Abstract

This study explored which subtypes of glutamate receptors in the dorsal facial area are involved in the interaction between glutamatergic and serotonergic actions in controlling common carotid arterial blood flow. Microinjection of glutamate (25–100 nmol), N-methyl- d-aspartate (NMDA; 1–4 nmol), or α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA; 0.5–2 nmol) into the dorsal facial area dose-dependently increased common carotid arterial blood flow. The potency order was AMPA>NMDA>glutamate. The glutamate-induced increase in common carotid arterial blood flow was reduced by pretreatment with either d-2-amino-5-phosphonopentanoate ( d-AP5; 2.5–5.0 nmol), or glutamate diethylester (25–50 nmol). The common carotid arterial blood flow was increased by ketanserin (1.0 nmol) and decreased by (±)-1-(2, 5-dimethoxy-4-iodopheny1)-2-aminopropane (1.0 nmol). Both effects were attenuated by pretreatment with either d-AP5 or glutamate diethylester. We conclude that activation of both NMDA and AMPA receptors in dorsal facial area is responsible for the increase in common carotid arterial blood flow, and AMPA receptor may play a greater role. Such response may be suppressed by 5-HT 2 action.

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