Changes in rubral multiunit activity after lesions in the interpositus nucleus of the cat

Abstract

The initial effect of an acute lesion in the central nervous system is loss of neural function. With time, however, restorative processes, generally termed 'compensation', may result in some degree of recovery of neural function. The mechanisms involved in recovery may include morphological changes in synaptic connections, a process described as neuroplasticity. Direct evidence for neuroplasticity in the mature mammalian central nervous system has been presented (for recent reviews, see refs. 3-6). Electrophysiological studies of the rubrospinal tract in the cat have shown evidence of neuroplasticity in which sprouting of axonal terminals (collateral sprouting) is thought to occur in the red nucleus following partially deafferenting lesions ~4. The demonstration of synaptic reorganization in this nucleus is based on evidence that the two major inputs to this nucleus, corticorubral and interpositorubral fibers, make synaptic connection with two separate portions of the membranes of rubral neurons. Tsukahara and co-workers12, la showed in the intact cat that excitatory postsynaptic potentials (EPSPs) evoked in rubral neurons by stimulating the ipsilateral pericruciate cortex had relatively slow rise times, long decay phases, and low peak amplitudes. EPSPs evoked by stimulating the contralateral interpositus nucleus displayed more rapid rise times, shorter decay phases, and greater peak amplitudes. They attributed these differences to segregation of synaptic terminals on rubral neurons, cortical fibers on distal dendrites and interpositus fibers on proximal dendrites and somas. The reorganization of cortical synaptic contacts on rubral neurons after partial deafferenration was investigated in chronic cats with lesions of the contralateral interpositus nucleus 14. They observed a progressive shortening of the rise times of cortically evoked EPSPs for 4~10 days after the lesions and no further change after longer intervals. These changes in cortically evoked EPSPs were thought to result from collateral sprouting of cortical fibers to innervate more proximal portions of rubral neurons. If neuroplasticity participates in the recovery of motor function after a lesion, it must do so not only through changes in postsynaptic potentials, but also through changes in patterns of spike activity directed toward brain stem and spinal nuclei. It is not clear what effect changes in EPSP wave forms may have on rubral spike activity. We have investigated this issue by recording spontaneous multiunit spike activity in