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Pressure‐induced depression of synaptic transmission in the cerebellar parallel fibre synapse involves suppression of presynaptic N‐type Ca 2+ channels
Author(s) -
Etzion Yoram,
Grossman Yoram
Publication year - 2000
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2000.00303.x
Subject(s) - excitatory postsynaptic potential , neurotransmission , chemistry , neuroscience , synaptic potential , postsynaptic potential , voltage dependent calcium channel , synaptic fatigue , biophysics , calcium , biology , inhibitory postsynaptic potential , receptor , biochemistry , organic chemistry
High pressure induces CNS hyperexcitability while markedly depressing synaptic transmitter release. We studied the effect of pressure (up to 10.1 MPa) on the parallel fibre (PF) synaptic response in biplanar cerebellar slices of adult guinea pigs. Pressure mildly reduced the PF volley amplitude and to a greater extent depressed the excitatory field postsynaptic potential (fPSP). The depression of the PF volley was noted even at supramaximal stimulus intensities, indicating an effect of pressure on the amplitude of the action potential in each axon. Low concentrations of TTX mimicked the effects of pressure on the PF volley without affecting the fPSP. Application ω‐conotoxin GVIA (ω‐CgTx) reduced the synaptic efficacy by 34.3 ± 2.7%. However, in the presence of ω‐CgTx the synaptic depression at pressure was significantly reduced. Reduced Ca 2+ entry by application of Cd 2+ or low [Ca 2+ ] o did not have a similar influence on the effects of pressure. Application of ω‐AGA IVA, ω‐AGA TK and Funnel‐web spider toxin did not affect the synaptic response in concentrations that usually block P‐type Ca 2+ channels, whilst the N/P/Q‐type blocker ω‐conotoxin MVIIC reduced the response to 52.7 ± 5.0% indicating the involvement of Q‐type channels and R‐type channels in the non‐N‐type fraction of Ca 2+ entry. The results demonstrate that N‐type Ca 2+ channels play a crucial role in the induction of PF synaptic depression at pressure. This finding suggests a coherent mechanism for the induction of CNS hyperexcitability at pressure.