Abstract

Publisher Summary This chapter describes the depression in Ia excitatory postsynaptic potentials (EPSPs) in cat motoneurons by Mn2+, Co2+, and some other agents. The changes in EPSPs produced by the divalent cations are illustrated by oscilloscope traces. It is found that if EPSPs were mediated purely by electrical transmission from afferent terminals, one would expect them to be noticeably sensitive to local anesthetics, such as procaine, injected inside motoneurons. Such injections reduce the resting input conductance and greatly depress the electrical excitability of motoneurons, whether tested by intracellular depolarizing currents or by antidromic activation, but they produce little or no change in low threshold EPSPs. There was a marked depression of the action potential but no corresponding change in EPSPs. These observations are compatible with the electrical hypothesis only if the site of generation of the presynaptic action potential cannot be reached by local anesthetics injected into the motoneuron, either because of excessive distance or because of selective junctional permeability. On the other hand, if transmission is chemical, the membrane channels activated synaptically are either refractory or inaccessible to the local anesthetics.

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