Activation of α-adrenoceptors indirectly facilitates sodium pumping in frog motoneurons

The effects of clonidine on Na + pumping in motoneurons of the isolated frog spinal cord was investigated using sucrose gap recordings from ventral roots. Na + pump activity, induced in motoneurons either by tetanizing the dorsal root or by rapidly exposing the cord to normal medium following 30 min in K +-free Ringer's solution (K +-activated hyperpolarizations), was increased by application of clonidine (100 μM). These actions of clonidine were blocked by the preferential α 2-adrenergic antagonist yohimbine, but not by α 1-adrenergic antagonist prazosin or the β-blocker propranolol. Clonidine's effects on Na + pumping appeared to be indirect (presumably via interneurons) because its effects on K +-activated hyperpolarizations were reduced by tetrodotoxin (TTX) or high concentrations of Mg 2+. This indirect mechanism involved activation of non-NMDA excitatory amino acid receptors. Thus, in the presence of clonidine, CNQX, but not APH, limited the ability of clonidine to enhance K +-activated hyperpolarizations. The AMPA receptor may play a role in the process. K +-activated hyperpolarizations were augmented by the presence of AMPA; NMDA had no effect. The present results are consistent with the idea that activation of α 2-adrenoceptors produces the following: the release of excitatory amino acids from interneurons; the activation of non-NMDA receptors on motoneurons; increased Na + influx and loading and increased Na + pump activity.