Abstract
Although catecholamines have been studied extensively, much is still unknown regarding their role in the control of neuronal excitability within the spinal cord. Therefore, I examined the effects of exogenously applied epinephrine (Epi) and norepinephrine (NE) on primary afferent terminals and motoneurons of the hemisected, superfused, frog spinal cord utilizing sucrose gap recording techniques.Application of Epi or NE to the cord evoked hyperpolarizing responses in both primary afferent terminals and motoneurons in the unstimulated cord. This response was apparently mediated through alpha(,2)-adrenoceptors since the potential change was mimicked by agonists and blocked by antagonists selective for this receptor. Depolarizing responses following the initial hyperpolarization were also seen--more frequently in motoneurons--and these responses were sensitive to beta-adrenergic antagonists.Electrically-evoked reflexes were studied using both AC and DC recording techniques. Low concentrations of Epi and NE facilitated reflexes evoked by stimulation of a dorsal root and recorded from an extensor nerve. This action was also produced by beta agonists and blocked by beta antagonists. Higher concentrations of catecholamines had an inhibitory effect on both the extensor and flexor reflexes and this action was only partially reversed by superfusion of alpha antagonists.Responses produced by excitatory amino acids were selectively altered by Epi and NE. Low concentrations of catecholamines potentiated the responses evoked by L-glutamate and L-aspartate, while higher concentrations depressed these responses. A specific interaction of the amines with two of the receptor subtype-selective agonists was discovered. Epi and NE potentiated N-methyl-D-aspartate (NMDA)-evoked responses by activation of beta receptors. Responses caused by quisqualate (QUIS) were reduced by alpha(,2)-adrenoceptor activation.In summary, complex responses evoked by catecholamines were found in the frog spinal cord. The potential changes produced by these compounds appeared to be caused both by direct actions of Epi and NE on spinal neurons as well as indirect effects occurring through interactions with other transmitter systems.