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Impaired endocannabinoid signalling in the rostral ventromedial medulla underpins genotype-dependent hyper-responsivity to noxious stimuli
2014, PainCitation Excerpt :Microinjection of cannabinoid compounds directly into the RVM have been shown to modulate neuronal firing in cells of the RVM under conditions of acute [50,54,55,57] and persistent [57] inflammatory pain, as determined by in vivo electrophysiological studies. The RVM has a dense population of serotonergic [3,11,46,61,78], GABAergic [2,56], and glutamatergic neurons [81]; however, the expression of CB1 receptors on GABAergic, glutamatergic, or serotonergic neurons in the RVM has yet to be confirmed anatomically (for review, see Rea et al. [70]). Moreover, to our knowledge, no studies to date have investigated serotonergic, GABAergic, or glutamatergic tone in the RVM of WKY vs SD rats.
Multiple roles of serotonin in pain control mechanisms -Implications of 5-HT<inf>7</inf>and other 5-HT receptor types
2013, European Journal of PharmacologyCitation Excerpt :From the nucleus raphe magnus, the nucleus paragigantocellularis and the ventral portion of the nucleus gigantocellularis in the rostroventral medulla, serotoninergic neurons project specifically into the superficial laminae of the dorsal horn of the spinal cord where primary afferent fibers convey nociceptive signals to second order (mainly spino-thalamic) neurons (Kwiat and Basbaum, 1992). In both rodents and cats, 5-HT terminals at the spinal level have an exclusive supraspinal origin because transection of the thoracic spinal cord leads to an extensive depletion of 5-HT and the disappearance of 5-HT immunoreactivity in the lumbar segments (Oliveras et al., 1977; Ruda et al., 1986). Direct electrical stimulation of the rostroventral medulla induces both the release of 5-HT at the spinal level and concomitant anti-nociceptive effects (Bourgoin et al., 1980; Cui et al., 1999; Hentall et al., 2006; Rivot et al., 1982).
Noxious stimulation excites serotonergic neurons: A comparison between the lateral paragigantocellular reticular and the raphe magnus nuclei
2013, PainCitation Excerpt :In line with these behavioral observations, spinal neuronal response to noxious stimuli is decreased by direct stimulation of the LPGi [42] or the RMg [29,59,80] through serotonin receptor activation at the spinal level [6,44,68]. Importantly, LPGi and RMg serotonergic neurons together constitute the B3 group [83], the major source of serotonin release within spinal superficial laminae [50–52,72,82]. Gau et al. [38] demonstrated that serotonergic neurons of the LPGi (located laterally to RMg wings) are also responsible for the inhibition of cardiac baroreflex induced by strong thermal noxious stimuli (⩾48°C).
Inhibition of opioid release in the rat spinal cord by serotonin 5-HT<inf>1A</inf> receptors
2007, Brain ResearchCitation Excerpt :5-HT1 receptors signal through Gi/o (Pauwels, 2000), which can inhibit opioid release by inactivating voltage-gated Ca2+ channels (Dolphin, 2003). Serotonergic terminals in the spinal cord are of supraspinal origin (Stamford, 1995), with a substantial fraction of the serotonin content of the dorsal horn originating in the nucleus raphe magnus (Oliveras et al., 1977). Although for some time it was believed that the bulbospinal pain inhibitory pathway was serotonergic, it is now clear that the serotonergic neurons in the nucleus raphe magnus are different from the ON and OFF cells that mediate descending facilitation and inhibition, respectively, of pain responses (Gao and Mason, 2000).
Influence of Serotonin on the Blood-Brain and the Blood-Spinal Cord Barriers
2004, Blood-Spinal Cord and Brain Barriers in Health and Disease
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