Biomedical subjects

J Glowinski

Publications and source records attributed to J Glowinski.

At least 91 records · Page 5Linked to original sources

PubMed1997

Activity and distribution of superoxide dismutase in the layers of polyester grafts.

The aim of the present study was to evaluate superoxide dismutase (Cu, Zn-SOD) activity in the principal layers of polyester grafts implanted into the abdominal aorta of dogs. The grafts were examined 7 days and 1, 4 and 12 months after the operation. It was found that SOD activity occurred in all polyester graft layers during the whole experiment. The neointima activity ws 1.5-fold lower during the 1st month; with the passage of time, it became 2-fold lower than in the normal aorta (p < 0.01). SOD activity in the medial and outer graft layers behaved similarly: it was lowest after 7 days, increased after 1 month and significantly decreased after 4 and 12 months (p < 0.01). Our study shows that the activity of SOD is low in polyester grafts and it can thus be inferred that protection against the superoxide anion is inadequate.

Animals↗

PubMed1997

Nicotine-induced inhibition of neuronal phospholipase A2.

A protective effect of nicotine against glutamate-induced neurotoxicity has previously been reported in cultured striatal and cortical neurons. The aim of this study was to investigate whether nicotine also inhibits glutamate-evoked arachidonic acid release from cultured striatal neurons. (-)-Nicotine selectively inhibited the release of [3H]-arachidonic acid induced by the joint stimulation of alpha-amino-3-isoxazol-5-propionic acid and metabotropic receptors, whereas the response evoked by the sole activation of N-methyl-D-aspartate receptors remained unchanged. The inhibitory effect of (-)-nicotine was not mediated by nicotinic receptors because it was neither reproduced by acetylcholine (in the presence of atropine) or 1,1-dimethyl-4-phenyl piperazinium, nor reversed by dihydro-beta-erythroidine or hexamethonium, two central nicotinic receptor antagonists. (-)-Nicotine, which induced rapidly desensitizing inward currents in 17% of striatal neurons, did not alter the alpha-amino-3-isoxazol-5-propionic acid-evoked currents. Moreover, (-)-nicotine did not inhibit the accumulation of inositol phosphate derivatives induced by agonists of glutamate metabotropic receptors. In fact, using the fluorogenic phospholipase A2 substrate 1,2-bis-(1-pyrenedecanoyl)-sn-glycero-3-phosphocholine, (-)-nicotine was found to inhibit both particulate and soluble phospholipase A2 activities from striatal neurons. Therefore, (-)-nicotine can modulate a neuronal response (arachidonic acid release) evoked by glutamate but this process is not involved in the neuroprotective effect of the drug on glutamate-induced neurotoxicity.

Animals↗

PubMed1997

Endogenic non-enzymatic antioxidative system of polyester grafts during their healing.

OBJECTIVE: Non-enzymatic low-molecular antioxidants are one of the important mechanisms which protect cells against the toxic effect of oxygen. The aim of the present study was to determine the content of glutathione, glutathione reductase, and ascorbic acid in the principal layers of polyester grafts. INTERVENTIONS AND MEASURES: The experiments were carried out on 24 mongrel dogs, in which polyester double velour DALLON grafts were implanted. Seven days, 1, 4, and 12 months after the operation the grafts were excised. The following were determined: glutathione content by use of a GSH-400 system, glutathione reductase activity by the method of Langdon and Mize, and ascorbic acid content by the Kyaw method. RESULTS: It was found that the glutathione content in the graft neointima was 33% lower, in the graft neomedia higher during the first 4 months, in the neoadventitia 50% lower after 4 months than in the corresponding layers of the aorta (p < 0.01). The activity of glutathione reductase was significantly higher in all the graft layers during 12 months' observation than in the normal aorta layers. The ascorbic acid content of the graft layers was lowest 7 days after the implantation, and then in time increased so that 12 months after the operation it reaches its highest values. CONCLUSIONS: Our study shows that low non-enzymatic antioxidative potential is not capable of proteoting the newly forming graft layers, particularly the neointima, against oxygen toxicity. Thus, it would be beneficial to administer antioxidants (vitamin C, vitamin E, and N-acetylcysteine).

