Search PubMed⌕ Search

Biomedical subjects

J Glowinski

Publications and source records attributed to J Glowinski.

At least 289 records · Page 16Linked to original sources
PubMed1985

Vasoactive intestinal polypeptide receptors linked to an adenylate cyclase, and their relationship with biogenic amine- and somatostatin-sensitive adenylate cyclases on central neuronal and glial cells in primary cultures.

The presence of vasoactive intestinal polypeptide (VIP) receptors coupled to an adenylate cyclase was demonstrated on membranes of neurons or glial cells grown in primary cultures originating from the cerebral cortex, striatum, and mesencephalon of mouse embryos. A biphasic pattern of activation was observed in all these cell types, involving distinct high- and low-apparent-affinity mechanisms. The absence of additive effects of VIP and 3,4-dihydroxyphenylethylamine (DA, dopamine), isoproterenol (ISO), and 5-hydroxytryptamine (5-HT, serotonin) suggests that the peptide receptors are colocated with each of the corresponding amine receptors on neuronal membranes of the three structures studied. The nonadditivity between the VIP- and ISO-induced responses on cortical and striatal glial membranes reveals as well a colocation of VIP and beta-adrenergic-sensitive adenylate cyclases on the same cells. A subpopulation of mesencephalic glia could possess only one of the two types of receptors, as a partial additivity of the VIP and ISO responses was seen. In addition, VIP modified the characteristics of the somatostatin inhibitory effect on adenylate cyclase activity of neuronal membranes from the cerebral cortex and striatum but not from those of the mesencephalon. On striatal and mesencephalic glial membranes the somatostatin inhibitory effect was observed only in the presence of VIP. However, as previously seen with ISO, the presence of VIP did not allow the appearance of a somatostatin inhibitory response on cortical glial membranes. This suggests that cortical glia are devoid of somatostatin receptors.

Adenylyl Cyclases↗
PubMed1984

Role of thalamic motor nuclei in bilateral regulation of serotoninergic transmission in cat basal ganglia.

The effects of unilateral application of GABA (10(-5) M) into thalamic motor nuclei (ventralis medialis-ventralis lateralis, VM-VL) on 5-HT transmission in basal ganglia were investigated in halothane-anaesthetized cats implanted with several push-pull cannulae. The release of [3H]5-HT continuously synthesized from [3H]tryptophan was estimated in both caudate nuclei (CN), both substantia nigrae (SN) and in the dorsal raphe nucleus (DRN). [3H]5-HT release was decreased in the two CN and in the two SN but was enhanced in the DRN when GABA was applied into the VM-VL. These results indicate that thalamic motor nuclei are involved in a bilateral regulation of serotoninergic transmission in the basal ganglia.

Animals↗
PubMed1984

Evidence for a dopaminergic innervation of the cat lateral habenula: its role in controlling serotonin transmission in the basal ganglia.

The presence of a dopaminergic innervation of the cat lateral habenula and its possible role in modulating serotonin transmission within the basal ganglia were investigated using both in vitro and in vivo approaches. A high density of [3H]spiroperidol binding sites with similar affinities for domperidone and apomorphine as those present in the cat striatum were found in the habenula. By means of the push-pull cannula technique, a substantial release of [3H]dopamine continuously formed from [3H]tyrosine was detected in the lateral habenula of halothane-anesthetized cats since the amount of [3H]catecholamines was enhanced in the presence of benztropine, an inhibitor of dopamine uptake into dopaminergic nerve terminals. Furthermore, in anesthetized animals with a push-pull cannula implanted in each caudate nucleus and substantia nigra habenular applications of dopamine (10(-7) M) reduced nigral but not striatal release of [3H]serotonin continuously formed from [3H]tryptophan. This change was prevented either by the delivery of domperidone to the lateral habenula or by the blockade of GABAergic transmission (picrotoxin 10(-5) M) in the dorsal raphe. These data support the involvement of habenulo-raphe pathways in the regulation of serotonin transmission in the cat basal ganglia and indicate that dopaminergic inputs to the lateral habenula participate in such a control.

Animals↗
PubMed1984

Distinct commissural pathways are involved in the enhanced release of dopamine induced in the contralateral caudate nucleus and substantia nigra by unilateral application of GABA in the cat thalamic motor nuclei.

