Prolonged inactivation of cortical pyramidal tract neurones in cats by distension of the carotid sinus.

1. We have investigated the effects of stimulating carotid sinus baroreceptors upon the activity of single cortical pyramidal tract cells (PT-cells) in anaesthetized cats.2. Extracellular potentials were recorded from PT-cells, which were driven orthodromically (1/sec) by stimulating thalamic nuclei (N. ventralis lateralis, N. ventralis posterolateralis) or afferent nerves in the contra-lateral forepaw. Baroreceptors were stimulated by inflating small balloons placed in the bifurcations of one or both common carotid arteries.3. Distension of the carotid sinus caused a prolonged depression of the orthodromically evoked discharge of eighteen of thirty-two PT-cells, the effect ranging from a 15% reduction in firing to complete cessation of activity (average reduction, 39%). The depression of firing outlasted the period of balloon inflation by an average of 85 sec; in some experiments inhibition persisted for as long as 2-3 min.4. Inflation of the balloon caused a reflex fall in arterial pressure (mean decrease, 29 mmHg), pressure reverting to the control level as soon as the balloon was deflated. Single fibre recording from the carotid sinus nerve confirmed that stimulation was confined to baroreceptors and that carotid chemoreceptors were unaffected by balloon distension.5. Depression of PT-cell activity could not be explained simply by a fall in cerebral blood flow resulting from the reflex fall in arterial blood pressure. When a comparable or greater degree of hypotension was produced by bleeding or peripheral vagal stimulation, PT-cell firing fell in a third of experiments but reverted immediately to the control level when arterial pressure was restored. Thus some factor other than a decrease in cerebral perfusion pressure was responsible for the prolonged inhibition evoked by carotid sinus distension.6. Our results are consistent with the hypothesis that baroreceptor input to the reticular formation exerts an ascending influence on cortical mechanisms, with prolonged inhibitory effects comparable to those previously demonstrated at spinal level.