Calcium homeostasis in rat sympathetic neurones: A primary role for the plasma membrane calcium ATPase

Patch-clamp experiments combined with indo-1 measurement of free intracellular Ca²⁺ concentration ([Ca²⁺]i) were used to determine the homeostatic systems involved in the maintenance of resting [Ca²⁺]i and the clearance of Ca²⁺ transients following activation of voltage-gated Ca²⁺ channels in neurones from rat superior cervical ganglion (SCG). In these neurones, the Ca²⁺ buffering capacity was estimated to be ≈ 1000 at [Ca²⁺]i close to rest and ≈ 250 at [Ca²⁺]i ≈ 1 μM and to involve at least two buffering systems with different affinities for Ca²⁺. Removal of extracellular Ca²⁺ led to a decrease in [Ca²⁺]i that was mimicked by the addition of La³⁺. This decrease in [Ca²⁺]i was more pronounced after inhibition of the endoplasmic reticulum Ca²⁺ uptake system (SERCA) and subsequent depletion of the intracellular stores. Inhibition of the plasma membrane Ca2+ pump (PMCA) by intracellular carboxyeosin or extracellular alkalisation (pH 9) both increased resting [Ca²⁺]i and prolonged the recovery of Ca²⁺ transients at peak [Ca²⁺]i 500 nM, recovery showed an additional plateau phase that was abolished in carbonyl cyanide m-chlorohydrazone (CCCP) or on omitting Na⁺ from the intracellular solution. Inhibition of the plasma membrane Na⁺/Ca²⁺ exchanger (NCX) and of SERCA had a small but significant effect on the rate of decay of these larger Ca²⁺ transients. However, neither of these mechanisms appeared to contribute substantially to the recovery from rises in [Ca²⁺]i below 1 μM. In conclusion, resting [Ca²⁺]i is maintained as the result of a passive Ca²⁺ influx regulated by a large Ca²⁺ buffering system, Ca²⁺ extrusion via a PMCA and Ca²⁺ transport from the intracellular stores. PMCA is also the principal Ca²⁺ extrusion system at low Ca²⁺ loads, with additional participation of the NCX and intracellular organelles at high [Ca²⁺]i

Limits of Calcium Clearance by Plasma Membrane Calcium ATPase in Olfactory Cilia

BACKGROUND: In any fine sensory organelle, a small influx of Ca(2+) can quickly elevate cytoplasmic Ca(2+). Mechanisms must exist to clear the ciliary Ca(2+) before it reaches toxic levels. One such organelle has been well studied: the vertebrate olfactory cilium. Recent studies have suggested that clearance from the olfactory cilium is mediated in part by plasma membrane Ca(2+)-ATPase (PMCA). PRINCIPAL FINDINGS: In the present study, electrophysiological assays were devised to monitor cytoplasmic free Ca(2+) in single frog olfactory cilia. Ca(2+) was allowed to enter isolated cilia, either through the detached end or through membrane channels. Intraciliary Ca(2+) was monitored via the activity of ciliary Ca(2+)-gated Cl(-) channels, which are sensitive to free Ca(2+) from about 2 to 10 microM. No significant effect of MgATP on intraciliary free Ca(2+) could be found. Carboxyeosin, which has been used to inhibit PMCA, was found to substantially increase a ciliary transduction current activated by cyclic AMP. This increase was ATP-independent. CONCLUSIONS: Alternative explanations are suggested for two previous experiments taken to support a role for PMCA in ciliary Ca(2+) clearance. It is concluded that PMCA in the cilium plays a very limited role in clearing the micromolar levels of intraciliary Ca(2+) produced during the odor response

Multiple Kinases Involved in the Nicotinic Modulation of Gamma Oscillations in the Rat Hippocampal CA3 Area

