Glutamate (Glu) stimulation of the dorsal facial area (DFA) in the medulla might induce an increase in common carotid arterial (CCA) blood flow in cats. Serotonin (5-HT) might inhibit glutamate release via 5-HT2 receptor in DFA to reduce the CCA blood flow. This study will explore which subtype(s) of Glu receptors in DFA were involved and the interaction between glutamatergic and serotonergic actions in DFA to regulate the CCA blood flow. Microinjection of Glu (25-100 nmol), N-methyl-D-aspartate (NMDA; 1-4 nmol), orα-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA; 0.5-2 nmol) increased CCA blood flow dose-dependently. The potency was AMPA>NMDA>Glu. The Glu-induced increase in CCA blood flow was reduced by pretreatment with either D-2-amino-5-phosphonopentanoate (D-AP5; 2.5-5.0 nmol), or glutamate diethylester (GDEE; 25-50 nmol). The CCA blood flow was increased by ketanserin (1.0 nmol), and decreased by (+/-)-1-(2, 5-dimethoxy-4-iodopheny1)-2-aminopropane (DOI; 1.0 nmol). Both effects were attenuated by pretreatment with either D-AP5 or GDEE respectively. We conclude that in the DFA, both NMDA and AMPA receptors are involved in regulating CCA blood flow and AMPA receptor exerts greater effect; such response may be modulated by 5-HT2 receptors.
