On the involvement of GABA in the analgesia produced by baclofen, muscimol and morphine
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GABA<inf>B</inf> receptors and pain
2018, NeuropharmacologyCitation Excerpt :In the early 90's it became evident that the systemic administration of (±)baclofen resulted in analgesic and anti-hyperalgesic effects in experimental models of acute and chronic pain at doses which were significantly lower than those required for muscle-relaxation. Baclofen exerted antinociceptive effects when administered directly in the CNS by intrathecal and intracerebroventricular injections (Sawynok and LaBella, 1982; Wilson and Yaksh, 1978). Consistent with a central site of action for baclofen, GABAB receptor antagonists injected intrathecally were able to prevent the analgesic effect of systemic baclofen (Malcangio et al., 1991).
The role of CA3 GABA<inf>B</inf> receptors on anxiolytic-like behaviors and avoidance memory deficit induced by D-AP5 with respect to Ca<sup>2 +</sup> ions
2017, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :Combining behavioral and electrophysiological approaches to investigate cellular and synaptic bases, Kobayashi et al., 2006 showed that once the CA3 circuit becomes more stable, it may cause a reduction in locomotor activity (Kobayashi et al., 2006). Baclofen has also been reported to possess muscle relaxant property (Hammond and Drower, 1984; Levy and Proudfit, 1977; Sawynok and LaBella, 1982; Wilson and Yaksh, 1978). Presynaptic GABABRs contribute to presynaptic inhibition (Fischer and Parnas, 1996) and the activation of postsynaptic GABABRs on pyramidal cells is highly effective in counteracting responses mediated by NMDARs (Staubli et al., 1999).
GABA and valproate modulate trigeminovascular nociceptive transmission in the thalamus
2010, Neurobiology of DiseaseCitation Excerpt :GABA has a complex modulatory role in the processing of tactile sensory information in the thalamus (Lee et al., 1994a; Lee et al., 1994b). The antinociceptive properties of GABAergic agonists are well described (Sawynok and LaBella, 1982; Vaught et al., 1985) and may in part be due to actions in the thalamus. Microiontophoresis of GABA inhibits nociceptive transmission in several thalamic nuclei (Olausson et al., 1994; Reyes-Vazquez et al., 1986; Yamashiro et al., 1994; Yamashiro et al., 1997) while interventions that increase the concentration of GABA in the thalamus are correlated with behavioural antinociception (Ipponi et al., 1999).
Vigabatrin attenuates the development and expression of tolerance to morphine-induced antinociception in mice
2009, Pharmacology Biochemistry and BehaviorIn vivo characterization of the effects of human hemokinin-1 and human hemokinin-1(4-11), mammalian tachykinin peptides, on the modulation of pain in mice
2008, Brain, Behavior, and ImmunityCitation Excerpt :γ-Aminobutyric acid (GABA) is well known as an inhibitory amino acid neurotransmitter in the central nervous system. Baclofen, a GABA receptor agonist, increases the pain threshold in rodents (Bartolini et al., 1981; Sawynok and LaBella, 1982), and picrotoxin and bicuculline, two GABA receptor antagonists, induce a dose-related antinociceptive effect through augmented release of GABA (Malcangio et al., 1992). The GABA uptake inhibitors, nipecotic acid, and its derivatives, SKF-100330A and SKF-89976A, display significant antinociceptive activity in the mouse tail immersion assay (Kendall et al., 1982; Zorn and Enna, 1985).