Primary Afferent Synaptic Modulation as a Mechanism of Behavioral Compensation Following Spinal Cord Lesion in the Frog

Abstract

Direct investigation of neuronal mechanisms responsible for recovery of function following lesions of the central nervous system (CNS) or its peripheral inputs is limited by the need for detailed knowledge of normal functional organization in the system under study. Without this knowledge it is generally impossible to say whether a neuronal change consequent to lesion is a symptom of deficit or an aspect of compensatory self-regulation. Various studies have shown that when a neuron is partly deafferented other inputs to the cell or its region can take over vacant synaptic sites (see, e.g., Cotman, Gall, Tsukahara, this vol.) in a manner analogous to the “sprouting” of motor axon terminals onto denervated muscle fibers. However, it is not easy to demonstrate that such substitution of synaptic input is functionally useful.