1986 Fiscal Year Final Research Report Summary
Studies on vestibular compensation following hemilabyrinthectomy
| Project/Area Number |
60480383
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
MIZUKOSHI Osamu Kyoto Pref. Univ. Med., Dept. of Otolaryngology, 医学部, 教授 (70079896)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Chifuyu ditto, 耳鼻咽喉科学教室, 助手 (20347462)
YASUDA Norio ditto, 耳鼻咽喉科学教室, 助手 (00182337)
水越 文和 京都府立医科大学, 耳鼻咽喉科学教室, 助手 (80166008)
YACHIBANA Masayoshi Kyoto Pref. Univ. Med., Dept. of Otolaryngology, 耳鼻咽喉科学教室, 助教授 (90112515)
MIZUKOSHI Fumikazu ditto (70079896)
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| Project Period (FY) |
1985 – 1986
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| Keywords | Vestibular compensation / Hemilabyrinthectomized rat / Lateral vestibular nucleus / Cholinergic neuron |
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| Research Abstract |
Neurochemical mechanisms underlying the occurrence of vestibular compensation (VC) were analyzed in male Wistar rats following hemilabyrinthectomy.
Surgical destruction of the right labyrinth caused symptoms of disequilibrium including head deviation toward the lesioned side and spontaneous nystagmus. However, these animals exhibited VC characterized by spontaneous disappearance of these symptoms.
Various drugs were administered systemically to hemilabyrinthectomized animals in order to study their influence on the course of VC. Among the drugs tested, those which are related to cholinergic and glutaminergic systems caused modification of the course of compensation, implying involvement of alterations in the function of those two transmitter systems in the occurrence of VC.
In order to investigate the possible role of cholinergic neurons in the occurrence of VC, neurochemical techniques were applied to the cholinergic neurons in the lateral vestibular nucleus (LVN) of rat at various time intervals following hemilabyrinthectomy. Acetylcholine content in the LVN after hemilabyrinthectomy showed no significant alteration. Similarly, no significant change in the activity of acetylcholinesterase in the nucleus was noted. On the other hand, choline acetyltransferase activity in the LVN of the non-lesioned side showed a slight but statistically significant decrease only 15 min after hemilabyrinthectomy. However, neither high affinity transport of choline in slices of the LVN nor high <K^+> -evoked release of [ <^3H> ]ACh from slices of the LVN was significantly altered 15 min after the operation. Furthermore, the specific binding of [ <^3H> ]quinuclidinyl benzilate to muscarinic acetylcholine receptor showed no significant changes under the same experimental conditions.
The present results suggest that the occurrence of VC may involve functional alterations in central cholinergic synapses, possibly not at the level of LVN.
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