Elsevier

Neuroscience

Volume 31, Issue 1, 1989, Pages 269-273
Neuroscience

Presynaptic auto- and allelo-receptor regulation of hypothalamic opioid peptide release

https://doi.org/10.1016/0306-4522(89)90049-3Get rights and content

Abstract

Recent studies have shown that inhibitory feedback mechanisms regulate the release of the endogenous opioid peptides β-endorphin (acting predominantly at μ opioid receptors in the brain), dynorphin (a κ opioid receptor ligand) and [Met]enkephalin (a δ opioid receptor ligand) from the rat hypothalamus. By using specific antagonists of the various opioid receptor types, it is shown that the release of these peptides from hypothalamic slices in vitro is not only controlled by homologous (auto)-receptors, but that cross-regulation between the three neuronal opioid receptor types also occurs; thus, the δ receptor antagonist N,N-diallyl-Tyr-Aib-Aib-Phe-Leu increases the release of all three peptides, the μ receptor antagonist d-tetrahydroisoquinoline-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH2 increases that of β-endorphin and dynorphin, and the κ receptor antagonist nor-binaltorphimine increases that of dynorphin; all these effects occur in the presence of tetrodotoxin, indicating a presynaptic site of action. We propose the term “allelo-receptors” to describe this particular form of neuronal regulation in which an endogenous ligand, acting via its own specific receptor, also regulates the release of related peptides which activate different classes of opioid receptors.

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Cited by (26)

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    2007, Brain Research
    Citation 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).

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