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Histamine and corticosterone modulate Acid sensing ion channels (ASICs) dependent long-term potentiation at the mouse anterior cingulate cortex.

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 ASIC-1a (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 ASIC-1a channels. During synaptic transmission, acidification of the synaptic cleft presumably due to the co-release of neurotransmitter and H+ from synaptic vesicles activates postsynaptic ASIC-1a 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 ASIC-1a regulate synaptic plasticity, reducing the threshold for LTP induction of glutamatergic EPSCs. Our findings suggest a new role for ASIC-1a mediating the neuromodulator action of histamine and corticosterone regulating specific forms of synaptic plasticity in the mouse ACC.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Natalia Gobetto M,González-Inchauspe Osvaldo D Uchitel C

doi

10.1016/j.neuroscience.2021.01.022

subject

Has Abstract

pub_date

2021-01-22 00:00:00

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(21)00029-4

pub_type

杂志文章

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