QUANTAL ANALYSIS OF PRESYNAPTIC INHIBITION, LOW [CA2-PRESSURE INTERACTIONS AT CRUSTACEAN EXCITATORY SYNAPSES(](0), AND HIGH)

The cellular mechanisms underlying the effects of high pressure, GABAe rgic presynaptic inhibition, and low [Ca2+](0) on glutamatergic excita tory synaptic transmission were studied in the opener muscle of the lo bster walking leg. Excitatory postsynaptic currents (EPSCs) were recor ded with or without prior stimulation of the inhibitor using a loose m acropatch clamp technique at atmospheric pressure and at 6.9 MPA heliu m pressure. High pressure reduced the mean EPSC amplitude and variance , decreased the quantal content (m), but did not affect the quantum cu rrent (q). Pressure shifted the median of the amplitude histogram to t he left by 1-2 q. Under normal pressure conditions, presynaptic inhibi tion and low [Ca2+](0) induced similar effects. However, quantal analy sis using a binomial frequency distribution model revealed that high p ressure and low [Ca2+](0) diminished n (available active zones) and sl ightly increased p (probability of release), but presynaptic inhibitio n reduced p and slightly increased n. At high pressure, presynaptic in hibition was reduced, at which time the major contributor to the inhib itory process appeared to be reduction in n and not p. The similarity of the alterations in quantal parameters of release at high pressure, low [Ca2+](0), and in some conditions of presynaptic inhibition is con sistent with the hypothesis that pressure reduces Ca2+ inflow into the presynaptic nerve terminals to affect the Ca2+-dependent quantal rele ase parameters n and p. (C) 1994 Wiley-Liss, Inc.