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- W3124619237 endingPage "160" @default.
- W3124619237 startingPage "145" @default.
- W3124619237 abstract "Increase in proton concentration [H+] or decrease in local and global extracellular pH occurs in both physiological and pathological conditions. Acid-sensing ion channels (ASICs), belonging to the ENaC/Deg superfamily, play an important role in signal transduction as proton sensor. ASICs and in particular ASIC1a (one of the six ASICs subunits) which is permeable to Ca2+, are involved in many physiological processes including synaptic plasticity and neurodegenerative diseases. Activity-dependent long-term potentiation (LTP) is a major type of long-lasting synaptic plasticity in the CNS, associated with learning, memory, development, fear and persistent pain. Neurons in the anterior cingulate cortex (ACC) play critical roles in pain perception and chronic pain and express ASIC1a channels. During synaptic transmission, acidification of the synaptic cleft presumably due to the co-release of neurotransmitter and H+ from synaptic vesicles activates postsynaptic ASIC1a channels in ACC of mice. This generates ASIC1a synaptic currents that add to the glutamatergic excitatory postsynaptic currents (EPSCs). Here we report that modulators like histamine and corticosterone, acting through ASIC1a regulate synaptic plasticity, reducing the threshold for LTP induction of glutamatergic EPSCs. Our findings suggest a new role for ASIC1a mediating the neuromodulator action of histamine and corticosterone regulating specific forms of synaptic plasticity in the mouse ACC." @default.
- W3124619237 created "2021-02-01" @default.
- W3124619237 creator A5003263760 @default.
- W3124619237 creator A5028940161 @default.
- W3124619237 creator A5039719881 @default.
- W3124619237 date "2021-04-01" @default.
- W3124619237 modified "2023-10-09" @default.
- W3124619237 title "Histamine and Corticosterone Modulate Acid Sensing Ion Channels (ASICs) Dependent Long-term Potentiation at the Mouse Anterior Cingulate Cortex" @default.
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