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ASIC1a regulates insular long-term depression and is required for the extinction of conditioned taste aversion.


ABSTRACT: Acid-sensing ion channel 1a (ASIC1a) has been shown to play important roles in synaptic plasticity, learning and memory. Here we identify a crucial role for ASIC1a in long-term depression (LTD) at mouse insular synapses. Genetic ablation and pharmacological inhibition of ASIC1a reduced the induction probability of LTD without affecting that of long-term potentiation in the insular cortex. The disruption of ASIC1a also attenuated the extinction of established taste aversion memory without altering the initial associative taste learning or its long-term retention. Extinction of taste aversive memory led to the reduced insular synaptic efficacy, which precluded further LTD induction. The impaired LTD and extinction learning in ASIC1a null mice were restored by virus-mediated expression of wild-type ASIC1a, but not its ion-impermeable mutant, in the insular cortices. Our data demonstrate the involvement of an ASIC1a-mediated insular synaptic depression mechanism in extinction learning, which raises the possibility of targeting ASIC1a to manage adaptive behaviours.

SUBMITTER: Li WG 

PROVIDER: S-EPMC5150990 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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ASIC1a regulates insular long-term depression and is required for the extinction of conditioned taste aversion.

Li Wei-Guang WG   Liu Ming-Gang MG   Deng Shining S   Liu Yan-Mei YM   Shang Lin L   Ding Jing J   Hsu Tsan-Ting TT   Jiang Qin Q   Li Ying Y   Li Fei F   Zhu Michael Xi MX   Xu Tian-Le TL  

Nature communications 20161207


Acid-sensing ion channel 1a (ASIC1a) has been shown to play important roles in synaptic plasticity, learning and memory. Here we identify a crucial role for ASIC1a in long-term depression (LTD) at mouse insular synapses. Genetic ablation and pharmacological inhibition of ASIC1a reduced the induction probability of LTD without affecting that of long-term potentiation in the insular cortex. The disruption of ASIC1a also attenuated the extinction of established taste aversion memory without alterin  ...[more]

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