigral afferent fibres and to influence the activity of nigral non-dopaminergic cells.

Afferent Pathways↗