5-Hydroxytryptamine3 receptor modulation of excitatory amino acid release in the rat nucleus tractus solitarius
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2021, Physiology and BehaviorCitation Excerpt :There are a large number of serotonergic inputs from the dorsal raphe (DR.) to the VTA which strongly promotes reward, and motivational function [61]. Serotonin (5-HT) has a modulatory role in glutamate transmission [62], especially in the brain areas controlling pain [63, 64]. The serotonergic modulatory effects on pain likely depend on the activated 5-HT receptor type and the action site.
5-HT<inf>3</inf> receptor-mediated neural transmission of cardiorespiratory modulation by the nucleus of the tractus solitarius
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2018, NeuropharmacologyCitation Excerpt :Thus dlPAG activation may be at the origin of serotonin release into the NTS, to ultimately activate presynaptic 5-HT3a receptors (Hosford et al., 2014), as found previously (Bernard et al., 2008). The activation of these receptors is at the origin of vagal presynaptic glutamatergic release into the NTS (Ashworth-Preece et al., 1995), and glutamate acts on GABAergic interneurones embedded with excitatory amino acid receptors (Callera et al., 1997; Sévoz et al., 1996). In turn, GABA inhibits second-order carotid chemoreflex neurons through activation of GABAA receptors, and may block tachypneic chemoreflex responses as it was found previously for bradycardic chemoreflex responses in awake and anaesthetised rats (Sévoz et al., 1997).
Key role of 5-HT<inf>3</inf> receptors in the nucleus tractus solitarii in cardiovagal stress reactivity
2017, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Central 5-HT3 receptors are known to mediate an excitatory action on target cells (Kito et al., 2012). Accordingly, administration of a 5-HT3 receptor agonist into the NTS increases the local release of endogenous glutamate from vagal afferents (Ashworth-Preece et al., 1995), resulting in increased activity in second-order neurons (Jeggo et al., 2005) (Fig. 2). We have shown that stimulation of NTS 5-HT3 receptors activates a pressor efferent pathway via indirect facilitation of NO and EAA receptor-mediated mechanisms (Sévoz-Couche et al., 2002), without modifying heart rate.
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