RT Journal Article
SR Electronic
T1 Acid-Sensing Ion Channel-1a Is Not Required for Normal Hippocampal LTP and Spatial Memory
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1828
OP 1832
DO 10.1523/JNEUROSCI.4132-12.2013
VO 33
IS 5
A1 Wu, Pu-Yeh
A1 Huang, Yu-Yin
A1 Chen, Chien-Chun
A1 Hsu, Tsan-Ting
A1 Lin, Yen-Chu
A1 Weng, Ju-Yun
A1 Chien, Ta-Chun
A1 Cheng, Irene H
A1 Lien, Cheng-Chang
YR 2013
UL http://www.jneurosci.org/content/33/5/1828.abstract
AB Acid-sensing ion channel-1a (ASIC1a) is localized in brain regions with high synaptic density and is thought to contribute to synaptic plasticity, learning, and memory. A prominent hypothesis is that activation of postsynaptic ASICs promotes depolarization, thereby augmenting N-methyl-d-aspartate receptor function and contributing to the induction of long-term potentiation (LTP). However, evidence for activation of postsynaptic ASICs during neurotransmission has not been established. Here, we re-examined the role of ASIC1a in LTP in the hippocampus using pharmacological and genetic approaches. Our results showed that a tarantula peptide psalmotoxin, which profoundly blocked ASIC currents in the hippocampal neurons, had no effect on LTP. Similarly, normal LTP was robustly generated in ASIC1a-null mice. A further behavioral analysis showed that mice lacking ASIC1a had normal performance in hippocampus-dependent spatial memory. In summary, our results indicate that ASIC1a is not required for hippocampal LTP and spatial memory. We therefore propose that the role of ASIC1a in LTP and spatial learning should be reassessed.