Targeted deletion of AKAP7 in dentate granule cells impairs spatial discrimination

eLife

Jenesa Chin¹  Michael Weisenhaus¹  Daniela Nachmanson¹  Brian W Jones¹  G Stanley McKnight¹  Christina A Sanford¹  Jennifer Deem¹  Margaret C Slack¹  Alex McKennon¹  Pablo E Castillo²  Thomas J Younts² 

[1] Department of Pharmacology, University of Washington School of Medicine, Seattle, United States;Dominick P Purpura Department of Neuroscience, Albert Einstein College of Medicine, New York, United States;

关键词: PKA anchoring;    synaptic plasticity;    spatial discrimination;   

DOI  :  10.7554/eLife.20695

来源: DOAJ

【 摘 要 】

Protein Kinase A (PKA) mediates synaptic plasticity and is widely implicated in learning and memory. The hippocampal dentate gyrus (DG) is thought to be responsible for processing and encoding distinct contextual associations in response to highly similar inputs. The mossy fiber (MF) axons of the dentate granule cells convey strong excitatory drive to CA3 pyramidal neurons and express presynaptic, PKA-dependent forms of plasticity. Here, we demonstrate an essential role for the PKA anchoring protein, AKAP7, in mouse MF axons and terminals. Genetic ablation of AKAP7 specifically from dentate granule cells results in disruption of MF-CA3 LTP directly initiated by cAMP, and the AKAP7 mutant mice are selectively deficient in pattern separation behaviors. Our results suggest that the AKAP7/PKA complex in the MF projections plays an essential role in synaptic plasticity and contextual memory formation.

【 授权许可】

Unknown