A neuropharmacological and electrophysiological study was carried out in order to investigate the mechanism of the sciatic and trigeminal evoked eyelid microvibration (SMV and TMV), and blink reflex (BR) in rabbits.
The results obtained wer e as follows;
1. The response of SMV, induced in the upper eyelid by sciatic nerve stimulation, was composed of three components, which had peak latencies of 44±10,63±11, and 84±7msec, respectively.
2. The pe ak latency of the nociceptive reflex (SNR), recorded simultaneously in the anterior tibial muscle, was 13±5 msec.
3. The latency time of SMV and S NR was not changed statistically by the repeated electric stimulation of the sciatic nerve, but the amplitude indicated habituation.
4. There was no difference in the latency time of SMV, induced in the left upper eyelid, between the response to the sciatic stimulation of the left site and that of right site.
5. Each SMV component was increased in amplitude by the low dose of barbiturate and decreased by the high dose. It was also suppressed, dose-dependently, by TRH. CD P choline suppressed the SMV1 and SMV
2 components, but increased that of SMV
3. Cardiazol increased SMV component in a low dose, but decreased it in a h i gh dose. The SMV was little influenced by amphetamine.
6. The amplitude of SNR increased w i th barbiturate and CDP-choline, but decreased with TRH, cardiazol and amphetamine.
7. SMV and SNR respon ded to most of the agents in the same way, but an antagonistic relationship was observed, in part, in the response between SMV and SNR.
8. Three components were also recorded in the TMV, their peak latencic s being 32±10,53±11 and 71±12 msec, respectively.
9. The BR recorded simultaneously consisted of two components; the peak latencies of which were 3 and 10±1 msec, respectively.
10. Barbiturate, TRH, cardiaz o l and morphine, administered intravenously, suppressed each TMV component, and the effect of morphine was the strongest. CDP-choline increa s e d each TMV component.
11. BR was sup pressed in amplitude by all agents.
12. The TMV and BR responses to these ag ents showed almost the same behavior.
13. A lesion in the sensory relay nucleus, such as posterolateral ventral nucleus (VPL)and posteromedial ventral nucleus (VPM), increased each TMV component, w h i le it decreased that of BR.
14. Impairments of the nucleus reticularis (RET), the nucleus centrum medianum (CM), the nucleus ventralis medialis pars lateralis (VML) and the nucleus lateralis posterior (LP ), which belong to the non-specific projection nuclei, also decreased each TMV component, and increased that of BR. There was no definite trend with TMV and B R respone when the nucleus ventralis anterior (VA) and the nucleus ventralis lateralis (VL ) were impaired.
15. The amplitude of each TMV component decreased with a lesion in the brain stem reticular formation (RF), while that of BR increased.
16. Lesion in the oculomotor nuclei (III-nucl. ) su ppressed each TMV component completely, but that of BR, moderately.
17. Impairment of the subthaIamus (STH) decreased the amplitude of the first component of TMV and that of BR.
18. Impairment of the cap sula interna (IC) and optic tract (OT) did not show any definite response in TMV and BR.
These results indicate that the TMV response appears to be the same as that of SMV in mediating, in part, the same relay nucleus or synapse of the central nervous system, and that it differs from BR in the mechanism of response.
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