Format

Send to

Choose Destination
Sci Rep. 2015 May 19;5:10143. doi: 10.1038/srep10143.

ASIC-dependent LTP at multiple glutamatergic synapses in amygdala network is required for fear memory.

Author information

1
Institute of Neuroscience, National Yang-Ming University, Taipei 112, Taiwan.
2
Molecular Medicine Program, Taiwan International Graduate Program, Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan.
3
Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan.
4
Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine and JST, CREST, Maebashi 371-8511, Japan.
5
1] Institute of Neuroscience, National Yang-Ming University, Taipei 112, Taiwan [2] Institute of Brain Science, National Yang-Ming University, Taipei 112, Taiwan [3] Brain Research Center, National Yang-Ming University, Taipei 112, Taiwan.

Abstract

Genetic variants in the human ortholog of acid-sensing ion channel-1a subunit (ASIC1a) gene are associated with panic disorder and amygdala dysfunction. Both fear learning and activity-induced long-term potentiation (LTP) of cortico-basolateral amygdala (BLA) synapses are impaired in ASIC1a-null mice, suggesting a critical role of ASICs in fear memory formation. In this study, we found that ASICs were differentially expressed within the amygdala neuronal population, and the extent of LTP at various glutamatergic synapses correlated with the level of ASIC expression in postsynaptic neurons. Importantly, selective deletion of ASIC1a in GABAergic cells, including amygdala output neurons, eliminated LTP in these cells and reduced fear learning to the same extent as that found when ASIC1a was selectively abolished in BLA glutamatergic neurons. Thus, fear learning requires ASIC-dependent LTP at multiple amygdala synapses, including both cortico-BLA input synapses and intra-amygdala synapses on output neurons.

PMID:
25988357
PMCID:
PMC4437300
DOI:
10.1038/srep10143
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center