Animals↗

PubMed1996

Stimulatory effect of arachidonic acid on the release of GABA in matrix-enriched areas from the rat striatum.

Arachidonic acid was shown to stimulate the release of preloaded [3H]GABA from microdiscs of tissue punched out in matrix-enriched areas of the rat striatum. This effect, which was calcium- and dose-dependent, persisted in the presence of inhibitors of arachidonic acid catabolism. Other fatty acids were less or not effective. Arachidonic acid also inhibited [3H]GABA uptake into purified striatal synaptosomes, however the arachidonic acid-evoked release of [3H]GABA persisted following inhibition of the GABA neuronal uptake process. The stimulatory effect of arachidonic acid on GABA release may largely result from the activation of a protein kinase C since the arachidonic acid response was reduced by several protein kinase C inhibitors. Arachidonic acid also dose-dependently stimulated the release of preloaded [3H]GABA from purified striatal synaptosomes. Similar results were obtained when synaptosomes were previously incubated with [3H]glutamine to study the release of endogenously synthesized [3H]GABA. Further indicating a direct action of the fatty acid on GABAergic neurons, the arachidonic acid-induced release of [3H]GABA from microdiscs was not modified in the presence of the D1 dopaminergic antagonist SCH23390 or of glutamatergic antagonists. Finally, the release of [3H]GABA evoked by the combined application of NMDA and carbachol (a treatment known to markedly stimulate arachidonic acid formation) was reduced by inhibitors of phospholipase A2 further indicating that endogenously formed arachidonic acid significantly facilitates the release of GABA in the striatum.

Animals↗

PubMed1996

The major astrocytic phosphoprotein PEA-15 is encoded by two mRNAs conserved on their full length in mouse and human.

Specific phosphoproteins are targets of numerous extracellular signals received by astrocytes. One such target, which we previously described, is PEA-15, a protein kinase C substrate associated with microtubules. Two cDNAs differing in the length of their 3'-untranslated region (3'UTR) were cloned from a mouse astrocytic library. Accordingly, Northern blots revealed two transcripts (1.7 and 2.5 kilobase pairs) abundant brain regions but also found in peripheral tissues. PEA-15-deduced protein sequence (130 amino acids) shared no similarity with known proteins but is 96% identical to its human counterpart. In addition, several regions of the 3'UTR share more than 90% identity between mouse and human. Different potential regulatory sequences are found in the 3'UTR, which also completely includes the proto-oncogene MAT1. The high level of conservation of both the coding and the untranslated regions and the differential tissular distribution of the two transcripts of this major brain phosphoprotein suggest that not only the protein but also the 3'UTR of PEA-15 mRNA play a role in astrocytic functions.

Amino Acid Sequence↗

PubMed1996

Mediodorsal thalamic evoked responses in the rat prefrontal cortex: influence of the mesocortical DA system.

The prefrontal cortex (PFC) receives a dopaminergic (DA) innervation from the ventral tegmental area (VTA) and is reciprocally connected with the mediodorsal thalamic nucleus (MD). The present study was performed in anaesthetized rats to determine the influence of the mesocortical DA system on excitatory responses evoked in the PFC by stimulation of MD: (1) short latency (< 4 ms) responses resulting from activation of the MD-PFC pathway; (2) long latency responses (> 10 ms) resulting from activation of recurrent collaterals of PFC neurons projecting to MD. Local DA application and VTA stimulation did not affect short latency responses but blocked long latency responses. These results suggest that the mesocortical DA system inhibits excitations by recurrent collaterals of the PFC-MD neurones but not the excitatory MD inputs to the PFC.

Animals↗

PubMed1996

Astrocytes protect neurons from hydrogen peroxide toxicity.

