Premium
Dual Ca 2 + modulation of glycinergic synaptic currents in rodent hypoglossal motoneurones
Author(s) -
Mukhtarov Marat,
Ragozzino Davide,
Bregestovski Piotr
Publication year - 2005
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2005.094862
Subject(s) - glycine receptor , neuroscience , neurotransmission , postsynaptic potential , long term potentiation , postsynaptic current , chemistry , excitatory postsynaptic potential , post tetanic potentiation , inhibitory postsynaptic potential , biology , glycine , receptor , biochemistry , amino acid
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.