Microinjections of nicotine (10-80 nmol), choline (10-160 nmol) and physostigmine (PHY), an acetylcholinesterase inhibitor, into the dorsal facial area (DFA) of urethane and α-chloralose-anesthetized cats, elicited a dose-dependent increase in the blood flow of the common carotid artery of the injected side. Nicotine-induced increase in CCA blood flow was attenuated by 66-83 % by prior microinjections of α-bungarotoxin (0.02 nmol), a selective antagonist for the nicotinic receptors containing α-7 subunits. The nicotinic response was reduced by 35-52 % by prior microinjections of mecamylamine (2 nmol), an antagonist for the nicotinic receptors containing α3b4 subunits. Blockade of excitatory amino acid (EAA) neurotransmission in the DFA did not attenuate the responses to nicotine-induced increase in CCA blood flow. We conclude that (1) The increase in CCA blood flow elicited by the administration of PHY result from the augmented action of ACh release from cholinergic terminals within the dorsal facial area; (2) ACh-synthesizing enzyme, choline acetyltransferase (CAT) containing neurons and nicotinic receptors are present in the DFA; (3) activation of these receptors results in increase in common carotid artery blood flow; (4) two different subtypes of nicotinic receptors (α-7 subunits, and α3b4 subunits) must be present in the DFA and the predominant type of nicotinic receptor in the DFA contains α-7 subunits and (6) excitatory amino acid receptors in the DFA are not involved in mediating responses to nicotine.