Recent reports indicate that neurons are particularly sensitive to hydrogen peroxide (H2O2). The present study was undertaken to investigate the putative role of astrocytes in the modulation of the neurotoxic effect of H2O2. The exposure to H2O2 of cultured striatal neurons from mouse embryos induced a concentration-dependent (10-1000 microM) cell death as estimated 24 hr later. Two methods were used to estimate neuronal survival: the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay or an enzyme-linked immunosorbent assay with antibodies directed against an antigen located in neurons (microtubule-associated protein-2). The neurotoxic effect of H2O2 on neurons cocultured with astrocytes was strongly attenuated compared with that observed on a pure population of neurons seeded at the same density. Moreover, the protective effect of astrocytes depended on the astrocytes/neurons ratio, a significant neuroprotection being detectable for 1 astrocyte to 20 neurons. Catalase seems to be the main hydrogen peroxidase activity involved in the neuroprotective effect of astrocytes. Indeed, in the culture conditions used, this enzymatic activity was enriched in this cell type compared with neurons; its inhibition, and not that of glutathione peroxidase, reduced the disappearance rate of the oxidant. On the contrary, glutathione peroxidase appeared to be the main enzymatic activity involved in the neuronal defense against H2O2 toxicity. Therefore, astrocytes could delay neuronal death in pathological situations in which H2O2 has been, at least partially, demonstrated to be involved.

Animals↗

PubMed1996

Prefrontal cortex inputs of the nucleus accumbens-nigro-thalamic circuit.

The functional organization of the cortico-nucleus accumbens-substantia nigra pars reticulata circuit was investigated in the rat using combined anatomical and electrophysiological approaches. The nucleus accumbens neurons which project to the substantia nigra pars reticulata are located in a circumscribed region of the core immediately adjacent and extending dorsally to the anterior commissure. As shown by retrograde and anterograde transports of wheatgerm agglutinin conjugated to horseradish peroxidase, the region of the nucleus accumbens related to the substantia nigra was found to receive bilateral inputs from restricted areas of the medial and lateral prefrontal cortex, i.e., prelimbic/medial orbital and dorsal agranular insular areas. The electrical stimulation of these medial and lateral prefrontal cortical areas induced excitatory responses in nucleus accumbens neurons projecting to the dorsomedial substantia nigra pars reticulata. Interestingly, an important proportion (61%) of the nucleus accumbens-nigral cells responding to the stimulation of the lateral prefrontal cortex were also excited by the stimulation of the medial prefrontal cortex, demonstrating the existence of a convergent influence of these cortical areas on single nucleus accumbens cells. Furthermore, the present data also show that the stimulation of the medial prefrontal cortex results in a powerful inhibition of the tonic firing of the substantia nigra pars reticulata neurons. In conclusion, this study reveals the existence of a functional link between the prefrontal cortex (prelimbic/medial orbital and agranular insular areas) and the nucleus accumbens neurons which innervate the dorsomedial region of the substantia nigra pars reticulata. Since the dorsomedial region of substantia nigra pars reticulata is known to project to subfields of the mediodorsal and ventromedial thalamic nuclei related to the prefrontal cortex, the present data further demonstrate the existence of a prefrontal-nucleus accumbens-thalamo-cortical circuit involving the substantia nigra pars reticulata.

Animals↗

PubMed1996

Distinct regulations by septide and the neurokinin-1 tachykinin receptor agonist [pro9]substance P of the N-methyl-D-aspartate-evoked release of dopamine in striosome- and matrix-enriched areas of the rat striatum.