The effects of diencephalic or telencephalic commissural sectioning on the changes in [3H]dopamine ([3H]DA) release from nerve terminals (in the caudate nucleus, CN) and dendrites (in the substantia nigra, SN) of the two nigro-striatal dopaminergic pathways induced by the application of GABA (10(-5) M, 30 min) into the left ventralis medialis (VM) or ventralis lateralis (VL) thalamic nuclei were investigated. Experiments were performed in halothane-anesthetized cats implanted with push-pull cannulae in both CN and SN. In unlesioned cats, GABA application into the left VM-VL increased [3H]DA release in both CN and in the contralateral SN confirming previous results. Sectioning of the thalamic massa intermedia only blocked the GABA-induced increase in [3H]DA release in the contralateral SN, the responses in both CN being preserved. Sectioning of the rostral part of the corpus callosum only prevented the GABA-induced increase in [3H]DA release in the contralateral CN, whereas [3H]DA release in the ipsilateral CN and in the contralateral SN was still enhanced. These results suggest that changes in [3H]DA release evoked in both CN and in the contralateral SN by GABA application into the left VM-VL might involve different mechanisms: those observed in the CN result from potent pre-synaptic influences mediated by the bilateral cortico-striatal projections; those induced in the contralateral SN are due to other types of messages involving or passing through the thalamic massa intermedia.

Animals↗
PubMed1984

Non-DA prefronto-cortical efferents modulate D1 receptors in the nucleus accumbens.

Bilateral injections of 6-OHDA in the ventral mesencephalic tegmentum (VMT) destroy the DA afferents of the nucleus accumbens but do not induce any denervation supersensitivity of the D1 receptors in the nucleus accumbens. Because other non-DA afferent fibers might also regulate D1 receptors in that structure, bilateral ablations of the prefrontal cortex were performed. This lesion induced a 55% decrease of [3H]glutamic acid high-affinity uptake activity in the nucleus accumbens. When the prefronto-cortical ablation was performed simultaneously with the bilateral injection of 6-OHDA in the VMT, a marked hypersensitivity of DA-sensitive adenylate cyclase activity was observed in the nucleus accumbens (+52% increase of Vmax and a two-fold decrease of the Kapp for DA) while the ablation of the prefrontal cortex alone induced only a +14% (P less than 0.01) increase of D1 receptors in that structure. These results indicate that the regulation of D1 receptors in the nucleus accumbens is not solely dependent on the presynaptic DA innervation and that other non-DA fibers, such as those of the cortico-nucleus accumbens pathway, might contribute to it.

Adenylyl Cyclases↗
PubMed1984

In vivo release of [3H]GABA in cat caudate nucleus and substantia nigra. II. Involvement of different thalamic nuclei in the bilateral changes induced by a nigral application of muscimol.

The contribution of motor and intralaminar thalamic nuclei to the changes of [3H]GABA release evoked in both caudate nuclei (CN) and both substantia nigra (SN) by a unilateral nigral application of muscimol (10(-6) M) was investigated on halothane-anaesthetized cats. Acute lesions were performed on one side of the thalamus at the level of either the ventralis medialis and ventralis lateralis (motor nuclei) or the centralis lateralis and paralamellar zone of the medialis dorsalis (intralaminar nuclei). The release of [3H]GABA neosynthesized from [3H]glutamine was measured by perfusing continuously a [3H]glutamine-enriched physiological medium through a push-pull cannula implanted in the 4 structures under investigation. After two hours of superfusion, muscimol (10(-6) M) was delivered for 60 min through the nigral push-pull cannula implanted ipsilaterally to the thalamic lesion. Evoked changes of [3H]GABA release were analyzed either in motor or intralaminar nuclei lesioned cats and compared to those observed in intact animals. Whatever the localization of the thalamic lesions was, an increased release of [3H]GABA was elicited locally in the SN and distally in the ipsilateral CN as in intact animals, suggesting that the responses induced ipsilaterally did not require nigro-thalamic pathways. On the contrary, in the contralateral CN changes of [3H]GABA release evoked by the nigral muscimol application were reversed by both types of thalamic lesion. Instead of a decreased release of [3H]GABA observed in intact cats, an increased release of [3H]GABA was detected in lesioned animals. In the contralateral SN, the response was reversed only after the intralaminar nuclei lesion. In this situation nigral muscimol application induced a decreased release of [3H]GABA in contrast to the enhanced release observed in intact and motor thalamic lesioned cats. The parallel increased release of [3H]GABA observed in the contralateral CN and SN in motor thalamic nuclei lesioned cats suggests an activation of the striatonigral cells by the nigral muscimol treatment. The asymmetrical changes of [3H]GABA release measured in the contralateral CN and SN in intact and intralaminar nuclei lesioned cats could indicate a presynaptic modulation of the [3H]GABA release acting either at the CN or the SN levels. The possible pathways involved in the interhemispheric transfer of information originating from one SN to the contralateral basal ganglia components are also discussed.

Animals↗
PubMed1984

Inhibitory influence of the mesocortical dopaminergic system on spontaneous activity or excitatory response induced from the thalamic mediodorsal nucleus in the rat medial prefrontal cortex.

