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      Opioids Hyperpolarize β-Endorphin Neurons via μ-Receptor Activation of a Potassium Conductance

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          Intracellular recordings were made from hypothalamic arcuate (ARC) neurons with biocytin-filled electrodes under current- and voltage-clamp in slices prepared from ovariectomized guinea pigs which were pretreated with estradiol. Forty-three neurons were identified after linking the intracellular biocytin with streptavidin-FΓΓC and subsequently were examined for β-endorphin immunoreactivity. Ten of these neurons were immunoreactive for β-endorphin. β-Endorphin neurons displayed the following passive membrane properties: RMP: –56 ± 2 mV; R<sub>in</sub>: 439 ± 66 MΩ; τ: 17.5 ± 2.4 ms; and often fired spontaneously (5.9 ± 2.2 Hz). These membrane characteristics were not different from identified neurons in the ARC that were not immunoreactive for β-endorphin. β-Endorphin neurons exhibited instantaneous inward rectification and time-dependent rectification. The µ-opioid agonist Tyr-ö-Ala-Gly-MePhe-Gly-ol (DAGO) decreased spontaneous firing, induced membrane hyperpolarization (12 ± 2 mV; range 6–22 mV) and decreased the R<sub>in</sub> (38 ± 4%) of the β-endorphin neurons. These effects of DAGO were blocked by the opioid antagonist naloxone (1 µ M) and were not blocked by 1 µ M TTX. DAGO-responsive cells were unaffected by either ĸ- or δ-receptor opioid agonists. These results indicate that µ-receptors may be autoreceptors on ARC β-endorphin neurons and that activation of opioid µ-receptors hyperpolarizes β-endorphin neurons via an increase in K<sup>+</sup> conductance. Therefore, opioid peptides may modulate opioid tone through an ‘ultra-short loop’ feedback control mechanism.

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          S. Karger AG
          03 April 2008
          : 52
          : 3
          : 268-275
          Department of Physiology, Oregon Health Sciences University, Portland, Oreg., USA
          125597 Neuroendocrinology 1990;52:268–275
          © 1990 S. Karger AG, Basel

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