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In vivo administration of corticotropin-releasing hormone at remote intervals following ischemia enhances CA1 neuronal survival and recovery of spatial memory impairments: a role for opioid receptors.
Behav Brain Res. 2008 Mar 17; 188(1):125-35.BB

Abstract

The contribution of corticotropin-releasing hormone (CRH) in the modulation of ischemia-induced cell death in vivo remains unclear. We characterized the impact of pre-ischemic administration of CRH (0, 0.1, 1, 5 microg, i.c.v., 15 min prior to vessel occlusion) on neuronal damage following global ischemia in rats. The injection of 5 microg CRH led to a 37% increase in CA1 neuronal survival compared to vehicle-treated ischemic animals, while pre-treatment with alpha-helical CRH (9-41) abolished this neuronal protection. A second objective aimed to determine whether CRH protection is maintained over weeks when the peptide is administered at remote time intervals following ischemia. Compared to vehicle-treated ischemic animals, administration of CRH 8h following global ischemia led to a 61% increase in CA1 neuronal survival observed 30 days post-ischemia. Neuronal protection translated into significant improvement of ischemia-induced spatial memory deficits in the radial maze. Finally, our findings demonstrated that selective blockade of kappa- and delta-opioid receptors (using nor-binaltorphimine and naltrindole, respectively) prior to CRH administration significantly reduced CA1 neuronal protection. These findings represent the first demonstration of enhanced neuronal survival following in vivo CRH administration in a global model of ischemia in rats. They also support the idea that CRH-induced neuroprotection involves opioid receptors activation.

Authors+Show Affiliations

University of Ottawa, School of Psychology, 11, Marie Curie, Vanier Building, Room 204, Ottawa, ON K1N 9A9, Canada.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18055027

Citation

Charron, Charlaine, et al. "In Vivo Administration of Corticotropin-releasing Hormone at Remote Intervals Following Ischemia Enhances CA1 Neuronal Survival and Recovery of Spatial Memory Impairments: a Role for Opioid Receptors." Behavioural Brain Research, vol. 188, no. 1, 2008, pp. 125-35.
Charron C, Fréchette S, Proulx G, et al. In vivo administration of corticotropin-releasing hormone at remote intervals following ischemia enhances CA1 neuronal survival and recovery of spatial memory impairments: a role for opioid receptors. Behav Brain Res. 2008;188(1):125-35.
Charron, C., Fréchette, S., Proulx, G., & Plamondon, H. (2008). In vivo administration of corticotropin-releasing hormone at remote intervals following ischemia enhances CA1 neuronal survival and recovery of spatial memory impairments: a role for opioid receptors. Behavioural Brain Research, 188(1), 125-35.
Charron C, et al. In Vivo Administration of Corticotropin-releasing Hormone at Remote Intervals Following Ischemia Enhances CA1 Neuronal Survival and Recovery of Spatial Memory Impairments: a Role for Opioid Receptors. Behav Brain Res. 2008 Mar 17;188(1):125-35. PubMed PMID: 18055027.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - In vivo administration of corticotropin-releasing hormone at remote intervals following ischemia enhances CA1 neuronal survival and recovery of spatial memory impairments: a role for opioid receptors. AU - Charron,Charlaine, AU - Fréchette,Sabrina, AU - Proulx,Geneviève, AU - Plamondon,Hélène, Y1 - 2007/11/04/ PY - 2007/09/13/received PY - 2007/10/21/revised PY - 2007/10/25/accepted PY - 2007/12/7/pubmed PY - 2008/5/20/medline PY - 2007/12/7/entrez SP - 125 EP - 35 JF - Behavioural brain research JO - Behav Brain Res VL - 188 IS - 1 N2 - The contribution of corticotropin-releasing hormone (CRH) in the modulation of ischemia-induced cell death in vivo remains unclear. We characterized the impact of pre-ischemic administration of CRH (0, 0.1, 1, 5 microg, i.c.v., 15 min prior to vessel occlusion) on neuronal damage following global ischemia in rats. The injection of 5 microg CRH led to a 37% increase in CA1 neuronal survival compared to vehicle-treated ischemic animals, while pre-treatment with alpha-helical CRH (9-41) abolished this neuronal protection. A second objective aimed to determine whether CRH protection is maintained over weeks when the peptide is administered at remote time intervals following ischemia. Compared to vehicle-treated ischemic animals, administration of CRH 8h following global ischemia led to a 61% increase in CA1 neuronal survival observed 30 days post-ischemia. Neuronal protection translated into significant improvement of ischemia-induced spatial memory deficits in the radial maze. Finally, our findings demonstrated that selective blockade of kappa- and delta-opioid receptors (using nor-binaltorphimine and naltrindole, respectively) prior to CRH administration significantly reduced CA1 neuronal protection. These findings represent the first demonstration of enhanced neuronal survival following in vivo CRH administration in a global model of ischemia in rats. They also support the idea that CRH-induced neuroprotection involves opioid receptors activation. SN - 0166-4328 UR - https://www.unboundmedicine.com/medline/citation/18055027/In_vivo_administration_of_corticotropin_releasing_hormone_at_remote_intervals_following_ischemia_enhances_CA1_neuronal_survival_and_recovery_of_spatial_memory_impairments:_a_role_for_opioid_receptors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(07)00571-2 DB - PRIME DP - Unbound Medicine ER -