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Serotonin in the solitary tract nucleus shortens the laryngeal chemoreflex in anaesthetized neonatal rats
Author(s) -
Donnelly William T.,
Bartlett Donald,
Leiter J. C.
Publication year - 2016
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep085716
Subject(s) - solitary tract , serotonin , nucleus , neuroscience , anatomy , medicine , biology , anesthesia , chemistry , receptor
New FindingsWhat is the central question of this study? Failure to terminate apnoea and arouse is likely to contribute to sudden infant death syndrome (SIDS). Serotonin is deficient in the brainstems of babies who died of SIDS. Therefore, we tested the hypothesis that serotonin in the nucleus of the solitary tract (NTS) would shorten reflex apnoea.What is the main finding and its importance? Serotonin microinjected into the NTS shortened the apnoea and respiratory inhibition associated with the laryngeal chemoreflex. Moreover, this effect was achieved through a 5‐HT 3 receptor. This is a new insight that is likely to be relevant to the pathogenesis of SIDS.The laryngeal chemoreflex (LCR), an airway‐protective reflex that causes apnoea and bradycardia, has long been suspected as an initiating event in the sudden infant death syndrome. Serotonin (5‐HT) and 5‐HT receptors may be deficient in the brainstems of babies who die of sudden infant death syndrome, and 5‐HT seems to be important in terminating apnoeas directly or in causing arousals or as part of the process of autoresuscitation. We hypothesized that 5‐HT in the brainstem would limit the duration of the LCR. We studied anaesthetized rat pups between 7 and 21 days of age and made microinjections into the cisterna magna or into the nucleus of the solitary tract (NTS). Focal, bilateral microinjections of 5‐HT into the caudal NTS significantly shortened the LCR. The 5‐HT 1a receptor antagonist, WAY 100635, did not affect the LCR consistently, nor did a 5‐HT 2 receptor antagonist, ketanserin, alter the duration of the LCR. The 5‐HT 3 specific agonist, 1‐(3‐chlorophenyl)‐biguanide, microinjected bilaterally into the caudal NTS significantly shortened the LCR. Thus, endogenous 5‐HT released within the NTS may curtail the respiratory depression that is part of the LCR, and serotonergic shortening of the LCR may be attributed to activation of 5‐HT 3 receptors within the NTS. 5‐HT 3 receptors are expressed presynaptically on C fibre afferents of the superior laryngeal nerve, and serotonergic shortening of the LCR may be mediated presynaptically by enhanced activation of inhibitory interneurons within the NTS.