Neurotransmitter regulation of luteinizing hormone-releasing hormone neuronal function.

This paper reviews some of the research which was performed in my laboratory over the past several years on neurotransmitter regulation of LHRH neuronal function. Evidence is provided that LHRH neurons are relatively unresponsiveness to norepinephrine in their normal resting state (plasma LH levels are low) and one cause of this may be due to inhibitory influences exerted by local GABA interneurons. Also described is evidence that concomitant with preovulatory LH surges and increases in hypothalamic NE secretion there also is an increase in tyrosine hydroxylase mRNA levels and in activity within medullary A1 noradrenergic neurons. As well, following orchidectomy, A1 neuronal TH mRNA levels, hypothalamic NE secretion and plasma LH concentrations increase. Moreover, electrical stimuli which evoke hypothalamic NE secretion also elevate TH mRNA levels in A1 noradrenergic neurons. These observations indicate that increases in hypothalamic NE secretion are due to increases in A1 neuronal activity. We also examined the effects of excitatory stimuli such as NMDA and NE on LHRH/LH release and determined if such secretion is coupled to increases in LHRH mRNA. Both neurotransmitters increase LHRH mRNA levels and LH secretion. However, these two events are not coupled as morphine, which amplifies NE-induced LHRH/LH release, also blocks NE-induced increases in LHRH mRNA levels. Evidence is presented that this amplifying effect of morphine is due to a suppression of tuberinfundibular dopamine secretion thus allowing NE to evoke the release of LHRH from axon terminals in the median eminence.(ABSTRACT TRUNCATED AT 250 WORDS)