Physiological aspects of synaptic plasticity: the Ia/motoneuron connection as a model

Abstract

Damage to peripheral nerves results in substantial changes in the function of spinal synapses that mediate the monosynaptic reflex. These alterations consist independently of those caused by axotomy of the postsynaptic neuron and those produced by axotomy of the presynaptic neuron. Synaptic transmission is depressed following interruption of either limb of the segmental reflex loop. These reductions in EPSP amplitude are largely reversed following reinnervation of the peripheral tissue by the cut fibers, whether or not the regenerating fiber finds the correct muscle. Alterations in synaptic transmission following damage to the spinal cord itself are more variable than those noted after peripheral nerve damage. Although segmental EPSPs are generally enhanced following spinal injury (if in fact changes do occur), these increases are superimposed on motoneuron hyperpolarization, making the net changes in reflex transmission unpredictable. Furthermore, the extent of motoneuron depolarization is also influenced by the amount of temporal summation of EPSPs during the high-frequency activation of group Ia fibers known to occur, for example, during normal walking. Because EPSP amplitude is not constant during such activation and is modulated differently at connections on different motoneurons, changes in effective levels of synaptic transmission after such lesions are very difficult to predict. Thus it is not surprising that it is not possible to make close correlations between changes in amplitude of EPSPs and reflex behavior following injury (but see chapter by M.E. Goldberger and M. Murray, this volume). These alterations in synaptic transmission can occur at a considerable physical distance from the site of injury, peripheral or central. They illustrate the interdependence in elements of the nervous system, which can also be seen as changes in properties of motoneurons themselves (e.g., input resistance, after-hyperpolarization, rheobase) following many of these injuries. Altered cell properties complicate the functional interpretation of synaptic changes obtained after injury but must be considered in evaluating the sequelae of lesions in the peripheral and central nervous system.