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Evidence that activation of both vagal and glossopharyngeal afferents cause the release of 5‐HT in the NTS
Author(s) -
Hosford Patrick Steven,
Millar Julian,
Ramage Andrew G
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.701.1
Subject(s) - sodium nitroprusside , chemistry , serotonin , baroreceptor , chemoreceptor , endocrinology , medicine , citalopram , anesthesia , 5 ht receptor , pharmacology , receptor , nitric oxide , heart rate , biochemistry , blood pressure
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.