Evidence that activation of both vagal and glossopharyngeal afferents cause the release of 5‐HT in the NTS

Abstract

Pharmacological studies indicate that 5‐HT is released in the nucleus tractus solitarii (NTS) in response to cardiovascular afferent activation. Experiments using a modified form of fast differential voltammetry were carried out to determine if this release of 5‐HT could be detected in the NTS. Rats were anaesthetized with [alpha]‐chloralose (120 mg kg−1; i.v), neuromuscular blocked and artificially ventilated. Activation of cardiopulmonary afferents by phenylbiguanide (PBG; i.a.) caused a transient rise in 5‐HT of 17.8 ± 2.5nM. Citalopram (1 mg kg−1; i.v.) had no effect, while the OCT3/PMAT inhibitor decynium‐22 (600 [micro]g kg−1, i.v.) potentiated this increase in 5‐HT from 18 ± 4 to 70 ± 11 nM. Increasing baroreceptor afferent input with i.v. noradrenaline increased 5‐HT release, while decreasing this input with i.v. sodium nitroprusside had no effect. Citalopram (1 mg kg−1) had no effect on these responses. Activation of the chemoreflex with i.a. sodium cyanide caused a maintained rise in 5‐HT of 27 ± 6 nM. The data supports the view that cardiovascular afferents cause the release of 5‐HT in the NTS.