| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Department of Physiology and Pharmacology (E.C.), Oregon Health & Science University, Portland, Oregon 97239; Department of Psychology (C.L.), Georgia State University, Atlanta, Georgia 30302; Department of Zoology and Physiology (J.D.R.), University of Wyoming, Laramie, Wyoming 82072; and Department of Zoology (F.L.M.), Oregon State University, Corvallis, Oregon 97331
Address all correspondence and requests for reprints to: Emma Coddington, Physiology and Pharmacology Department, L334, 3181 SW Sam Jackson Park Road, Oregon Health & Science University, Portland, Orgeon 97239. E-mail: ecodding{at}willamette.edu.
For animals in the wild, survival depends on being able to detect and respond rapidly to danger by switching from risky (e.g. conspicuous courtship) to survival-oriented behaviors. Very little is known about the hormonal or neuroendocrine mechanisms that control the rapid switch in behavioral state that occurs when an animal detects threats or other stressors. Prior studies with rough-skinned newts (Taricha granulosa), an amphibian model, found that stress-induced suppression of male sexual behaviors (amplectic clasping) involves corticosterone (CORT) and that this steroid hormone uses a novel membrane receptor and modulates the responsiveness of medullary neurons in clasp-controlling neural circuits. We provide evidence that this rapid suppression of male sex behaviors, when induced by either acute stress or CORT administration, involves activation of endocannabinoids signaling in the hindbrain. In a series of behavioral studies, administration of a cannabinoid antagonist, AM281, blocked the suppressive effects of exposure to acute stress or an injection of CORT on the performance of clasping behaviors in sexually active males. Similarly, in electrophysiological studies, prior treatment with AM281 blocked CORT-induced suppression of spontaneous neuronal activity and sensory responsiveness of hindbrain neurons in clasp-controlling neural circuits. These data suggest that, in response to acute stress, elevated CORT concentration increases endocannabinoid signaling in the hindbrain and alters sexual behaviors by modulating the excitability of medullary circuits.
This article has been cited by other articles:
![]() |
R.R Thompson, P.S Dickinson, J.D Rose, K.A Dakin, G.M Civiello, A Segerdahl, and R Bartlett Pheromones enhance somatosensory processing in newt brains through a vasotocin-dependent mechanism Proc R Soc B, July 22, 2008; 275(1643): 1685 - 1693. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Rossi, V. De Chiara, A. Musella, H. Kusayanagi, G. Mataluni, G. Bernardi, A. Usiello, and D. Centonze Chronic Psychoemotional Stress Impairs Cannabinoid-Receptor-Mediated Control of GABA Transmission in the Striatum J. Neurosci., July 16, 2008; 28(29): 7284 - 7292. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Denver Endocannabinoids Link Rapid, Membrane-Mediated Corticosteroid Actions to Behavior Endocrinology, February 1, 2007; 148(2): 490 - 492. [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |