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Abstract
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.