Targeted deletion of AKAP7 in dentate granule cells impairs spatial discrimination.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 27911261.
- Also identified by DOI 10.7554/eLife.20695 and PMC identifier 5135391.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
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.
Medical subject headings
- A Kinase Anchor Proteins
- CA3 Region, Hippocampal
- Cerebellar Nuclei
- Gene Knockout Techniques
- Mossy Fibers, Hippocampal
- Spatial Behavior