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Mutagenesis and knockout models: hypothalamic-pituitary-adrenocortical system


Keck, M E; Müller, M B (2005). Mutagenesis and knockout models: hypothalamic-pituitary-adrenocortical system. In: Holsboer, F; Ströhle, A. Anxiety and Anxiolytic Drugs. Berlin [etc.]: Springer, 113-141.

Abstract

Hyperactivity of central neuropeptidergic circuits such as the corticotropin-releasing hormone (CRH) and vasopressin (AVP) neuronal systems is thought to play a causal role in the etiology and symptomatology of anxiety disorders. Indeed, there is increasing evidence from basic science that chronic stress-induced perturbation of CRH and AVP neurocircuitries may contribute to abnormal neuronal communication in conditions of pathological anxiety. Anxiety disorders aggregate in families, and accumulating evidence supports the notion that the major source of familial risk is genetic. In this context, refined molecular technologies and the creation of genetically engineered mice have allowed us to specifically target individual genes involved in the regulation of the elements of the CRH (e.g., CRH peptides, CRH-related peptides, their receptors, binding protein). During the past few years, studies performed in such mice have complemented and extended our knowledge. The cumulative evidence makes a strong case implicating dysfunction of CRH-related systems in the pathogenesis of anxiety disorders and depression and leads us beyond the monoaminergic synapse in search of eagerly anticipated strategies to discover and develop better therapies.

Hyperactivity of central neuropeptidergic circuits such as the corticotropin-releasing hormone (CRH) and vasopressin (AVP) neuronal systems is thought to play a causal role in the etiology and symptomatology of anxiety disorders. Indeed, there is increasing evidence from basic science that chronic stress-induced perturbation of CRH and AVP neurocircuitries may contribute to abnormal neuronal communication in conditions of pathological anxiety. Anxiety disorders aggregate in families, and accumulating evidence supports the notion that the major source of familial risk is genetic. In this context, refined molecular technologies and the creation of genetically engineered mice have allowed us to specifically target individual genes involved in the regulation of the elements of the CRH (e.g., CRH peptides, CRH-related peptides, their receptors, binding protein). During the past few years, studies performed in such mice have complemented and extended our knowledge. The cumulative evidence makes a strong case implicating dysfunction of CRH-related systems in the pathogenesis of anxiety disorders and depression and leads us beyond the monoaminergic synapse in search of eagerly anticipated strategies to discover and develop better therapies.

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Additional indexing

Item Type:Book Section, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute for Regenerative Medicine (IREM)
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2005
Deposited On:05 Sep 2011 09:05
Last Modified:16 Aug 2016 10:14
Publisher:Springer
Series Name:Handbook of Experimental Pharmacology
Number:169
ISSN:0171-2004
ISBN:978-3-540-22568-3
Related URLs:http://www.springer.com/978-3-540-22568-3
http://opac.nebis.ch/F/?local_base=EBI01&con_lng=GER&func=find-b&find_code=090&request=001525466
PubMed ID:16594256

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