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• W1497758044 abstract "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 Ca 2 + imaging in hypoglossal motoneurones from rat and mouse brainstem slices, we address here the role of cytoplasmic Ca 2 + (Ca i ) in glycinergic synapse modulation. Ca 2 + 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 Ca 2 + ‐dependent increase in amplitude and decay prolongation. Both presynaptic inhibition and postsynaptic potentiation were completely prevented by strong Ca i buffering (20 m m BAPTA). Our findings demonstrate two independent mechanisms by which Ca 2 + modulates glycinergic synaptic transmission: (i) presynaptic inhibition of glycine release and (ii) postsynaptic potentiation of GlyR‐mediated responses. This dual Ca 2 + ‐induced regulation might be important for feedback control of neurotransmission in a variety of glycinergic networks in mammalian nervous systems." @default.
• W1497758044 created "2016-06-24" @default.
• W1497758044 creator A5007553002 @default.
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• W1497758044 date "2005-12-01" @default.
• W1497758044 modified "2023-10-13" @default.
• W1497758044 title "Dual Ca²⁺ modulation of glycinergic synaptic currents in rodent hypoglossal motoneurones" @default.
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• W1497758044 doi "https://doi.org/10.1113/jphysiol.2005.094862" @default.
• W1497758044 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1464266" @default.
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