Neuronal synchronization at gamma band frequency (20–80 Hz, γ oscillations) is closely associated with higher brain function, such as learning, memory and attention. Nicotinic acetylcholine receptors (nAChRs) are highly expressed in the hippocampus, and modulate hippocampal γ oscillations, but the intracellular mechanism underlying such modulation remains elusive. We explored multiple kinases by which nicotine can modulate γ oscillations induced by kainate in rat hippocampal area CA3 in vitro. We found that inhibitors of cyclic AMP dependent kinase (protein kinase A, PKA), protein kinase C (PKC), N-methyl-D-aspartate receptor (NMDA) receptors, Phosphoinositide 3-kinase (PI3K) and extracellular signal-related kinases (ERK), each individually could prevent the γ oscillation-enhancing effect of 1 μM nicotine, whereas none of them affected baseline γ oscillation strength. Inhibition of the serine/threonine kinase Akt increased baseline γ oscillations and partially blocked its nicotinic enhancement. We propose that the PKA-NMDAR-PI3K-ERK pathway modifies cellular properties required for the nicotinic enhancement of γ oscillations, dependent on a PKC-ERK mediated pathway. These signaling pathways provide clues for restoring γ oscillations in pathological conditions affecting cognition. The suppression of γ oscillations at 100 μM nicotine was only dependent on PKA-NMDAR activation and may be due to very high intracellular calcium levels

Les photographes étrangers dans la France de l’entre-deux-guerres

Photographers from abroad in France during the inter-war period. Between the two wars, many foreigners settled in France. The artists amongst them come from countries which are not representative of the countries of immigrants’ origins as a whole. Where photographers are concerned, a quarter come from Germany and another quarter from Hungary, fleeing the political situation after Admiral Horty’s seizure of power. These Hungarian photographers often came from avant-garde milieux, and they had a far-reaching influence on French photography which, for many years, has gone unrecognized.Wanaverbecq Annie-laure. Les photographes étrangers dans la France de l’entre-deux-guerres. In: Histoire de l'art, N°15, 1991. Varia. pp. 61-77

Depolarization-induced release of endocannabinoids by murine dorsal motor nucleus of the vagus nerve neurons differentially regulates inhibitory and excitatory neurotransmission.

International audienceNumerous studies, focused on the hypothalamus, have recently implicated endocannabinoids (EC) as orexigenic factors in the central control of food intake. However, the EC system is also highly expressed in the hindbrain autonomic integrator of food intake regulation, i.e. the dorsal vagal complex (DVC). Previous studies have shown that exogenous cannabinoids, by acting on cannabinoid 1 receptor (CB1R), suppress GABAergic and glutamatergic neuronal transmission in adult rat dorsal motor nucleus of the vagus nerve (DMNV), the principal efferent compartment of the DVC. However, no endogenous release of EC has been demonstrated in DVC to date. Using patch-clamp techniques on mouse coronal brainstem slices, we confirmed that both inhibitory and excitatory neurotransmission were depressed by WIN 55,212-2, a CB1R agonist. We demonstrated that DMNV neurons exhibited a rapid and reversible depolarization-induced suppression of electrically evoked GABAergic IPSCs (eIPSCs), classically known as DSI (depolarization-induced suppression of inhibition), while spontaneous or miniature IPSCs activity remained unaltered. Further, no depolarization-induced suppression of glutamatergic eEPSCs (DSE) occurred. Our results indicate that DSI was blocked by SR141716A (Rimonabant), a selective CB1R antagonist, and was dependent on calcium elevation in DMNV neurons, suggesting a release of EC in the DVC. Moreover, the analysis of the paired-pulse ratio, of the coefficient of variation and of the failure rate of eIPSCs support the fact that EC-mediated suppression of GABAergic inhibition takes place at the presynaptic level. These results show for the first time that DMNV neurons release EC in an activity-dependent manner, which in turn differentially regulates their inhibitory and excitatory synaptic inputs

Evidence for PKD2L1‐positive neurons distant from the central canal in the ventromedial spinal cord and Medulla

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Cholinergic Axons Modulate GABAergic Signaling among Hippocampal Interneurons via Postsynaptic 7 Nicotinic Receptors

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Evidence for PKD2L1‐positive neurons distant from the central canal in the ventromedial spinal cord and medulla of the adult mouse

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Signaling Microdomains Define the Specificity of Receptor-Mediated InsP3 Pathways in Neurons

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