ROLES OF 2ND-MESSENGER SYSTEMS AND NEURONAL-ACTIVITY IN THE REGULATION OF LORDOSIS BY NEUROTRANSMITTERS, NEUROPEPTIDES, AND ESTROGEN - A REVIEW

Citation
Lm. Kow et al., ROLES OF 2ND-MESSENGER SYSTEMS AND NEURONAL-ACTIVITY IN THE REGULATION OF LORDOSIS BY NEUROTRANSMITTERS, NEUROPEPTIDES, AND ESTROGEN - A REVIEW, Neuroscience and biobehavioral reviews, 18(2), 1994, pp. 251-268
Citations number
305
Categorie Soggetti
Neurosciences,"Behavioral Sciences
ISSN journal
01497634
Volume
18
Issue
2
Year of publication
1994
Pages
251 - 268
Database
ISI
SICI code
0149-7634(1994)18:2<251:RO2SAN>2.0.ZU;2-H
Abstract
Many neurotransmitters and neuropeptides can affect the rodent feminin e sexual behavior, lordosis, when administered in the ventromedial hyp othalamus (VMH), midbrain central gray (MCG), or other brain regions. A survey of the electrophysiological and biochemical actions of these neural agents revealed that there is a very consistent association bet ween lordosis facilitation with both the activation of the phosphoinos itide (PI) pathway and the excitation of VMH and MCG neurons. In contr ast, lordosis inhibition is associated, less consistently, with altera tions of the adenylate cyclase (AC) system and the inhibition of neuro nal activity. The findings that lordosis could be facilitated by going beyond membrane receptors and directly activating the PI pathway, sug gest that this second-messenger pathway is a common mediator for the l ordosis-facilitating agents. Furthermore, as in the case of stimulatin g membrane receptors, direct activation of this common mediator also r equires estrogen priming for lordosis facilitation. Therefore, it is l ikely that the PI pathway is modulated by estrogen in the permissive a ction of estrogen priming. Indeed, a literature review shows that estr ogen can affect selective isozymes of key enzyme families of the PI pa thway at various levels. Such selective modulations, at several levels , could easily alter the course of a PI cascade; thence, the eventual functional outcome. These findings prompt us to propose that estrogen enables lordosis to be facilitated by a selective modulation of the PI pathway.