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Acid‐sensing ion channel‐1a (ASIC1a) contributes to fear and associated autonomic/cardiovascular responses

Understanding fear mechanisms may suggest new therapies for anxiety and its cardiovascular sequela. Previous studies suggest that ASIC1a is enriched in fear circuit structures and is critical for fear behavior. Here we tested the hypothesis that ASIC1a mediates both behavioral and cardiovascular responses to fear. Arterial blood pressure and heart rate (HR) were recorded by radio telemetry in conscious wild type (n = 3) and ASIC1a‐null mice (n = 4) before and during exposure to the fear‐evoking predator odor trimethylthiazoline (TMT) from foxes. Fear‐related freezing behavior was quantified from video recordings. Baseline mean arterial pressure (MAP) and HR did not differ between genotypes. In wild‐type mice, TMT‐induced freezing was accompanied by a reduction in HR and MAP; HR decreased from 795 ± 6 (−TMT) to 374 ± 28 beats/min (+ TMT), and MAP fell from 155 ± 11 to 88 ± 6 mmHg (P < 0.05). Blocking peripheral muscarinic receptors with methylscopolamine reduced TMT‐evoked bradycardia and hypotension, but not freezing. A control odor (butyric acid) failed to evoke freezing, bradycardia or hypotension. In ASIC1a‐null mice, the effects of TMT on freezing, HR, and MAP were attenuated. We conclude: 1) fear‐evoked freezing is accompanied by a parasympathetic‐mediated decrease in HR and a decrease in MAP, and 2) ASIC1a is critically involved in behavioral and autonomic/cardiovascular fear responses (AHA 0760046Z).