The effects of septide (a short substance P C-terminal analogue) and of the neurokinin-1 receptor agonist [Pro9]substance P on the N-methyl-D-aspartate (50 microM)-evoked release of [3H]dopamine (continuously synthesized from [3H]tyrosine) were investigated in the absence or the presence of the selective neurokinin-1 receptor antagonist RP 67580 in selected striosome- and matrix-enriched areas of the rat striatum. Experiments were performed in vitro using a microsuperfusion procedure described previously. At a concentration of 0.1 microM, septide and [Pro9]substance P stimulated the spontaneous release of [3H]dopamine in striosome-enriched areas similarly. However, in this compartment, these peptides induced larger and opposite effects on the N-methyl-D-aspartate (50 microM)-evoked release of [3H]dopamine (estimated in the absence of magnesium). Indeed, septide markedly enhanced the N-methyl-D-aspartate response, while [Pro9]substance P largely reduced the N-methyl-D-aspartate-evoked release of [3H]dopamine. Septide also enhanced the N-methyl-D-aspartate response in the matrix, but [Pro9]substance P was without effect. When used alone, at 0.1 or 1 microM, RP 67580 reduced by about 33% the N-methyl-D-aspartate-evoked release of [3H]dopamine in striosome-enriched areas. In contrast, in the matrix, the N-methyl-D-aspartate response was enhanced in the presence of a low concentration of the antagonist, while the higher concentration was ineffective. In striosomes, the reducing effect of [Pro9]substance P and the enhancing action of septide on the N-methyl-D-aspartate response were respectively blocked in the presence of low and high concentrations of RP 67580, while the stimulatory effect of septide on the N-methyl-D-aspartate response in the matrix was prevented with both concentrations of the neurokinin-1 receptor antagonist. Finally, the co-application of [Pro9]substance P (0.1 microM) with septide (0.1 microM) abolished the enhancing effect of septide on the N-methyl-D-aspartate-evoked release of [3H]dopamine in both striatal compartments. Altogether, these results suggest that substance P and eventually one of its metabolites, substance P(6-11) or another endogenous tachykinin released under the action of N-methyl-D-aspartate, contribute to the regulation of [3H]dopamine release in both striatal compartments. They also extend previous observations which allowed us to demonstrate that the local circuits contributing to the presynaptic regulation of [3H]dopamine release differ in striosome- and matrix-enriched areas. Furthermore, in agreement with observations made in some peripheral tissues, the present results support the existence of "septide-sensitive" tachykinin receptors in the rat striatum or alternatively of septide sensitive sites on tachykinin neurokinin-1 receptors distinct from those sensitive to neurokinin-1 receptor agonists, coupled to distinct transducing systems, and thus leading to biological responses which differ from those evoked by neurokinin-1 receptor agonists.

Animals↗

PubMed1996

Reduced glucose metabolism enhances the glutamate-evoked release of arachidonic acid from striatal neurons.

Glucose deprivation potentiates the glutamate receptor-evoked release of arachidonic acid from cultured mouse striatal neurons. In this study we investigated whether this potentiation would be modified by the end-products of glycolysis. These enhanced responses were completely reversed by the addition of increasing concentrations of either lactate or pyruvate. This reversal was not due to increased osmolarity as substituting sucrose for lactate or pyruvate did not mimic their effects. In contrast, in the presence of glucose, neither lactate nor pyruvate was effective. Furthermore, these monocarboxylic acids rescued neuronal respiration in the absence of glucose. Inhibiting glycolysis with iodoacetate in the presence of glucose reproduced the potentiated glutamate-evoked release of arachidonic acid observed following glucose deprivation and reduced neuronal respiration to the same extent as that observed in the absence of glucose. All of these effects were overcome by the addition of either lactate or pyruvate. The reversal of the potentiated glutamate-evoked release of arachidonic acid by lactate or pyruvate was inhibited by a specific inhibitor of monocarboxylic acid transport, alpha-cyano-4-hydroxycinnamic acid, suggesting that lactate and pyruvate act intracellularly. Therefore, we propose that the enhanced release of arachidonic acid evoked by glutamate during glucose deprivation results from reduced glycolysis and hence from a depletion of lactate or pyruvate.

Animals↗

PubMed1996

Cyclothiazide unmasks an AMPA-evoked release of arachidonic acid from cultured striatal neurones.

