This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Balasubramanian, B. Articles by Mani, S. K. Search for Related Content PubMed PubMed Citation Articles by Balasubramanian, B. Articles by Mani, S. K.

Nonclassical Mechanisms of Progesterone Action in the Brain: I. Protein Kinase C Activation in the Hypothalamus of Female Rats

Department of Molecular and Cellular Biology (B.B., W.P., A.R., J.Z.C., S.K.M.), Baylor College of Medicine, and Department of Neurobiology and Anatomy (A.N.M., P.K.D.), The University of Texas Medical School, Houston, Texas 77030

Address all correspondence and requests for reprints to: Shaila Mani, Ph.D., Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030-3411. E-mail: smani{at}bcm.tmc.edu.

The modulation of gene regulation by progesterone (P) and its classical intracellular regulation by progestin receptors in the brain, resulting in alterations in physiology and behavior has been well studied. The mechanisms mediating the short latency effects of P are less well understood. Recent studies have revealed rapid nonclassical signaling action of P involving the activation of intracellular signaling pathways. We explored the involvement of protein kinase C (PKC) in P-induced rapid signaling in the ventromedial nucleus of the hypothalamus (VMN) and preoptic area (POA) of the rat brain. Both the Ca²⁺-independent (basal) PKC activity representing the activation of PKC by the in vivo treatments and the Ca⁺²-dependent (total) PKC activity assayed in the presence of exogenous cofactors in vitro were determined. A comparison of the two activities demonstrated the strength and temporal status of PKC regulation by steroid hormones in vivo. P treatment resulted in a rapid increase in basal PKC activity in the VMN but not the POA. Estradiol benzoate priming augmented P-initiated increase in PKC basal activity in both the VMN and POA. These increases were inhibited by intracerebroventricular administration of a PKC inhibitor administered 30 min prior to P. The total PKC activity remained unchanged demonstrating maximal PKC activation within 30 min in the VMN. In contrast, P regulation in the POA significantly attenuated total PKC activity ± estradiol benzoate priming. These rapid changes in P-initiated PKC activity were not due to changes in PKC protein levels or phosphorylation status.

This article has been cited by other articles:

				B. Balasubramanian, W. Portillo, A. Reyna, J. Z. Chen, A. N. Moore, P. K. Dash, and S. K. Mani Nonclassical Mechanisms of Progesterone Action in the Brain: II. Role of Calmodulin-Dependent Protein Kinase II in Progesterone-Mediated Signaling in the Hypothalamus of Female Rats Endocrinology, November 1, 2008; 149(11): 5518 - 5526. [Abstract] [Full Text] [PDF]