Artigo Acesso aberto Revisado por pares

Exposure to chronic psychosocial stress and corticosterone in the rat: Effects on spatial discrimination learning and hippocampal protein kinase Cγ immunoreactivity

1997; Wiley; Volume: 7; Issue: 4 Linguagem: Inglês

10.1002/(sici)1098-1063(1997)7

ISSN

1098-1063

Autores

Harm J. Krugers, B. R. K. Douma, Gerda Andringa, B. Bohus, Jakob Korf, Paul G.M. Luiten,

Tópico(s)

Hormonal Regulation and Hypertension

Resumo

HippocampusVolume 7, Issue 4 p. 427-436 Research Article Exposure to chronic psychosocial stress and corticosterone in the rat: Effects on spatial discrimination learning and hippocampal protein kinase Cγ immunoreactivity Harm J. Krugers, Corresponding Author Harm J. Krugers [email protected] Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsInstitute of Neurobiology, University of Amsterdam, Kruislaan 320, 1098 SM, Amsterdam, The NetherlandsSearch for more papers by this authorBas R.K. Douma, Bas R.K. Douma Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorGerda Andringa, Gerda Andringa Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The Netherlands Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorBéla Bohus, Béla Bohus Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorJakob Korf, Jakob Korf Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorPaul G.M. Luiten, Paul G.M. Luiten Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The Netherlands Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this author Harm J. Krugers, Corresponding Author Harm J. Krugers [email protected] Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsInstitute of Neurobiology, University of Amsterdam, Kruislaan 320, 1098 SM, Amsterdam, The NetherlandsSearch for more papers by this authorBas R.K. Douma, Bas R.K. Douma Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorGerda Andringa, Gerda Andringa Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The Netherlands Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorBéla Bohus, Béla Bohus Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorJakob Korf, Jakob Korf Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this authorPaul G.M. Luiten, Paul G.M. Luiten Department of Biological Psychiatry, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The Netherlands Department of Animal Physiology, Graduate School for Behavioral and Cognitive Neurosciences, University of Groningen, The NetherlandsSearch for more papers by this author First published: 07 December 1998 https://doi.org/10.1002/(SICI)1098-1063(1997)7:4 3.0.CO;2-FCitations: 98AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Previous reports have demonstrated a striking increase of the immunoreactivity of the γ-isoform of protein kinase C (PKCγ-ir) in Ammon's horn and dentate gyrus (DG) of rodent hippocampus after training in a spatial orientation task. In the present study, we investigated how 8 days of psychosocial stress affects spatial discrimination learning in a hole board and influences PKCγ-ir in the hippocampal formation. The acquisition of both reference memory and working memory was significantly delayed in the stressed animals during the entire training period. With respect to cellular plasticity, the training experience in both nonstressed and stressed groups yielded enhanced PKCγ-ir in the CA1 and CA3 regions of the posterior hippocampus but not in subfields of the anterior hippocampus. Stress enhanced PKCγ-ir in the DG and CA3 pyramidal cells of the anterior hippocampus. In stressed animals that were subsequently trained, the PKCγ-ir was increased in the posterior CA1 region to the same level as that found in nonstressed trained animals. Stress apparently abrogated the PKCγ-ir training response in the CA3 region. In a second experiment, the elevation of plasma corticosterone levels to values that are found during stress did not significantly influence reference memory scores but slightly and temporarily affected working memory. The training-induced enhancement of PKCγ-ir in the CA1 region was similar in trained and corticosterone-treated trained animals, but the learning-induced PKCγ-ir response in the posterior CA3 area was absent after corticosterone pretreatment. These results reveal that prolonged psychosocial stress causes spatial learning deficits, whereas artificial elevation of corticosterone levels to the levels that occur during stress only mildly affects spatial memory performance. 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