title: Role of autonomic nervous system for development and suppression of motion sickness in Suncus murinus.
abstract: 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.
authors.affiliation: Department of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Japan. a80503@mail.ecc.u-tokyo.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Uchino
authors.forename: K
authors.initials: K
authors.lastname: Ishii
authors.forename: M
authors.initials: M
authors.lastname: Kuwahara
authors.forename: S
authors.initials: S
authors.lastname: Ebukuro
authors.forename: H
authors.initials: H
authors.lastname: Tsubone
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D005730:Ganglionic Blockers / Q000627:therapeutic use*; D018738:Hexamethonium / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009038:Motion; D009041:Motion Sickness / Q000188:drug therapy* / Q000503:physiopathology*; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D012788:Shrews / Q000502:physiology*; D013045:Species Specificity; D014839:Vomiting / Q000517:prevention & control
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D005730:Ganglionic Blockers; D018727:Muscarinic Antagonists; D018738:Hexamethonium; D001285:Atropine; D007545:Isoproterenol; D000109:Acetylcholine; D009638:Norepinephrine