The Journal of Neurophysiology Vol. 79 No. 1 January 1998, pp. 181-189
Copyright ©1998 The American Physiological Society

EPSP Amplitude Modulation at the Rat Ia-Alpha Motoneuron Synapse: Effects of GABA_B Receptor Agonists and Antagonists

Kavita R. Peshori, William F. Collins III, and Lorne M. Mendell

Department of Neurobiology and Behavior, State University of New York at Stony Brook, New York 11794-5230

Peshori, Kavita R., William F. Collins III, and Lorne M. Mendell. EPSP amplitude modulation at the rat Ia-alpha motoneuron synapse: effects of GABA_B receptor agonists and antagonists. J. Neurophysiol. 79: 181-189, 1998. The object of this study was to examine the relationship between excitatory postsynaptic potential (EPSP) amplitude, posttetanic potentiation, and EPSP amplitude modulation at synapses made by group Ia afferents on motoneurons in the rat. These relationships were evaluated in cells in untreated rats and in cells in rats treated with the -aminobutyric acid-B (GABA_B) receptor agonist baclofen and antagonist CGP-35348, which were used to manipulate Ca²⁺ entry into presynaptic terminals and consequently probability of transmitter release from them. There was no evidence for postsynaptic action of these drugs from measurement of their effects on motoneuron properties. During high-frequency stimulation (32 shock bursts at 167 Hz), EPSP amplitude either decreased (negative modulation) or increased (positive modulation) in response to successive stimuli at different connections. In untreated rats this frequency-dependent amplitude modulation behavior was inversely but weakly correlated with EPSP amplitude measured at low frequency. Intravenous (iv) administration of the GABA_B agonist, baclofen, produced a marked and progressive decrease in EPSP amplitude measured at low frequency coincident with a change in frequency-dependent EPSP amplitude modulation toward more positive values (synaptic facilitation). In contrast, an increase in EPSP amplitude occurred after iv administration of the GABA_B antagonist CGP-35348 that was accompanied by a negative shift in EPSP amplitude modulation during high-frequency stimulation. The negative shift in EPSP amplitude modulation (synaptic depression) after CGP-35348 application was much smaller than the positive shift induced by baclofen when normalized to the change in EPSP amplitude. Posttetanic potentiation decreased after baclofen but did not increase after CGP-35348. The relationship between modulation and EPSP amplitude was much steeper after GABA_B receptor manipulation in either direction than that observed in the population of motoneurons in untreated preparations. This suggests that in the rat differences in probability of release play at most a small role in determining EPSP amplitude across the motoneuron pool.

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