Presynaptic auto- and allelo-receptor regulation of hypothalamic opioid peptide release
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Cited by (26)
30 years of dynorphins - New insights on their functions in neuropsychiatric diseases
2009, Pharmacology and TherapeuticsNaloxone rapidly evokes endogenous kappa opioid receptor-mediated hyperalgesia in naïve mice pretreated briefly with GM1 ganglioside or in chronic morphine-dependent mice
2007, Brain ResearchCitation Excerpt :By contrast, our experimental paradigm using NLX-evoked hyperalgesia in GM1-treated mice as a model system appears to provide a more sensitive assay to demonstrate that kelatorphan inhibition of the degradation of endogenous opioid agonists can, indeed, potentiate NLX-evoked analgesia. Previous studies have suggested that presynaptic inhibitory opioid autoreceptors participate in a negative feedback system regulating the local release of endogenous opioid agonists from nociceptive neurons (Bourgoin et al., 1991; Jhamandas et al., 1984; Nikolarakis et al., 1989; Ueda et al., 1986, 1987). The pharmacological properties of these putative presynaptic inhibitory opioid autoreceptors activated by endogenous opioid agonists released at nociceptive nerve terminals in the spinal cord differ significantly from conventional presynaptic inhibitory (Gi/Go-coupled) and excitatory (Gs-coupled) opioid receptors that are activated by exogenous or endogenous opioid agonists and result in inhibition or stimulation of action-potential-initiated release of neurotransmitters from these nerve terminals (Bourgoin et al., 1991; Burns et al., 1990; Langer, 1981, 1997; Nikolarakis et al., 1989; Starke et al., 1989; see below).
Effect of chronic treatment with morphine, midazolam, and both together on β-endorphin levels in the rat
1996, Brain Research BulletinImmunocytochemical localization of delta opioid receptors in mouse brain
1995, Journal of Chemical Neuroanatomy