Mandatory neuropeptide-steroid signaling for the preovulatory luteinizing hormone-releasing hormone discharge.
In this article I have examined various aspects of the complex spatio-temporal patterning of peptidergic signaling that lead to synchronized development of neural events for the preovulatory LHRH discharge on proestrus. Undoubtedly, the integration of these events is orchestrated by both ovarian steroids, E2 and P. Evidence accumulated in recent years has failed to affirm the perceived notion that E2 is an adequate peripheral signal for the timely, robust discharge of LHRH on proestrus. The current understanding is shaped by the thesis that the concerted central actions of E2 and P are mediated by a host of regulatory peptides produced locally in the hypothalamus, and steroids, in general, augment the production and release of both inhibitory and excitatory peptides in a timely fashion to facilitate the preovulatory LHRH discharge. Since these peptidergic pathways appear mandatory for signal transfer, considerable recent research has been devoted first to identifying the signals that selectively participate in the induction of preovulatory LHRH (LH) surge, and then to trace the route of signal transmission that ultimately leads to LHRH hypersecretion on the afternoon of proestrus (Fig. 1). The peptidergic pathways that propagate and transmit impulses for the preovulatory LHRH discharge reside in the SCN-MPN-MPOA-ARC-ME neural complex (Fig. 1). The timely initiation of these impulses is entrained to the photo-periodic input reaching the SCN by the retino-hypothalamic tract. The evidence is already in place to show that further information processing is transduced in the MPN; however, the nature of neurochemical signaling between the two sites remains to be deciphered. The available evidence favors a mandatory participation of inhibitory (EOP and NPK) and excitatory (NPY, GAL, NT, and AII) messenger molecules within the SCN-MPN-MPOA-ARC-ME complex (Fig. 1). It is possible that the relevant information from the SCN-MPN is conveyed caudally to the ARC in order to initiate a chain of events for disinhibition/excitation of the NPY-EOP network and to affect LHRH neurosecretion at the perikaryal level in the MPOA and at axon terminals in the ME. Also, either concurrently or on a time-delayed basis, the relevant information from the MPN may be relayed to the MPOA via the local peptidergic network comprised of NT, EOP, NPK, and GAL. This transmission may initially be critical for elicitation of antecedent neurosecretory events in the ME and to ultimately evoke the preovulatory LHRH surge.(ABSTRACT TRUNCATED AT 400 WORDS)
Kalra
S P
SP
Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610-0244.
D000818:Animals; D004967:Estrogens / Q000502:physiology*; D005246:Feedback; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism*; D006801:Humans; D007031:Hypothalamus / Q000502:physiology; D008297:Male; D009479:Neuropeptides / Q000502:physiology*; D011359:Proestrus / Q000502:physiology*; D011374:Progesterone / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
D004967:Estrogens; D009479:Neuropeptides; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone