Intraspinally mediated state‐dependent enhancement of motoneurone excitability during fictive scratch in the adult decerebrate cat

Abstract

This is the first study to report on the increase in motoneurone excitability during fictive scratch in adult decerebrate cats. Intracellular recordings from antidromically identified motoneurones revealed a decrease in the voltage threshold for spike initiation (V(th)), a suppression of motoneurone afterhyperpolarization and activation of voltage-dependent excitation at the onset of scratch. These state-dependent changes recovered within 10-20 s after scratch and could be evoked after acute transection of the spinal cord at C1. Thus, there is a powerful intraspinal system that can quickly and reversibly re-configure neuronal excitability during spinal network activation. Fictive scratch was evoked in spinal intact and transected decerebrate preparations by stroking the pinnae following topical curare application to the dorsal cervical spinal cord and neuromuscular block. Hyperpolarization of V(th) occurred (mean 5.8 mV) in about 80% of ipsilateral flexor, extensor or bifunctional motoneurones during fictive scratch. The decrease in V(th) began before any scratch-evoked motoneurone activity as well as during the initial phase in which extensors are tonically hyperpolarized. The V(th) of contralateral extensors depolarized by a mean of +3.7 mV during the tonic contralateral extensor activity accompanying ipsilateral scratch. There was a consistent and substantial reduction of afterhyperpolarization amplitude without large increases in motoneurone conductance in both spinal intact and transected preparations. Depolarizing current injection increased, and hyperpolarization decreased the amplitude of rhythmic scratch drive potentials in acute spinal preparations indicating that the spinal scratch-generating network can activate voltage-dependent conductances in motoneurones. The enhanced excitability in spinal preparations associated with fictive scratch indicates the existence of previously unrecognized, intraspinal mechanisms increasing motoneurone excitability.