Beta-endorphin alters electrical activity of gonadotropin releasing hormone neurons located in the terminal nerve of the teleost medaka (Oryzias latipes).

ABSTRACT

Endogenous opioid peptides (EOPs) are an important class of modulators of the hypothalamo-pituitary axis; treatment with opiates leads to inhibition of GnRH and LH secretion and suppression of reproductive functions. However, little work has been done to investigate the effect of opiates on the electrical activity of GnRH neurons, which ultimately controls GnRH secretion. The purpose of the present study was to investigate the effects of the EOP beta-endorphin on electrical activity of GnRH neurons located in the terminal nerve (TN) associated with the olfactory bulb. We used an excised intact brain preparation from transgenic medaka in which green fluorescent protein (GFP) is genetically expressed in TN-GnRH neurons. These GFP-expressing neurons were then targeted for whole-cell current clamp recordings. Treatment with beta-endorphin led to changes in several characteristics of electrical activity, including depolarization of membrane potential and a decrease in spike amplitude--similar to that observed in response to depolarizing high K(+) treatment. This finding suggests a model in which beta-endorphin depolarizes membrane potential leading to Na(+)-channel inactivation, and subsequent suppression of action-potential amplitude. On the other hand, beta-endorphin had no effect on membrane potential in synaptically isolated GnRH neurons. These results suggest that beta-endorphin is acting indirectly on TN-GnRH neurons to inhibit action potential firing.