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Accueil > Agenda > Les séminaires Jean Roche > Signalisation calcique liée au glutamate dans les interneurones de la couche (...)

Signalisation calcique liée au glutamate dans les (...)

Lundi 12 décembre 2005,11h, salle Lissitzky.

Bibliographie

1 : Curr Opin Neurobiol. 2005 Jun ;15(3):275-81.

Presynaptic calcium stores and synaptic transmission.

Collin T, Marty A, Llano I.

CNRS UMR8118, Laboratoire de Physiologie Cerebrale, UFR Biomedicale, Universite Paris 5, 45 rue des Saints Peres, 75006 Paris, France.

Following the gradual recognition of the importance of intracellular calcium stores for somatodendritic signaling in the mammalian brain, recent reports have also indicated a significant role of presynaptic calcium stores. Ryanodine-sensitive stores generate local, random calcium signals that shape spontaneous transmitter release. They amplify spike-driven calcium signals in presynaptic terminals, and consequently enhance the efficacy of transmitter release. They appear to be recruited by an association with certain types of calcium-permeant ion channels, and they induce specific forms of synaptic plasticity. Recent research also indicates a role of inositoltrisphosphate-sensitive presynaptic calcium stores in synaptic plasticity.


2 : Neurosci Lett. 2005 Jun 10-17 ;381(1-2):149-53. Epub 2005 Feb 25.

Involvement of ryanodine receptors in IP3-mediated calcium signalling in neurons. A modelling approach.

Louvet L, Collin T.

Laboratoire de Neurobiologie Cellulaire, Faculte des Sciences, Universite de Picardie Jules Verne, 33 rue Saint Leu, 80039 Amiens cedex, Paris.

Phospholipase C (PLC)-coupled metabotropic receptors trigger the release of intracellular Ca2+ through activation of IP3 receptors (IP3Rs). Increasing evidence suggests that they can also and perhaps more efficiently mobilize Ca2+ through ryanodine receptors (RyRs). We constructed a model allowing a variable PLC stimulation level (via the parameter gamma) as well as a variable involvement of RyRs (via the parameter A). The sole presence of RyRs (A not = 0) affected the basal Ca2+ concentration [Ca2+]i. To keep Ca2+ below 160 nM, we fixed the upper limit of A to 0.2, a value that is compatible with the numerical ratio between RyRs and IP3Rs in cerebellar Purkinje neurons. Metabotropic responses were simulated by abruptly raising the value of gamma to various levels. In the absence of RyRs, the model starts to oscillate with gamma=0.4. For lower levels of PLC stimulation (gamma< or =0.3), the presence of RyR is capable of triggering an oscillatory signal. When A< or =0.18, the frequency of the Ca2+ oscillations augments from 0.1 to 1.3 Hz as a function of gamma. Conversely, as the frequency increases, the amplitude of the oscillations is reduced from 1 microM to 50 nM. With higher values of A, the oscillating pattern is definitively inhibited. It is concluded that RyRs have the potentiality to strikingly affect the temporal pattern of the Ca2+ signalling triggered by IP3-related metabotropic responses.


3 : J Neurosci. 2005 Jan 5 ;25(1):96-107.

Developmental changes in parvalbumin regulate presynaptic Ca2+ signaling.

Collin T, Chat M, Lucas MG, Moreno H, Racay P, Schwaller B, Marty A, Llano I.

Laboratory of Cerebral Physiology, Centre National de la Recherche Scientifique, University Paris 5, 75006 Paris, France.

Certain interneurons contain large concentrations of specific Ca2+-binding proteins (CBPs), but consequences on presynaptic Ca2+ signaling are poorly understood. Here we show that expression of the slow CBP parvalbumin (PV) in cerebellar interneurons is cell specific and developmentally regulated, leading to characteristic changes in presynaptic Ca2+ dynamics (Ca(i)). Using whole-cell recording and fluorescence imaging, we studied action potential-evoked Ca(i) transients in axons of GABA-releasing interneurons from mouse cerebellum. At early developmental stages [postnatal days 10-12 (P10-P12)], decay kinetics were significantly faster for basket cells than for stellate cells, whereas at P19-P21 both interneurons displayed fast decay kinetics. Biochemical and immunocytochemical analysis showed parallel changes in the expression levels and cellular distribution of PV. By comparing wild-type and PV(-/-) mice, PV was shown to accelerate the initial decay of action potential-evoked Ca(i) signals in single varicosities and to introduce an additional slow phase that summates during bursts of action potentials. The fast initial Ca(i) decay accounts for a previous report that PV elimination favors synaptic facilitation. The slow decay component is responsible for a pronounced, PV-dependent, delayed transmitter release that we describe here at interneuron-interneuron synapses after presynaptic bursts of action potentials. Numerical simulations account for the effect of PV on Ca(i) kinetics, allow estimates for the axonal PV concentration (approximately 150 microm), and predict the time course of volume-averaged Ca(i) in the absence of exogenous buffer. Overall, PV arises as a major contributor to presynaptic Ca(i) signals and synaptic integration in the cerebellar cortex.


4 : Neuron. 2004 Nov 18 ;44(4):701-13. Osmotic tension as a possible link between GABA(A) receptor activation and intracellular calcium elevation.

Chavas J, Forero ME, Collin T, Llano I, Marty A.

Laboratoire de Physiologie Cerebrale, CNRS UMR 8118, Universite Paris 5, 45 rue des Saints Peres, 75006 Paris, France.

Intracellular calcium concentration rises have been reported following activation of GABA(A) receptors in neonatal preparations and attributed to activation of voltage-dependent Ca(2+) channels. However, we show that, in cerebellar interneurons, GABA(A) agonists induce a somatodendritic Ca(2+) rise that persists at least until postnatal day 20 and is not mediated by depolarization-induced Ca(2+) entry. A local Ca(2+) elevation can likewise be elicited by repetitive stimulation of presynaptic GABAergic afferent fibers. We find that, following GABA(A) receptor activation, bicarbonate-induced Cl(-) entry leads to cell depolarization, Cl(-) accumulation, and osmotic tension. We propose that this tension induces the intracellular Ca(2+) rise as part of a regulatory volume decrease reaction. This mechanism introduces an unexpected link between activation of GABA(A) receptors and intracellular Ca(2+) elevation, which could contribute to activity-driven synaptic plasticity.


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