Short communicationIdentification of 5-HT3 binding sites in rat spinal cord synaptosomal membranes
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Cited by (69)
Descending facilitation from the brainstem determines behavioural and neuronal hypersensitivity following nerve injury and efficacy of pregabalin
2008, PainCitation Excerpt :In this study, spinal ondansetron predictably reduced neuronal responses to mechanical stimuli in SAP-injected normal animals, yet following the ablation of medullary MOR cells, ondansetron now enhanced neuronal responses to noxious mechanical stimuli. Biphasic modulatory effects of spinal 5HT on sensory transmission through spinal 5HT3 receptors have been reported [7,15–17,33]. Thus, hypoalgesia induced by 5HT3 receptor stimulation on acute pain has been reported [16,17], possibly via the facilitation of spinal GABA release.
Descending facilitatory control of mechanically evoked responses is enhanced in deep dorsal horn neurones following peripheral nerve injury
2004, Brain ResearchCitation Excerpt :Using in vivo electrophysiology, we extend previous behavioural studies to demonstrate that spinal 5HT3 receptors are implicated in the descending facilitatory control of mechanical, and to a lesser degree, thermal-evoked responses of deep dorsal horn neurones. 5HT3 receptors are predominantly localised in the superficial dorsal horn where they are expressed on nerve terminals of small-diameter afferents (a subgroup of nonpeptidergic, non-IB4 afferent fibres) and on a small population of dorsal horn neurones [18,25,33,49,54]. Electrophysiological and behavioural evidence suggests that these receptors perform a pronociceptive function in the spinal cord [1,21,36,54] presumably through enhancement of transmitter release from nerve terminals, although a paradoxical antinociceptive role of this receptor has also been reported [10,19].
Suppression of the micturition reflex in urethane-anesthetized rats by intracerebroventricular injection of WAY100635, a 5-HT<inf>1A</inf> receptor antagonist
2003, Brain ResearchCitation Excerpt :Electrical or chemical stimulation of the raphe nuclei also inhibited the micturition reflex [1,18,19]. 5-HT and serotonergic drugs may influence micturition by acting on multiple receptors (5-HT1, 5-HT2 and 5-HT3) which are present in the spinal cord dorsal horn and in the autonomic and sphincter motor nuclei [12,21,26,33], in addition to receptors in the brain including 5-HT1A receptors on serotonergic neurons in the raphe nucleus. Previous studies in the rat revealed that i.v., i.t. or intracerebroventricular (i.c.v.) administration of the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), facilitated reflex bladder activity [17], whereas i.v. or i.t. administration of 5-HT1A antagonists (WAY100635 or NAD-299) blocked micturition [15,16,25,31].