Joint receptors modulate short and long latency muscle responses in the awake cat.

Nerve cuff electrodes were chronically implanted around multiple peripheral nerves in adult cats, including the medial and posterior articular nerves (MAN and PAN) to the knee while EMG electrodes were implanted into seven hindlimb muscles. Randomized load perturbations producing mid-range knee flexions at varying angular velocities were subsequently applied to awake cats. Recordings were initially obtained with knee joint innervation intact and then after local anaesthetic or saline control solution was injected into the knee. Averaged neurogram and EMG responses to the imposed movements were utilized to assess the contribution of joint mechanoreceptor activity to the evoked muscle responses. Additionally, spike-triggered averaging techniques and peri-stimulus time histograms of single joint afferent units isolated from the articular nerve cuffs were utilized to characterize unitary joint receptor responses. The averaged whole nerve response to knee joint perturbations on each of the cuffed articular nerves revealed phasic increases in activity relative to constant background levels. The earliest phasic responses on the articular nerves were initiated at latencies that were too short to be voluntary, occurring in the short latency (reflex) period. Detectable joint receptors were not recruited until after the earliest excitatory responses of agonist/antagonist muscle pairs acting across the knee had occurred, presumably resulting in mechanical loading of the knee joint capsule and subsequent activation of articular mechanoreceptors. Introduction of local anaesthetic into the knee was accompanied by marked diminution in joint afferent activity. Perturbation-evoked muscle responses were characterized by increased activity above background levels in all seven muscles studied, including antagonist muscle pairs. Local anaesthetic-mediated loss of knee joint mechanoreceptor input altered the latency, amplitude and duration of EMG responses in each muscle. The effect of joint anaesthesia in the short latency period was a generalized decrease in all muscle responses relative to normal and saline controls. The loss of afferent input after joint anaesthesia was also associated with altered muscle responses during the long latency period, when both reflex and voluntary mechanisms could potentially contribute to the generation of EMG activity. Interestingly, long latency activity after joint anaesthesia was characterized by "unbalancing" in the EMG responses of some antagonist muscle pairs. This alteration of normal antagonist pair co-contraction patterns served to increase the magnitude of the imposed perturbations, rather than to bring the movements under control. Analysis of single joint afferents isolated from whole joint nerve recordings demonstrated that some joint afferent units were tonically active at quiescent, mid-range knee positions. Additionally, isolated afferents demonstrated different time courses of response to imposed perturbations.(ABSTRACT TRUNCATED AT 400 WORDS)