The α1- and α2-adrenoceptor and muscarinic responses of normal and axotomized bullfrog sympathetic ganglia

Abstract

When neurones in bullfrog paravertebral sympathetic ganglia are studied by means of the sucrose-gap technique, muscarinic agonists produce a biphasic response (an initial hyperpolarization of ganglionic C cells followed by a depolarization of ganglionic B cells). Activation of ganglionic α2-adrenoceptors promotes hyperpolarization. The present experiments with selective α1- and α2-adrenoceptor agonists and antagonists provided evidence for the existence of hitherto undescribed α1-adrenoceptors, which are responsible for the production of depolarizing responses in these ganglia. Fifteen to twenty-five days after cutting postganglionic axons (axotomy), there was a nonselective depression of both α1- and α2-adrenoceptor mechanisms but little change in muscarinic responses. These results argue against the hypothesis that C cells assume all the properties of B cells after axotomy. Since the α-selective agonist phenylephrine failed to depolarize axotomized ganglia, it is unlikely that an α1-adrenoceptor mechanism is prominent in axotomized neurones as it is in some immature adrenergic neurones. The data are consistent with the idea that axotomy selectively affects the properties of certain types of cation channels and raise questions as to the mechanisms involved in regulating the expression and maintenance of specific neurotransmitter responses on ganglionic neurones.Key words: axotomy, α-adrenoceptor mechanisms, muscarinic receptors, sympathetic ganglion, frog.