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Critical role of the 65-kDa isoform of glutamic acid decarboxylase in consolidation and generalization of Pavlovian fear memory

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84944

Sangha S, Narayanan,  RT
Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Zitation

Bergado-Acosta, J., Sangha S, Narayanan, R., Obata K, Pape, H., & Stork, O. (2008). Critical role of the 65-kDa isoform of glutamic acid decarboxylase in consolidation and generalization of Pavlovian fear memory. Learning Memory, 15(3), 163-171. doi:10.1101/lm.705408.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0013-CA0F-4
Zusammenfassung
Evidence suggests that plasticity of the amygdalar and hippocampal GABAergic system is critical for fear memory formation. In this study we investigated in wild-type and genetically manipulated mice the role of the activity-dependent 65-kDa isozyme of glutamic acid decarboxylase (GAD65) in the consolidation and generalization of conditioned fear. First, we demonstrate a transient reduction of GAD65 gene expression in the dorsal hippocampus (6 h post training) and in the basolateral complex of the amygdala (24 h post training) during distinct phases of fear memory consolidation. Second, we show that targeted ablation of the GAD65 gene in Gad65−/− mice results in a pronounced context-independent, intramodal generalization of auditory fear memory during long-term (24 h or 14 d) but not short-term (30 min) memory retrieval. The temporal specificity of both gene regulation and memory deficits in Gad65 mutant mice suggests that GAD65-mediated GABA synthesis is critical for the consolidation of stimulus-specific fear memory. This function appears to involve a modulation of neural activity patterns in the amygdalo-hippocampal pathway as indicated by a reduction in theta frequency synchronization between the amygdala and hippocampus of Gad65−/− mice during the expression of generalized fear memory.