Cysteamine Attenuates the Decreases in TrkB Protein Levels and the Anxiety/Depression-Like Behaviors in Mice Induced by Corticosterone Treatment

Hdl Handle:
http://hdl.handle.net/10675.2/760
Title:
Cysteamine Attenuates the Decreases in TrkB Protein Levels and the Anxiety/Depression-Like Behaviors in Mice Induced by Corticosterone Treatment
Authors:
Kutiyanawalla, Ammar; Terry, Alvin V.; Pillai, Anilkumar
Abstract:
Objective: Stress and glucocorticoid hormones, which are released into the circulation following stressful experiences, have been shown to contribute significantly to the manifestation of anxiety-like behaviors observed in many neuropsychiatric disorders. Brain-derived neurotrophic factor (BDNF) signaling through its receptor TrkB plays an important role in stress-mediated changes in structural as well as functional neuroplasticity. Studies designed to elucidate the mechanisms whereby TrkB signaling is regulated in chronic stress might provide valuable information for the development of new therapeutic strategies for several stress-related psychiatric disorders.; Materials and Methods: We examined the potential of cysteamine, a neuroprotective compound to attenuate anxiety and depression like behaviors in a mouse model of anxiety/depression induced by chronic corticosterone exposure.; Results: Cysteamine administration (150 mg/kg/day, through drinking water) for 21 days significantly ameliorated chronic corticosterone-induced decreases in TrkB protein levels in frontal cortex and hippocampus. Furthermore, cysteamine treatment reversed the anxiety and depression like behavioral abnormalities induced by chronic corticosterone treatment. Finally, mice deficient in TrkB, showed a reduced response to cysteamine in behavioral tests, suggesting that TrkB signaling plays an important role in the antidepressant effects of cysteamine.; Conclusions: The animal studies described here highlight the potential use of cysteamine as a novel therapeutic strategy for glucocorticoid-related symptoms of psychiatric disorders.
Citation:
PLoS One. 2011 Oct 19; 6(10):e26153
Issue Date:
19-Oct-2011
URI:
http://hdl.handle.net/10675.2/760
DOI:
10.1371/journal.pone.0026153
PubMed ID:
22039440
PubMed Central ID:
PMC3198436
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Department of Psychiatry and Health Behavior: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorKutiyanawalla, Ammaren_US
dc.contributor.authorTerry, Alvin V.en_US
dc.contributor.authorPillai, Anilkumaren_US
dc.date.accessioned2012-10-26T20:30:39Z-
dc.date.available2012-10-26T20:30:39Z-
dc.date.issued2011-10-19en_US
dc.identifier.citationPLoS One. 2011 Oct 19; 6(10):e26153en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22039440en_US
dc.identifier.doi10.1371/journal.pone.0026153en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/760-
dc.description.abstractObjective: Stress and glucocorticoid hormones, which are released into the circulation following stressful experiences, have been shown to contribute significantly to the manifestation of anxiety-like behaviors observed in many neuropsychiatric disorders. Brain-derived neurotrophic factor (BDNF) signaling through its receptor TrkB plays an important role in stress-mediated changes in structural as well as functional neuroplasticity. Studies designed to elucidate the mechanisms whereby TrkB signaling is regulated in chronic stress might provide valuable information for the development of new therapeutic strategies for several stress-related psychiatric disorders.en_US
dc.description.abstractMaterials and Methods: We examined the potential of cysteamine, a neuroprotective compound to attenuate anxiety and depression like behaviors in a mouse model of anxiety/depression induced by chronic corticosterone exposure.en_US
dc.description.abstractResults: Cysteamine administration (150 mg/kg/day, through drinking water) for 21 days significantly ameliorated chronic corticosterone-induced decreases in TrkB protein levels in frontal cortex and hippocampus. Furthermore, cysteamine treatment reversed the anxiety and depression like behavioral abnormalities induced by chronic corticosterone treatment. Finally, mice deficient in TrkB, showed a reduced response to cysteamine in behavioral tests, suggesting that TrkB signaling plays an important role in the antidepressant effects of cysteamine.en_US
dc.description.abstractConclusions: The animal studies described here highlight the potential use of cysteamine as a novel therapeutic strategy for glucocorticoid-related symptoms of psychiatric disorders.en_US
dc.rightsKutiyanawalla et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectMedicineen_US
dc.subjectMental Healthen_US
dc.subjectPsychiatryen_US
dc.subjectAnxiety Disordersen_US
dc.subjectPsychologyen_US
dc.subjectDevelopmental Psychologyen_US
dc.subjectExperimental Psychologyen_US
dc.titleCysteamine Attenuates the Decreases in TrkB Protein Levels and the Anxiety/Depression-Like Behaviors in Mice Induced by Corticosterone Treatmenten_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3198436en_US
dc.contributor.corporatenameDepartment of Psychiatry and Health Behavior-
dc.contributor.corporatenameDepartment of Pharmacology and Toxicology-

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