Since the medial prefrontal cortex receives converging projections from the mediodorsal nucleus of the thalamus (MD) and the dopaminergic neurons located in the ventromedial mesenscephalic tegmentum (VMT) the responses of cortical neurons to ipsilateral VMT and MD stimulation (50-150 microA; 0.2-0.5 ms duration) were analyzed in ketamine anaesthetized rats. MD stimulation at 1 Hz blocked the firing of 99% of the spontaneously active cortical units tested (mean latency, 15 ms; mean duration, 182 ms). MD stimulation at 5-10 Hz evoked single spike responses (mean latency, 16 ms) in 80% of the units tested. Ten to 15 days after kainic acid injection into the MD the number of cortical neurons inhibited (1 Hz) or excitated (5-10 Hz was reduced to 57 and 18%, respectively. Following stimulation of the VMT (at a frequency of 1-5 Hz), 85% of cortical neurons showed an arrest of spontaneous firing occurring after a mean latency of 17 ms and lasting 109 ms on the average. Most of the cells displaying the VMT inhibitory effect were excitated by MD stimulation. Moreover VMT stimulation, applied 3-45 ms before that of MD, blocked the excitation induced by MD in 75% of the units tested. After injection of 6-hydroxydopamine into the medial forebrain bundle or intraperitoneal administration of alpha-methyl-paratyrosine (alpha-MpT), the number of units tested responding to VMT stimulation was of 19 and 35%, respectively. Moreover in these treated rats, the proportion of excitatory responses to MD blocked by VMT stimulation was reduced to 5 and 6%.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1984

Biogenic amine-sensitive adenylate cyclases in primary culture of neuronal or glial cells from mesencephalon.

Primary cultures of virtually pure mesencephalic neurons (5 days) or glials (4 weeks) from 14-day-old mouse embryo were obtained using appropriate medium. Membranes prepared from neuronal cells contained mainly serotonin and beta 1-adrenergic-sensitive adenylate cyclases. However, a low but significant classical dopamine-sensitive adenylate cyclase activity (D1 receptor) was detected. Contrasting with the data obtained from a previous study on striatal neurons no adenosine-sensitive adenylate cyclase was found on mesencephalic neurons. Study on the additive effects of the 3 biogenic amines-sensitive adenylate cyclases indicated that: all neuronal cells having dopamine receptors possess beta 1-adrenergic receptors (no additivity); beta 1-adrenergic and serotonin receptors on the one hand, and dopamine and serotonin receptors on the other hand, were coupled with independent adenylate cyclase systems localized either on two different domains of the same cell or on different cells (complete additivity). Membranes prepared from primary mesencephalic cultures of glial cells contained a mixture of beta 1- and beta 2-adrenergic receptor subtypes coupled with an adenylate cyclase (70% and 30%, respectively). No dopamine- or serotonin-sensitive adenylate cyclase was detected on mesencephalic glial cells.

Adenylyl Cyclases↗
PubMed1984

Adaptive reaction of nigral neurons following lesion of their ventromedial-thalamic projection field.

The response of reticulata-nigral neurons to injury of their ventromedial-thalamic (VM) projection was studied in the rat, by the autoradiographic [14C]deoxyglucose method. Electrolytic lesion of the VM induced reversible: reticulata hypoexcitability; and hyporesponsiveness of areas receiving reticulata efferents, to nigral electrical stimulus. The results suggest that distal axonal injury (in the VM) induces reversible rearrangement of functional properties in the nigral parent cells and their uninjured collaterals, as a retrograde reaction.

Afferent Pathways↗
PubMed1984

Pharmacological study on the mixed CCK8/DA meso-nucleus accumbens pathway: evidence for the existence of storage sites containing the two transmitters.

The mixed CCK8/DA meso-nucleus accumbens pathway was used as a model to study the effects of some pharmacological treatments on the two coexisting transmitters. Reserpine (7 mg/kg i.p.), which depletes monoamine vesicles, induced as early as 1 h following its injection a selective decrease (36%) of CCK8 levels in the posterior part of the nucleus accumbens, an area innervated by the mixed CCK8/DA projection. In contrast, this treatment was without effect on CCK8 levels in the anterior nucleus accumbens and the ventral striatum, two areas which contain distinct CCK8 and DA innervations. Apomorphine (5 mg/kg i.p.), which is known to inhibit the firing rate of DA cells, did not block the reserpine- induced decrease in CCK8 levels suggesting that reserpine is acting on CCK8 storage. This mechanism of action was further substantiated by results obtained with alpha-methyl-p-tyrosine (alpha-MpT, 200 mg/kg i.p.) since no change in CCK8 levels was observed 4 h after this treatment. However, a selective decrease (35%) in CCK8 levels was found in the posterior part of the nucleus accumbens 20 h after two successive alpha-MpT injections. This suggested that long-term interruption of DA transmission resulted in an activation of CCK8/DA cells leading to a release of CCK8. The partial effect of reserpine on total CCK8 stores in CCK8/DA fibers suggests that the peptide is distributed in two types of storage compartments, one of them being sensitive to reserpine and possibly corresponding to mixed CCK8/DA vesicles.

