[Functional role of muscarinic M1 receptor for the ganglionic transmission in the rat superior cervical ganglion].

To elucidate the sympathetic ganglia transmission via muscarinic M1 receptor subtype, we focused on the external carotid nerve (ECN), which branches from the superior cervical ganglion and innervates the thyroid gland. In addition, thyroid blood flow (TBF) was measured by a Laser Doppler blood flow meter as an indicator for the function of ECN. A relatively specific M1 agonist, AF102B, elicited a burst depolarization of ECN and an increase in TBF. Pretreatment with a selective M1 antagonist, pirenzepine, inhibited these responses. Superior cervical ganglionectomy also suppressed the AF102B-induced increase in TBF. In contrast, electric stimulation of the sympathetic trunk elicited a TBF decrease. Nicotinic receptor agonist, DMPP (dimethylphenylpiperazinium) evoked a short-term ECN depolarization, but decreased the TBF. These responses were blocked by nicotinic receptor antagonist, hexamethonium (C6), but not only by pirenzepine. Pretreatment with nitric oxide (NO) synthase inhibitor, L-NAME, suppressed the AF102B-induced increase in TBF. These findings suggest that the M1 receptor subtype may modulate the sympathetic ganglionic transmission which has a mechanism different from nicotinic transmission in terms of functional roles, i.e., blood flow changes. Furthermore, the NO system might be involved in sympathetic ganglia transmission via the M1 receptor subtype in the rat cervical ganglion.