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      Gonadal Hormones Humour the Brain

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          The relationship between the brain and the endocrine system is now seen to extend far beyond the regulation of somatic hormone production by the hypothalamus and pituitary: the brain itself can be considered both as an endocrine organ, producing hormones that act both within and outside the central nervous system, and as a target for hormones. The current extent of this concept with respect to the gonadal hormones was explored at a recent meeting (‘Hormones and the Brain’, Third Endocrinology Colloquium of the Fondation Ipsen, Paris, December 8, 2003). The discussion, reviewed in this article, ranged from intracellular signalling pathways and intercellular networks regulating hormone production and action in the central nervous system to hormone involvement in the generation of sexual behaviour and in development, plasticity, neuroprotection and repair. The hormonal contribution to psychiatric and neurodegenerative illnesses was also examined. The picture presented is complex, with layers of controls and with hormones that have diverse actions at different sites in the central nervous system. This richness of actions and functions is providing some interesting leads for developing new therapeutics.

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          Most cited references 25

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          Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

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            CB1 cannabinoid receptors and on-demand defense against excitotoxicity.

            Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons.
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              Limbic corticotropin-releasing hormone receptor 1 mediates anxiety-related behavior and hormonal adaptation to stress.

              Corticotropin-releasing hormone (CRH) is centrally involved in coordinating responses to a variety of stress-associated stimuli. Recent clinical data implicate CRH in the pathophysiology of human affective disorders. To differentiate the CNS pathways involving CRH and CRH receptor 1 (Crhr1) that modulate behavior from those that regulate neuroendocrine function, we generated a conditional knockout mouse line (Crhr1(loxP/loxP)Camk2a-cre) in which Crhr1 function is inactivated postnatally in anterior forebrain and limbic brain structures, but not in the pituitary. This leaves the hypothalamic-pituitary-adrenocortical (HPA) system intact. Crhr1(loxP/loxP)Camk2a-cre mutants showed reduced anxiety, and the basal activity of their HPA system was normal. In contrast to Crhr1 null mutants, conditional mutants were hypersensitive to stress corticotropin and corticosterone levels remained significantly elevated after stress. Our data clearly show that limbic Crhr1 modulates anxiety-related behavior and that this effect is independent of HPA system function. Furthermore, we provide evidence for a new role of limbic Crhr1 in neuroendocrine adaptation to stress.

                Author and article information

                S. Karger AG
                November 2004
                20 August 2004
                : 79
                : 6
                : 287-295
                Todmorden, Lancashire, UK
                80045 Neuroendocrinology 2004;79:287–295
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 48, Pages: 9
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