Abstract
The suppressive effect of opioid administration on secretion of luteinizing hormone (LH) probably originates primarily in the hypothalamus1–5. Furthermore, the endogenous ligands of the opiate receptors (endorphins) seem to exert a tonic inhibition on the hypothalamic–pituitary–LH axis, as blockade of opiate receptors by the narcotic antagonist naloxone causes a pronounced increase in the release of LH3,4. However, it is unknown which of the particular endorphins present in the hypothalamus is responsible for this tonic inhibition. In addressing this issue we hypothesized that a similar effect to that obtained by blocking receptors with naloxone would be achieved by reducing the concentration of a specific endorphin at the receptors using antibodies against specific opioid peptides. We report here that both anti-β-endorphin antibodies and anti-dynorphini1-13 antibodies, when injected into the arcuate nucleus of the mediobasal hypothalamus (MBH) of immature female rats, caused an increase in serum LH. Anti-methionine-enkephalin (Met-enkephalin) antibodies did not affect LH levels. We conclude that β-endorphin and dynorphin rather than Met-enkephalin have a role in regulation of LH secretion in immature female rats. These may represent the first data ascribing a specific physiological function to a particular endorphin
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Schulz, R., Wilhelm, A., Pirke, K. et al. β-Endorphin and dynorphin control serum luteinizing hormone level in immature female rats. Nature 294, 757–759 (1981). https://doi.org/10.1038/294757a0
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DOI: https://doi.org/10.1038/294757a0
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