“…These findings are consistent with the expression of GABA A Rs along sensory axons ( Bhisitkul et al., 1990 ; Oyelese et al., 1997 ), with the well-documented role of GABA A R signaling in trigeminal pathway nociception ( Dieb and Hafidi, 2015 ; Jang et al., 2017 ; Kaushal et al., 2016 ; Martin et al., 2010 ; Wei et al., 2013 ), with the efficacy of GABA-modulating drugs in some patients with TN ( Granger et al., 1995 ; White et al., 2000 ) ( Table S6 ), and with the established importance of GABA A R disinhibition and consequent neuronal hyperexcitability in neuropathic pain ( Dieb and Hafidi, 2015 ; Jang et al., 2017 ; Martin et al., 2010 ). These observations support our speculation that frequent co-occurrence of anxiety, depression, and other psychiatric conditions with TN, especially those in younger patients ( Mousavi et al., 2016 ) (often unresponsive to MVD) ( Hamlyn, 1997a ), may reflect pleiotropy of germline variants impacting other aspects of GABA signaling.…”