Single cell activity in the noradrenergic A-5 region: responses to drugs and peripheral manipulations of blood pressure.

Single unit recordings were obtained from the region of the A-5 noradrenergic cell group in the ventrolateral tegmentum at the level of the exiting VIIth nerve. In this region a distinct cell population was identified which exhibited moderate spontaneous rates of activity, a regular firing pattern, wide action potentials, and a characteristic response to sensory stimulation consisting of a brief excitation followed by a more prolonged period of inhibition. Simultaneous visualization of recording sites and catecholamine cells by fluorescence histochemistry indicated a close association between the location of the recorded units and the A-5 noradrenergic cell group. Antidromic responses could be elicited by stimulation of the spinal cord and forebrain indicating that A-5 cells project both anteriorly and posteriorly. The spontaneous activity of A-5 cells was invariably suppressed by low doses of clonidine and L-amphetamine, while adjacent cells showed varying responses to these agents. The effects of clonidine and L-amphetamine could be reversed by low doses of the alpha2-adrenoceptor antagonist, piperoxane. When applied by microiontophoresis, clonidine and norepinephrine were effective in inhibiting A-5 neurons. The rank order of inhibitory potencies for agonists applied microiontophoretically to A-5 neurons was characteristic of an alpha2-receptor (i.e. clonidine greater than norepinephrine greater than phenylephrine). Thus, the physiological and pharmacological properties of the A-5 neurons closely matched those previously reported for noradrenergic neurons elsewhere. Sixty percent of A-5 neurons responded to peripherally induced changes in blood pressure with reciprocal changes in spontaneous firing rate. Increases in blood pressure led to decreases in spontaneous activity while decreases in pressure led to the opposite response. These observations are consistent with the proposed vasomotor role for the A-5 noradrenergic cell group.