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The Acid-sensing ion channel (ASIC) family consists of proton-gated sodium channels that are primarily expressed in the central and peripheral nervous systems. These channels function as sensors for extracellular acidification, which occurs during physiological processes like synaptic transmission and pathological conditions such as ischemia, inflammation, and tissue injury. ASICs are critical mediators of pain perception and are implicated in the neuronal damage following stroke. The specific mention of 'Heavy metal ions, Gd' refers to a well-documented pharmacological profile where polyvalent cations, including Gadolinium (Gd3+), Lead (Pb2+), and Nickel (Ni2+), act as potent inhibitors of ASIC currents. While Gadolinium is a non-specific blocker often used in research to study ASICs and other mechanosensitive channels, it is not the target itself but rather a tool for its modulation. ASICs remain a significant area of drug development for novel analgesics and neuroprotective agents.
Inhibition of proton-gated sodium currents through pore blockade or allosteric modulation of the extracellular domain.
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