Animals↗
PubMed1984

Effects of electrical stimulation of various midline thalamic nuclei on the bilateral release of dopamine from dendrites and nerve terminals of neurons in the nigro-striatal dopaminergic pathways.

The effects of electrical stimulation of midline thalamic nuclei on the release of [3H]dopamine ( [3H]DA) were determined in both substantiae nigrae (SN) and caudate nuclei of halothane-anesthetized cats using the push-pull cannula method. [3H]DA release was increased in the four structures following stimulation of the interanteromedialis nucleus (IAM) but only enhanced in both SN when nucleus reuniens (RE) was stimulated. In contrast, no effect was detected after delivery of the stimuli to nucleus centralis medialis. These results indicate that the anterior part of the thalamic massa intermedia (IAM and RE particularly) is involved in the bilateral regulation of DA release from nerve terminals and dendrites of the nigro-striatal dopaminergic neurons.

Afferent Pathways↗
PubMed1984

Role of the thalamus in the bilateral regulation of dopaminergic and GABAergic neurons in the basal ganglia.

In halothane-anaesthetized cats implanted with several push-pull cannulae the release of dopamine from nerve terminals and dendrites of the two nigrostriatal dopaminergic pathways is shown to be asymmetrically or symmetrically regulated bilaterally when dopaminergic or GABAergic drugs are infused into one side of the nigra. Nigrothalamic GABAergic neurons may intervene in the asymmetrical regulation, as sagittal section of the thalamic massa intermedia blocks the contralateral effects induced by dopaminergic drugs. The role of thalamic nuclei in the bilateral regulation of dopamine and GABA release in the caudate nucleus and substantia nigra is further demonstrated by studies showing that (1) electrical stimulation of thalamic motor nuclei induces bilateral asymmetrical changes in dopamine release resembling the changes evoked by unilateral sensory stimuli or stimulation of cerebellar nuclei; (2) electrical stimulation of intralaminar or some midline thalamic nuclei leads to bilateral (or contralateral) symmetrical changes in dopamine release, some of these effects being comparable to those induced by unilateral stimulation of the motor cortex; (3) unilateral lesions of motor or intralaminar thalamic nuclei reverse the changes in GABA release in the contralateral caudate nucleus or substantia nigra induced by unilateral infusion of muscimol into the nigra; and (4) unilateral infusion of GABA into thalamic motor nuclei induces bilateral symmetrical regulation of dopamine release in caudate nuclei by means of presynaptic facilitatory influences.

Animals↗
PubMed1984

A peptidases-resistant glycosylated analogue of substance P-(5-11). Specificity towards substance P receptors.

Glycosylated analogues of the C-terminal heptapeptide of substance P either free or blocked on the N-terminal glutamine were synthesized in order to develop a metabolically stable peptide that would have an increased specificity for one type of receptor. Of the analogue described, (N-alpha-Boc-beta-D-Glc-p (1----5) Gln) -Gln-Phe-Phe-Gly-Leu-Met-NH2 is highly resistant to degradation on exposure to rat hypothalamic slices. This glycosylated peptide is about one third as potent as substance P in eliciting contractions of the guinea-pig ileum and is almost devoided of affinity for the 125I-Bolton Hunter-SP specific binding sites on rat brain synaptosomes.

Animals↗
PubMed1984

Local cerebral metabolic effects induced by nigral stimulation following ventromedial thalamic lesions. I: Basal ganglia and related motor structures.

The effects of unilateral electrical stimulation of the substantia nigra (SN) were mapped in the extrapyramidal system of conscious rats bearing ventromedial thalamic (VM) lesions, using the quantitative autoradiographic 14C-deoxyglucose method. SN-stimulation in VM-intact rats resulted in metabolic activation within the deep layer of superior colliculus, subthalamic nucleus, ventrolateral thalamus and sensory-motor cortex ipsilaterally, and bilaterally in the reticulata, compacta, centrolateral and ventromedial thalamus, striatum, globus pallidus and entopeduncular nucleus. SN-stimulation 8 days following ipsilateral VM-lesion, induced activation only within the ipsilateral compacta, subthalamic and entopeduncular nuclei and the globus pallidus and in addition, the reticulata bilaterally. However, SN-stimulation 30 days following VM-injury elicited bilateral metabolic activation in all the examined structures. It is concluded that the VM-thalamic nucleus mediates information from one SN to the ipsilateral motor cortex and striatum, as well as to the extrapyramidal components of the contralateral hemisphere. Moreover, due to the plasticity of the central nervous system, one month following the VM-lesion transmission of information from the SN to all the bilateral components of this network is reestablished.

Animals↗