The voltage-gated sodium channel Na v 1.8 is known to function in the transmission of pain signals induced by cold, heat, and mechanical stimuli. Sequence variants of human Na v 1.8 have been linked to altered cardiac conduction. We identified an allele of Scn10a encoding the α-subunit of Na v 1.8 among mice homozygous for N -ethyl- N -nitrosourea-induced mutations. The allele creates a dominant neurobehavioral phenotype termed Possum , characterized by transient whole-body tonic immobility induced by pinching the skin at the back of the neck (“scruffing”). The Possum mutation enhanced Na v 1.8 sodium currents and neuronal excitability and heightened sensitivity of mutants to cold stimuli. Striking electroencephalographic changes were observed concomitant with the scruffing-induced behavioral change. In addition, electrocardiography demonstrated that Possum mice exhibited marked sinus bradycardia and R-R variability upon scruffing, abrogated by infusion of atropine. However, atropine failed to prevent or mitigate the tonic immobility response. Hyperactive sodium conduction via Na v 1.8 thus leads to a complex neurobehavioral phenotype, which resembles catatonia in schizophrenic humans and tonic immobility in other mammals upon application of a discrete stimulus; no other form of mechanosensory stimulus could induce the immobility phenotype. Our data confirm the involvement of Na v 1.8 in transducing pain initiated by cold and additionally implicate Na v 1.8 in previously unknown functions in the central nervous system and heart.