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This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 569/3/817    most recent jphysiol.2005.094862v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mukhtarov, M. Articles by Bregestovski, P. Search for Related Content PubMed PubMed Citation Articles by Mukhtarov, M. Articles by Bregestovski, P.

¹ Institut de Neurobiologie de la Méditerranée (INMED) INSERM U29, 163, route de Luminy, 13273 Marseille cedex 09, France
² Dipartimento di Fisiologia Umana e Farmacologia, Università La Sapienza, Roma, P le A. Moro 5, I-00185, Italy
³ Istituto Neurologico Mediterraneo (Neuromed), Pozzilli (IS), Italy

Glycinergic synapses are implicated in the coordination of reflex responses, sensory signal processing and pain sensation. Their activity is pre- and postsynaptically regulated, although mechanisms are poorly understood. Using patch-clamp recording and Ca²⁺ imaging in hypoglossal motoneurones from rat and mouse brainstem slices, we address here the role of cytoplasmic Ca²⁺ (Ca_i) in glycinergic synapse modulation. Ca²⁺ influx through voltage-gated or NMDA receptor channels caused powerful transient inhibition of glycinergic IPSCs. This effect was accompanied by an increase in both the failure rate and paired-pulse ratio, as well as a decrease in the frequency of mIPSCs, suggesting a presynaptic mechanism of depression. Inhibition was reduced by the cannabinoid receptor antagonist SR141716A and occluded by the agonist WIN55,212-2, indicating involvement of endocannabinoid retrograde signalling. Conversely, in the presence of SR141716A, glycinergic IPSCs were potentiated postsynaptically by glutamate or NMDA, displaying a Ca²⁺-dependent increase in amplitude and decay prolongation. Both presynaptic inhibition and postsynaptic potentiation were completely prevented by strong Ca_i buffering (20 mM BAPTA). Our findings demonstrate two independent mechanisms by which Ca²⁺ modulates glycinergic synaptic transmission: (i) presynaptic inhibition of glycine release and (ii) postsynaptic potentiation of GlyR-mediated responses. This dual Ca²⁺-induced regulation might be important for feedback control of neurotransmission in a variety of glycinergic networks in mammalian nervous systems.

(Received 18 July 2005; accepted after revision 24 August 2005; first published online 25 August 2005)
Corresponding author P. Bregestovski: Institut de Neurobiologie de la Méditerranée, INSERM U29, 163, route de Luminy, 13273 Marseille cedex 09, France.  Email: pbreges{at}inmed.Univ-mrs.fr

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