To clarify the role of autonomic nervous function in
motion sickness, the effect of agents that act on the autonomic nervous system on the motion stimuli-induced
emesis was studied in two strains of Suncus murinus (Jic:SUN-Her and Jic:SUN-Ler) with congenitally different sensitivity to
veratrine sulfate. We demonstrated significant differences between the two strains in sensitivity to motion stimuli.
Isoproterenol (2.5 mg kg(-1), s.c.) significantly prolonged the latency to the first
emetic episode induced by motion stimuli and significantly decreased the number of
emetic episodes in Jic:SUN-Her suncus. Hexamethoium (2.0 mg kg(-1), s.c.) tended to shorten the latency in Jic:SUN-Ler.
Acetylcholine (1.2 mg kg(-1), s.c.) enhanced the
emetic response in Jic:SUN-Ler, but
atropine (4.0 mg kg(-1), s.c.) suppressed motion stimuli-induced
emetic response in Jic:SUN-Her. These results suggest that the predominance of parasympathetic nervous activity is relevant to the enhancement of motion stimuli-induced
emetic response, whereas the predominance of sympathetic nervous activity suppresses motion stimuli-induced
emetic response.
Norepinephrine (0.8 mg kg(-1), s.c.) enhanced motion stimuli-induced
emesis contrary to
isoproterenol in Jic:SUN-Ler although both drugs are
adrenergic agents. However,
atropine pretreatment (4.0 mg kg(-1), s.c.) inhibits
norepinephrine-induced
emetic response. It was considered that
norepinephrine-induced
emetic response might be dependent on a secondary increase of parasympathetic nervous activity due to bororeflex. Moreover, the different
emetic response in Jic:SUN-Her and Jic:SUN-Ler suncus to motion stimuli and
drug administration mentioned above indicated that different participation of autonomic nervous activity and/or afferent information from the baroreceptor in the
emetic response may exist between these animal groups.