Lack of long-term potentiation, non-cholinergic transmission and muscarinic inhibition in cat superior cervical ganglia innervated by nodose ganglion cells.

In anesthetized cats, in which a nodose-superior cervical ganglion (SCG) anastomosis had been performed 6-9 months earlier, the nictitating membrane contraction evoked by electrical stimulation of the cervical vagus nerve ipsilateral to the anastomosis was recorded. The competence of nodose neurons in regulation the multiple synaptic mechanisms of the sympathetic ganglion was tested by comparing this response with the responses to stimulation of (self-reinnervated SCG). The response of the nictitating membrane ipsilateral to the anastomosis was smaller and had a lower EC50 for hexamethonium (C6) than the responses of the nictitating membrane ipsilateral to the intact or sutured CST. A 40 Hz 10s stimulus train to the intact or sutured CST produced potentiation of ganglionic transmission lasting 1 hour or longer, while a similar stimulus train to the anastomosed cervical vagus nerve produced no potentiation. During block of ganglionic nicotinic transmission with C6, CST or vagus nerve stimulation evoked responses which increased in amplitude with increasing stimulus frequency and were blocked by the selective muscarinic receptor antagonist pirenzepine. When the anticholinesterase eserine was added, the responses evoked by preganglionic stimulation decreased in amplitude in the intact SCG, as previously shown [7], and in the self-reinnervated SCG. This effect, which is due to inhibition mediated by muscarinic receptors selectively blocked by AF-DX116, was absent in the anastomosed SCG. During block of ganglionic transmission with C6 and atropine, a 40 Hz stimulus train to the intact or to the sutured CST evoked a slow, small amplitude contraction that was enhanced by naloxone. This response, most likely mediated by peptides [6], was absent in the anastomosed SCG.(ABSTRACT TRUNCATED AT 250 WORDS)