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Quantal analysis of presynaptic inhibition, low [Ca 2+ ] 0 , and high pressure interactions at crustacean excitatory synapses
Author(s) -
Golan Hava,
Moore Homer J.,
Grossman Yoram
Publication year - 1994
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890180408
Subject(s) - excitatory postsynaptic potential , postsynaptic current , chemistry , neurotransmission , biophysics , glutamatergic , postsynaptic potential , inhibitory postsynaptic potential , neuroscience , glutamate receptor , biology , biochemistry , receptor
Abstract The cellular mechanisms underlying the effects of high pressure, GABAergic presynaptic inhibition, and low [Ca 2+ ] 0 on glutamatergic excitatory synaptic transmission were studied in the opener muscle of the lobster walking leg. Excitatory postsynaptic currents (EPSCs) were recorded with or without prior stimulation of the inhibitor using a loose macropatch clamp technique at atmospheric pressure and at 6.9 MPA helium pressure. High pressure reduced the mean EPSC amplitude and variance, decreased the quantal content (m), but did not affect the quantum current (q). Pressure shifted the median of the amplitude histogram to the left by 1–2 q. Under normal pressure conditions, presynaptic inhibition and low [Ca 2+ ] 0 induced similar effects. However, quantal analysis using a binomial frequency distribution model revealed that high pressure and low [Ca 2+ ] 0 diminished n (available active zones) and slightly increased p (probability of release), but presynaptic inhibition reduced p and slightly increased n. At high pressure, presynaptic inhibition was reduced, at which time the major contributor to the inhibitory process appeared to be reduction in n and not p. The similarity of the alterations in quantal parameters of release at high pressure, low [Ca 2+ ] 0 , and in some conditions of presynaptic inhibition is consistent with the hypothesis that pressure reduces Ca 2+ inflow into the presynaptic nerve terminals to affect the Ca 2+ ‐dependent quantal release parameters n and p. © 1994 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.