CHEMICAL-STIMULATION OF CARDIAC RECEPTORS ATTENUATES LOCOMOTION IN MESENCEPHALIC CATS

The purpose of the present investigation was to determine whether chem ical stimulation of cardiac receptors is sufficient to inhibit locomot ion. Decerebrate, unanesthetized cats were induced to walk on a treadm ill by electrically stimulating the mesencephalic locomotor region (ML R). Cardiac receptors were stimulated by injecting nicotine (62.3 +/- 8.6 mu g/kg, mean +/- SE) into the pericardial sac. Cardiac nerve acti vity was reversibly blocked by injecting procaine (2%) into the perica rdial sac. Locomotion was monitored by using bipolar needle electrodes inserted into the lateral gastrocnemius (LG) and tibialis anterior (T A) muscles. integrated electromyographic (iEMG) activity from each mus cle was quantified on a step-by-step basis. Intrapericardial (ipc) nic otine inhibited locomotion and evoked the coronary chemoreflex. Blood pressure and heart rate decreased significantly by 45.6 +/- 7.1 mmHg a nd 59.3 +/- 12.3 beats/min, respectively. Nicotine ipc significantly r educed iEMG activity by 24-28% in the LG muscles. The TA muscles were not affected consistently by ipc nicotine. The locomotor inhibition an d the depressor reflex paralleled each other and occurred within 5 s o f nicotine injection. Procaine ipc blocked the nicotine-induced locomo tor inhibition and depressor reflex. The effects of procaine were larg ely reversible, because ipc nicotine reduced iEMG activity in the LG ( 25-46%) but not in the TA muscles after washing procaine from the peri cardial sac. These results demonstrate that cardiac receptors sensitiv e to nicotine inhibit MLR-induced locomotion in the decerebrate cat. T hese findings indicate the presence of a neural pathway from the heart whereby endogenous stimuli could reflexly alter motor control.