1995
DOI: 10.1016/0304-3940(95)11564-5
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5-Hydroxytryptamine3 receptor modulation of excitatory amino acid release in the rat nucleus tractus solitarius

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Cited by 43 publications
(23 citation statements)
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“…Indeed, we found that the inhibitory effect of dPAG electrical or chemical stimulation on PECR could be blocked not only by intra-NTS microinjections of a 5-HT 3 receptor antagonist, granisetron, but also by local microinjections of a GABA A receptor antagonist, bicuculline. Taking into account these and previous data, it can be hypothetized that the inhibition by dPAG stimulation of the cardiovagal component of the baroreceptor reflex implies the following sequence: 1) excitation (by electrical or chemical stimulation) of dPAG cell bodies triggers the release of endogenous 5-HT within the NTS and consequently the activation of local presynaptic 5-HT 3 receptors (21, 23); 2) stimulation of these receptors on vagal afferent fibers promotes the local release of glutamate (1), which, in turn, activates GABAergic interneurons; and 3) the resulting stimulation of GABA A receptors finally exerts an inhibitory influence on NTS neurons at the origin of the aortic and carotid cardiac responses of the baroreceptor reflex.…”
Section: Discussionmentioning
confidence: 81%
“…Indeed, we found that the inhibitory effect of dPAG electrical or chemical stimulation on PECR could be blocked not only by intra-NTS microinjections of a 5-HT 3 receptor antagonist, granisetron, but also by local microinjections of a GABA A receptor antagonist, bicuculline. Taking into account these and previous data, it can be hypothetized that the inhibition by dPAG stimulation of the cardiovagal component of the baroreceptor reflex implies the following sequence: 1) excitation (by electrical or chemical stimulation) of dPAG cell bodies triggers the release of endogenous 5-HT within the NTS and consequently the activation of local presynaptic 5-HT 3 receptors (21, 23); 2) stimulation of these receptors on vagal afferent fibers promotes the local release of glutamate (1), which, in turn, activates GABAergic interneurons; and 3) the resulting stimulation of GABA A receptors finally exerts an inhibitory influence on NTS neurons at the origin of the aortic and carotid cardiac responses of the baroreceptor reflex.…”
Section: Discussionmentioning
confidence: 81%
“…Similarly, presynaptic inhibition of GABA release is mediated by 5-HT 1A [90,95,96] and 5-HT 1B receptors [88,117]. By activation of 5-HT 3 receptors, instead, 5-HT stimulates the release of either glutamate [7,57,185] or GABA [90,96,179]. Also 5-HT 2 receptors were shown to stimulate GABA release [2] and to either increase [2,72,177] or reduce [118] glutamate release in distinct structures.…”
Section: Modes Of Interactionmentioning
confidence: 99%
“…For example, in tractus solitarius nucleus [7], dorsal vagal motor nucleus [185] and area postrema [57] 5-HT stimulates glutamate release by activation of pre-synaptic 5-HT 3 receptors. In suprachiasmatic nucleus, pre-synaptic 5-HT 1B receptors inhibit retinal input [151] whereas 5-HT 7 receptors reduce glutamate effects at a post-synaptic level [155]; by these effects, serotonin changes neuronal responsiveness to light stimuli and participates to the regulation of circadian rhythms.…”
Section: Modulation Of Glutamate Transmissionmentioning
confidence: 99%
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