Abstract
Lateral geniculate neurons of anesthetized cats were studied with microelectrodes to determine whether the mechanisms underlying the prolonged depression in synaptic transfer, referred to as second subnormality (SS), which follows optic nerve tetanization occur in presynaptic or postsynaptic elements. Extracellularly recorded excitatory postsynaptic potentials (EPSP) were found to be reduced in amplitude during SS; subsequent tetanization resulted in potentiation of the depressed EPSP followed by a return to depressed levels (SS). During SS, cells which no longer responded to optic nerve stimulation continued to discharge spontaneously at the same rate as they had prior to tetanization, suggesting that tetanization of a portion of the presynaptic inputs to these cells does not alter their responsiveness to other inputs. These findings indicate that SS results from an alteration of presynaptic elements.
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