Mu-Opioid receptors modulate noradrenaline release from the rat hippocampus as measured by brain microdialysis
References (35)
- et al.
The inhibitory effect of opioid and α2-adrenoceptor agonists on cardiac sensory neurones is pertussis toxin-insensitive
Eur. J. Pharmacol.
(1992) - et al.
Regional differences in the regulation of dopamine and noradrenaline release in medial frontal cortex, nucleus accumbens and caudate-putamen: a microdialysis study in the rat
Brain Res.
(1992) - et al.
Effect of naloxone-precipitated morphine withdrawal on noradrenaline release in rat hippocampus in vivo
Eur. J. Pharmacol.
(1992) - et al.
Chronic morphine and testosterone treatment: effects on norepinephrine and serotonin metabolism and gonadotropin secretion in male rats
Brain Res.
(1988) - et al.
Basic characteristics of noradrenaline release in the hippocampus of intact and 6-hydroxydopamine-lesioned rats as studied by in vivo microdialysis
Brain Res.
(1988) - et al.
Pertussis toxin inhibits the antinociceptive action of morphine in the rat
Eur. J. Pharmacol.
(1986) - et al.
Pertussis toxin abolishes the antinociception mediated by opioid receptors in rat spinal cord
Eur. J. Pharmacol.
(1987) Increased brain norepinephrine metabolism correlated with analgesia produced by the periaquaductal gray injection of opiates
Brain Res.
(1985)- et al.
The effects of acute and chronic administration of morphine on norepinephrine turnover in rat brain regions
Biochem. Pharmacol.
(1977) - et al.
Epinephrine, norepinephrine, dopamine and serotonin: differential effects of acute and chronic stress on regional brain amines
Brain Res.
(1982)
Nucleus accumbens and amygdala are possible substrates for the aversive stimulus effects of opiate withdrawal
Neuroscience
Opioid receptor regulation of the release of norepinephrine in brain
Neuropharmacology
Opioid receptor regulation of 5-hydroxytryptamine release from the rat hippocampus measured by in vivo microdialysis
Brain Res.
Morphine and beta endorphin inhibit release of noradrenaline from cerebral cortex but not of dopamine from rat striatum
Nature
Acceleration of cerebral noradrenaline turnover after morphine withdrawal and its retardation by acute morphine administration in rats
Naunyn-Schmiedeberg's Arch. Pharmacol.
The K+-induced increases in noradrenaline and dopamine release are accompanied by reductions in the release of their intraneuronal metabolites from the rat anterior hypothalamus
Naunyn-Schmiedeberg's Arch. Pharmacol.
Quantitative autoradiographic analysis of mu and delta opioid binding sites in the rat hippocampal formation
J. Comp. Neurol.
Cited by (30)
Shell/core differences in mu- and delta-opioid receptor modulation of dopamine efflux in nucleus accumbens
2008, NeuropharmacologyCitation Excerpt :In order to minimize the concentration gradient around the probe and, therefore, to maximize the anatomical specificity of the pharmacological treatments (i.e. to reduce the possibility of diffusion at significant concentrations at distant sites to the analyzed subregion), we selected the lowest dose of these opioid drugs that, in preliminary experiments, produced a significant effect on DA levels. These low doses were equal to, or somewhat lower than, those used in other studies (Dourmap et al., 1997; Matsumoto et al., 1994; Piepponen et al., 1999; Yokoo et al., 1994; Yoshioka et al., 1993). After the 20 min period of retrodialysis application of the drugs, the experiments were continued over an additional period of 100 min.
Effects of chronic desipramine treatment on α<inf>2</inf>-adrenoceptors and μ-opioid receptors in the guinea pig cortex and hippocampus
2008, European Journal of PharmacologyInfluence of glial cells in the dopamine releasing effect resulting from the stimulation of striatal δ-opioid receptors
2007, NeuroscienceCitation Excerpt :Moreover, this indicates that the dopamine release, although modulated by glutamate, could be maintained at the same level despite the disruption of glutamatergic transmission. The present results confirm previous experiments (Dourmap et al., 1991; Matsumoto et al., 1994; Billet et al., 2004) showing that the selective δ-opioid receptor agonist DPDPE (Mosberg et al., 1983) increases both glutamate and dopamine dialysate levels in the striatum via δ-opioid receptors (Schad et al., 1996; Billet et al., 2004). The local infusion of l-αAA into the striatum increased significantly, 20 min later, both glutamate and dopamine dialysate levels.
Knockout of the mu opioid receptor enhances the survival of adult-generated hippocampal granule cell neurons
2007, NeuroscienceCitation Excerpt :Indirectly, MOR could regulate neurogenesis by altering the levels of pro-survival factors in the dentate gyrus. MOR activity has been shown to be involved in the regulation of a number of neurotransmitters in the hippocampus including acetylcholine (ACh, Lapchak et al., 1989; Kaplan et al., 2004), GABA (Drake and Milner, 1999, 2002; Akaishi et al., 2000), and norepinephrine (NE, Matsumoto et al., 1994). GABA modulates neurogenesis, but appears to do so by altering cell differentiation, not survival (Tozuka et al., 2005; Karten et al., 2006).
Opioid systems in the dentate gyrus
2007, Progress in Brain ResearchCitation Excerpt :Opioids cause presynaptic inhibition of certain subcortical afferents to the DG. Neurochemical measures of transmitter release showed that the stimulated release of serotonin (Yoshioka et al., 1993), norepinephrine (Jackisch et al., 1984; Matsumoto et al., 1994), and acetylcholine (Jackisch et al., 1986) were each directly inhibited by opioid receptor activation. The ionic mechanisms of these inhibitory presynaptic actions have not been directly defined because it is difficult to electrophysiologically record from hippocampal nerve terminals, but molecular mechanisms that have been suggested include activation of delayed rectifying potassium channels (Wimpey and Chavkin, 1991), opioid inhibition of voltage-sensitive calcium channels by Gβγ binding (Herlitze et al., 1996; Ikeda, 1996), or direct inhibition of the vesicular fusion machinery by opioid receptor activation (Scholz and Miller, 1992; Capogna et al., 1996).