The joint, but not independent, activation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) and metabotropic glutamate receptors induces liberation of arachidonic acid from cultured mouse striatal neurones. We examined whether blocking AMPA receptor desensitisation with cyclothiazide would modify this response. Cyclothiazide strongly potentiated the combined AMPA/(1 S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD)-evoked release of arachidonic acid (EC50 of approximately 7 microM) but did not modulate the basal, ACPD, or NMDA response. The enhanced liberation of arachidonic acid, observed in the presence of cyclothiazide, was due to the appearance of a genuine AMPA response that was independent of an associative activation of metabotropic receptors. The potentiated and nonpotentiated AMPA responses were inhibited by both competitive [2,3-di-hydroxy-6-nitro-7-sulphamoylbenzo (f) quinoxaline] and 2,3-benzodiazepine noncompetitive (GYKI 53655 and GYKI 52466) receptor antagonists. Cyclothiazide was equally effective at potentiating the AMPA response in either the presence or absence of glucose, suggesting that the increased glutamate-evoked arachidonic acid release observed in these cells under conditions of glucose deprivation is not due to reduced AMPA receptor desensitisation. The enhanced liberation of arachidonic acid measured in the presence of cyclothiazide appeared to result from a large (fourfold) elevation of the AMPA-induced increase in intracellular calcium level. Therefore, an AMPA-evoked mobilisation of arachidonic acid could potentially contribute to non-NMDA receptor-mediated neurotoxicity, which has been observed in neuronal cells in the presence of cyclothiazide.

Animals↗

PubMed1996

Cooperative contributions of cholinergic and NMDA receptors in the presynaptic control of dopamine release from synaptosomes of the rat striatum.

In the presence of magnesium, although ineffective alone, N-methyl-D-aspartate (NMDA, 10(-3) M plus glycine 10(-6) M) stimulated the release of [3H]-dopamine ([3H]-DA) continuously synthesized from [3H]-tyrosine when applied with ACh, the amplitude of the NMDA response being dependent on the ACh concentration. Experiments performed with nicotine, oxotremorine and the antagonists hexamethonium and atropine indicated that both muscarinic and nicotinic receptors are involved in the permissive effect of ACh on the NMDA response. Data obtained in the absence of magnesium or with increasing concentrations of magnesium revealed that the permissive effect of ACh on the NMDA-evoked release of [3H]-DA results from removal of the magnesium block of NMDA receptors. The NMDA-evoked release of [3H]-DA observed in the presence of ACh, nicotine or oxotremorine (10(-3) M) was blocked by either of the protein kinase C inhibitors staurosporine (10(-8) M) and chelerythrine (5 x 10(-7) M). However, these drugs were without effect on responses induced by ACh, nicotine or oxotremorine alone and by NMDA (10(-3) M, in the absence of magnesium). Supporting further the involvement of a protein kinase C activation in the permissive effects of ACh or the cholinergic agonists, NMDA (10(-3) M) stimulated the release of [3H]-DA in the presence of both magnesium and phorbol 12-myristate 13-acetate (10(-6) M) or 1 -oleoyl-2-acetyl-glycerol (10(-4) M), and the NMDA response was markedly potentiated by ionomycin (10(-7) M) used at a concentration that stimulated [3H]-DA release to about the same degree as ACh (10(-4) M). Therefore, besides their depolarizing action, ACh, nicotine and oxotremorine could eliminate the magnesium block of NMDA receptors by activation of protein kinase C.

Acetylcholine↗

PubMed1995

Excitatory responses evoked in prefrontal cortex by mediodorsal thalamic nucleus stimulation: influence of anaesthesia.

