1991 Fiscal Year Final Research Report Summary
Habituation to motion sickness and learning and memory
| Project/Area Number |
02670763
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Osaka University |
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Principal Investigator |
TAKEDA Norikai Osaka University Medical School, Assistant Professor, 医学部, 助手 (30206982)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUNAGA Toru Osaka University Medical School, Professor and Chairman, 医学部, 教授 (10101271)
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| Project Period (FY) |
1990 – 1991
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| Keywords | Motion Sickness / Habituation / Acetylcholine / Learning And Memory / Scopolamine / Anticholinsterase |
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| Research Abstract |
The effects of the anti-cholinergic drug scopolamine and of the cholinergics pbysostigmine and neostigmine on habituation to motion sickness in rats were first examined using. pica. measured as eating of kaolin. as a behavioral index of motion sickness in. rats. Rats were rotated around two axes for 1 h once a day for 10-11 days. Rotation-induced kaolin intake of control rats gradually decreased from day 9 of daily rotation. Test rats were not treated for the first 3 days. given drugs on day 4-7 of rotation and then again given no drugs for the next 3 or 4 days. Rotation-induced kaolin intake of test rats was compared to that of controls. Results showed that scopolamine administration facilitated habituat ion to rotation, whereas physostigmine'. a central acting choli'nesteratse inhibitor, suppressedit and neostigmine, a-peripheral active cholinesterase inhibitor. had no effect on habituation at all. These findings suggested that the central cholinergic neuron system play an important role in the neural mechanisms of habituation to motion in rats. 'Then. the effect of specific cholinergic destruction in hippocampus dn habituation to motion sickness was examined. After injection of nerve arouth factor-diphtheria toxin conjugate In the bilateral hippocampus, kaolin intake induced by linear motion was suppressed. This finding demonstrated that the septohippocampus cholinergic system is involved in the development of motion sickness. All these findings suggested that acetylcholine in the hippocampus transmits the information of the past sensory memory and that it is involved in neural store mechanisms of motion sickness.
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