Involvement of α 1-adrenoceptors in the depolarizing but not the hyperpolarizing responses of motorneurones in the neonate rat to noradrenaline

Abstract

Superfusion of the hemisected lumbar spinal cord in the neonate rat with solutions containing 10 −6 to 10 −3 M noradrenaline (NA), elicited graded depolarizations recorded from ventral roots, with a mean EC 50 value of 15.1 ± 1.5 μM (mean ± SEM, n = 37). Repeated concentration—response curves to NA could be determined from the same preparation. Adrenaline had a similar depolarizing action (EC 50 9.9 ± 1.7 μM, n = 11). Blockade of neuronal uptake of NA by desipramine (2 × 10 −6 M) caused some potentiation of submaximal responses to NA and shifted the EC 50 to 6.0 ± 1.7 μM (mean ± SEM, n = 14). The depolarizing response to NA was unaffected by dl-propranolol (10 −7 M) or yohimbine (10 −7 M). Prazosin (5 × 10 −9, 10 −8 and 10 −7 M) reduced the responses and caused a progressive rightward shift of the concentration-response curve. The onset of blockade by prazosin was slow, superfusion for at least 90–120 min being required before the blockade plateaued. Prazosin (5 × 10 −7 and 10 −8M) caused a surmountable blockade, the apparent pA, being 8.3 ± 0.2 (mean ± SEM, N = 9). Depolarizations induced by NA were also antagonised by phentolamine (10 −6M). An initial hyperpolarizing response to NA was unmasked after exposure to prazosin in 90% of preparations and was associated with a reduction in the spontaneous activity of the motorneurones. Both the hyperpolarization and reduction in spontaneous activity were attenuated by yohimbine. It is concluded that NA evokes a direct depolarizing response in lumbar motorneurones in the neonate rate, mediated by an α 1-adrenoceptor. The hyperpolarizing response revealed after α 1-adrenoceptor blockade may be mediated by an α 2-adrenoceptor.