The prefrontal cortex and the mediodorsal thalamic nucleus are reciprocally connected through excitatory amino acid pathways. Cortical excitatory responses resulting from activation of either the mediodorsal thalamic nucleus-prefrontal cortex pathway (short latency) or the recurrent collaterals of prefrontal cortex-mediodorsal thalamic nucleus neurons (long latency) can be discriminated mainly by their latency. The present study was undertaken to compare the effects of halothane and ketamine anaesthesia on these cortical excitatory responses and to establish their pharmacological characteristics using microiontophoretic application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D,L-2-amino-5-phosphonovaleric acid (APV), the specific antagonists of D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptors respectively. The number of prefrontal cortex cells which presented short or long latency excitatory responses was smaller in halothane- than in ketamine-anaesthetized rats. Whatever the anaesthetic used, short latency responses were blocked by CNQX and not affected by APV. Long latency responses were mainly blocked by APV and occasionally by CNQX in halothane-anaesthetized rats, while they were only blocked by CNQX in ketamine-anaesthetized animals. Therefore, halothane seems to preferentially reduce evoked responses mediated by AMPA receptors while ketamine completely abolishes evoked responses involving NMDA receptors. Moreover, the present data confirm that excitatory responses resulting from the activation of the mediodorsal thalamic nucleus-prefrontal cortex pathway are mainly mediated by AMPA receptors. In addition, they demonstrate that cortical responses linked to the activation of recurrent collaterals from prefrontal cortex-mediodorsal thalamic nucleus neurons involve both AMPA and NMDA receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1995

Inhibition of hippocampoprefrontal cortex excitatory responses by the mesocortical DA system.

The prefrontal cortex (PFC) receives dopaminergic (DA) afferents from the ventral tegmental area (VTA) and excitatory inputs from the hippocampal formation. The present electrophysiological experiments performed in anaesthetized rats demonstrate that activation of the mesocortical DA system blocked the spontaneous activity of PFC neurones and the excitatory responses induced by hippocampal stimulation. These data indicate that there is a convergence in the effects of hippocampal and DA mesocortical afferents on common PFC neurones. Furthermore, a population of PFC neurones responding to hippocampal stimulation could be identified as projecting to either the nucleus accumbens and/or the VTA, suggesting that the hippocampus exerts an indirect influence on these two structures through the PFC.

Animals↗

PubMed1995

Inhibition by anandamide of gap junctions and intercellular calcium signalling in striatal astrocytes.

Anandamide, an endogenous arachidonic acid derivative that is released from neurons and activates cannabinoid receptors, may act as a transcellular cannabimimetic messenger in the central nervous system. The biological actions of anandamide and the identity of its target cells are, however, still poorly documented. Here we show that anandamide is a potent inhibitor of gap-junction conductance and dye permeability in striatal astrocytes. This inhibitory effect is specific for anandamide as compared to co-released congeners or structural analogues, is sensitive to pertussis toxin and to protein-alkylating agents, and is neither mimicked by cannabinoid-receptor agonists nor prevented by a cannabinoid-receptor antagonist. Glutamate released from neurons evokes calcium waves in astrocytes that propagate via gap junctions, and may, in turn, activate neurons distant from their initiation sites in astrocytes. We find that anandamide blocks the propagation of astrocyte calcium waves generated by either mechanical stimulation or local glutamate application. Thus, by regulating gap-junction permeability, anandamide may control intercellular communication in astrocytes and therefore neuron-glial interactions.

Animals↗

PubMed1995

Oxygen free radicals enhance the nitric oxide-induced covalent NAD(+)-linkage to neuronal glyceraldehyde-3-phosphate dehydrogenase.

