Trigeminal reflex regulation of sympathetic neural communication strategies in human muscle sympathetic nerve activity

This study tested the hypothesis that during localized facial cooling the human trigeminal reflex regulates sympathetic neuronal communication strategies. In fifteen healthy individuals we measured action potential (AP) discharge in muscle sympathetic nerve activity (MSNA; peroneal microneurography and continuous wavelet transform) during baseline (BSL) and three minutes of trigeminal nerve stimulation (TGS; cold pack on face). Face temperature and discomfort were measured. TGS increased total integrated MSNA via differential regulation of sympathetic AP discharge versus AP recruitment. TGS increased sympathetic AP discharge frequency (BSL: 216 ± 150, TGS-1: 511 ± 335, TGS-2: 476 ± 323, TGS-3: 340 ± 160 APs/min, all P < 0.01). By contrast, TGS recruited previously silent larger sympathetic APs during TGS-1 and TGS-2, but not TGS-3 (BSL: 13 ± 3, TGS-1: 18 ± 4, TGS-2: 17 ± 4 clusters, both P < 0.01, TGS-3: 15 ± 4 clusters, P = 0.17). Compared to BSL, the sympathetic AP latency-size relationship was reset downwards to faster latencies during TGS-1 (Δ-63 ± 6 ms, P < 0.01) and TGS-2 (Δ-31 ± 13 ms, P = 0.02) but not TGS-3 (Δ-8 ± 1 ms, P = 0.32). Across BSL and TGS sympathetic AP recruitment ( r = 0.58; P < 0.01) and latency ( r = -0.52; P < 0.01) were related to perceptual discomfort but not face temperature. Thus, during localized facial cooling, trigeminal reflex activation and perceptual discomfort increase the discharge of previously active sympathetic neurons, recruit previously silent larger neurons, and reduce neuronal discharge latency.