The nature of postasphyxial rigidity examined by intracellular recording from motoneurons

Abstract

The spinal cord of cats was asphyxiated for about 30 min by increasing the pressure in the dural cavity above the blood pressure. The resulting rigidity in the hind legs was investigated with intracellular methods 2 weeks after asphyxiation. Spontaneous action potentials were obtained which originated in three structures. Spikes were recorded from primary afferent fibers. Some of these could be identified as afferents of stretch receptors in extensor muscles by the enhanced rate of discharge when the rigid leg was flexed. Spontaneous spikes were also obtained from motor fibers. These structures were identified by antidromic stimulation. More complicated potentials were obtained from structures which were probably motoneuron somas. In a few instances the identification was made by antidromic stimulation. The potentials consisted of spikes and small potential fluctuations in the interspike interval. The latter were considered to be synaptic noise. In a regularly discharging soma the spike was followed by a (relative) hyperpolarization after which the soma depolarized until threshold for the subsequent spike was reached. Somas discharging at low frequency exhibited an irregular base line due to the synaptic noise. Depolarizations of greater magnitude were caused presumably by bunching of excitatory postsynaptic potentials; these occasionally elicited a spike. Flexion of the rigid hind leg tended to cause an increase in the rate of the “spontaneous” discharging soma, or to initiate an impulse train in quiet somas. It was concluded that the postasphyxial rigidity investigated is of a reflexogenic nature.