Nitric oxide (NO) induces a covalent modification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from various tissues. This phenomenon, which has previously been interpreted as an auto-ADP-ribosylation, is in fact a covalent binding of NAD+ to the enzyme. In the present study, we show that 3-morpholino-sydnonimine (SIN-1) is much more efficient than sodium nitroprusside (SNP) in stimulating the covalent labelling of GAPDH from cultured striatal neurones in the presence of [adenylate-32P]NAD+ (877 +/- 110 and 266 +/- 33% increase in NAD(+)-labelling induced by maximally effective concentrations of SIN-1 and SNP respectively). The difference in the efficacy of both NO-generating compounds could be due to the additional release of superoxide by SIN-1, since superoxide dismutase and the nitrone 5,5'-dimethyl pyrroline-1-oxide markedly inhibited the SIN-1-induced covalent binding of NAD+ to GAPDH. Catalase and selective scavengers of hydroxyl radicals, mannitol and dimethyl sulphoxide, did not alter the SIN-1-induced covalent modification of GAPDH, ruling out the involvement of hydroxyl radicals in this phenomenon. Supporting further a role of oxygen free radicals in the NAD+ linkage to GAPDH, pyrogallol, a superoxide generator, which alone was ineffective, potentiated the SNP-evoked response. The NAD+ linkage to neuronal GAPDH measured in the presence of NO and superoxide probably involves sulphydryl groups, since the radiolabelling of the protein was reversed by exposure to HgCl2 and prevented by pretreatment with the alkylating agent N-ethylmaleimide. Moreover, the NO-induced inhibition of GAPDH activity was enhanced by pyrogallol, which was ineffective alone. In conclusion, the present study indicates that superoxide anions potentiate NO-induced covalent NAD(+)-linkage to GAPDH and enzyme inactivation.

Animals↗

PubMed1995

Homotypic and heterotypic coupling mediated by gap junctions during glial cell differentiation in vitro.

Intercellular communication mediated by gap junctions was investigated during oligodendrocyte differentiation in primary and secondary cell cultures from newborn and adult rats. Two types of communication were considered: ionic coupling and dye-coupling between similar oligodendrocytes selected at the same stage of differentiation (homotypic) and dye-coupling between oligodendrocytes and astrocytes (heterotypic). Intercellular diffusion of fluorescent probes and double whole-cell recordings were used to test the incidence of dye and ionic communication respectively. Progenitor cells, identified with A2B5 antibodies, were characterized by the absence of ionic and dye-coupling, whereas oligodendrocytes, identified with galactosylceramide antibodies, exhibited both types of communication. This homotypic coupling was inhibited by various uncoupling agents, but unaffected by treatments which increased the intracellular concentration of cAMP. In cocultures of astrocytes and oligodendrocytes, Lucifer yellow and sulphorhodamine B were exchanged in both directions. This heterotypic dye-coupling, which could be blocked by octanol, first appeared after 3 weeks in culture and increased to an incidence of 25% after 6 weeks, a developmental pattern comparable to homotypic dye-coupling between oligodendrocytes. In contrast, during the same period, progenitors and microglia were never observed to be dye-coupled with astrocytes.

Animals↗

PubMed1995

Heterogeneous topographical distribution of the striatonigral and striatopallidal neurons in the matrix compartment of the cat caudate nucleus.

The topographical organization of the striatonigral projection was investigated in the cat by comparing the localization and the intensity of labelling of retrogradely labelled cells in the caudate nucleus following one or multiple injections of horseradish peroxidase-wheat germ agglutinin into the center or along the rostrocaudal axis of the substantia nigra pars reticulata. Second, the localizations of retrogradely labelled striatopallidal neurons and of clusters of aggregated striatonigral neurons (as outlined by the transport of 14C-material) were compared in cats that received four horseradish peroxidase-wheat germ agglutinin injections into the internal segment of the globus pallidus and three nigral injections of 14C-amino acids into the substantia nigra pars reticulata. Two types of striatonigral neurons located predominantly within the matrix compartment were identified: poorly collateralized aggregated cells distributed in clusters and more numerous collateralized cells distributed outside the clusters. In addition, two cell types were distinguished within each cluster of aggregated neurons. Those innervating the center of the substantia nigra pars reticulata were observed after a single nigral injection of the tracer, whereas those projecting to distinct sites of the substantia nigra pars reticulata along a rostrocaudal axis were observed only after multiple injections. Striatal neurons innervating the internal segment of the globus pallidus were heterogeneously distributed predominantly within the matrix but outside the clusters of aggregated striatonigral neurons. Together, these results provide further evidence for the heterogeneity of the matrix and for the complexity of matrix striatonigral connections that send both diverging and converging signals to the substantia nigra pars reticulata.

Acetylcholinesterase↗