In order to clarify the functional significance of the sciatic evoked eyelid microvibration (SMV) and the electrical change of sciatic evoked palpebral reflex (SPR), it was studied neuropharmacologically in rabbits.
(1) As the results of th e sciatic nerve stimulation, the early 3 negative responses (N₁, N₂ and N₃),1 positive response (P) and late 4 negative responses (N₄, N₅, N₆ and N₇)were obsered in the cerebral cortex. The early componets were hardly suppressed by intravenous administration of morphine, while the late components were mildly suppressed.
(2) Sciatic nerve stimulation resulted in 3 small negative responses (HN₁, HN₂ and HN₃)followed by 3 large negative responses (HN4, HN5 and HN6) in the hippocampus. All hippocampal components were suppressed by intravenous injection of morphine.
(3) Painting of procaine directly on the sciatic nerve su p pressed not only N₁ and N₂components in the cerebral cortex, but also all components in the hippocampus.
(4) The lesions of the nucleus ventralis posteromedialis (VPM) and the nucleus ventralis posterolateralis (VPL) which are the sensory relay nuclei suppressed each component in the cerebral oortex. N₂, N₃, N₄, N₅, N₆ and N₇components were notably inhibited by the VPM lesion. The VPL lesion markedly inhibited P, N₄ and N₅.
(5) The lesions of the nucleus ventralis anterior (VA) and the nucleus centrum medianum (CM) which belong to the diffuse thalamo-cortical projection system suppressed, each component in the cerebral cortex. The CM lesion was especially effective in inhibiting the cerebral cortex responses to sciatic nerve stimulation.
(6) Each component o f the hippocampus was suppressed by the VPM and the VPL lesions. In particular, the VPL lesion markedly inhibited the HN₂ and HN₃ components.
(7) Each component in the hippocampus was also suppressed by th e VA and the CM lesions. The VA lesion produced greater inhibition of the hippocampal components than the CM lesion did.
(8) The SMV response induced in the upper eyelid by sciatic nerve stimulation was composed of 3 components (SMV₁, SMV₂ and SMV₃), which had peak latencies of 51 msec,71 msec, and 92. msec, respectively.
(9) Each component o f SMV was markedly, suppressed' by. intravenous administration of morphine or by painting of procaine.
(10) The lesion of VPM o r VPL suppressed each component of SMV. The inhibition produced by the VPM lesion was greater than the inhibition produced by the VPL lesion.
(11) The lesion of VA increased the amplitude of each component in SMV, while the lesion of CM decreased it.
(12) With the impair ments of the brain stem reticular formation (RF) or the oculomotor nuclei, all components of SMV disappeared:
(13) Each component of SM V was inhibited when the cerebral cortex was resected, and almost disappeared when tbe hippocampus was further resected.
(14). The SPR response induced in, the upper eyelid b y sciatic nerve stinulation was composed of 3 components (SPR₁, SPR₂ and. SPR₃), of which peak latencies were 52 msec, msec and: 113 msec, respectively.

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The mechanism of photo-evoked eyelid microvibration (MV) was studied in unanesthetized rabbits by giving a series of electrical stimulation on the subcortical structures (such as caudate nucleus, globus pallidus, putamen, amygdaloid nucleus, hippocampus and ventrolateral nucleus of thalamus) or by destroying them electrically.
1. Five components were observed in the MV in response to the photic stimulation. They were named MV₁, MV₂, MV₃, MV₄ and MV₅and their peak latencies were 33.1,44.1,57.3,70.0 and 83.0 msec respectively.
2. The influence on the amplitude of MV by electrical stimulation of subcortical structures was studied with frequencies of 3Hz and 100 Hz. Stimulation of the caudate nucleus with 100 Hz suppressed MV to a greater degree than with 3 Hz.
3. Stimulation of the putamen with 3 Hz suppressed MV to a greater degree than with 100 Hz.
4. Stimulation of the globus pallidus with 3 Hz and 100 ', Hz potentiated MV, and the Potentiation was stronger with 100 Hz.
5. Stimulation of amygdaloid nucleus had either facilitatory or inhibitory effect on MV, depending on the site of stimulation. Inhibitory effect was often observed with stimula t i on of the ventral part of the amygdaloid nucleus.
6. MV was depressed by stimulation of the hippocampus with both frequencies, especially with 100 Hz.
7. Stimulation of the ventrolateral nucleus of the thalamus suppressed MV. Its effect was not dependent on the difference in freqency.
8. MV either increased or decreased in amplitude with stimulation of the internal capsule. In the same animal, the effect on MV was the same with the two diffenent frequencies o f stimulation. In the potentiated case, stimulation of the internal capsule with 100 H z increased to a greater extent than with 3 Hz.
9. MV was recorded 10,60 and 120 minutes after generating a electrical lesion in the caudate nuclei. MV slowly increased step by step after destruction of the bilateral cauda t e nuclei, while MV gradually decreased after destruction of the globus pallidus.
10. MV increased after destruction of the putamen and the maximal response was usually obtained at 60 minutes. In some cases, MV either increased or decreased at 10 min u tes.
11. Destruction of the amygdaloid nucleus markedly potentiated MV, especially, at a later time.
12. Potentiation of MV was observed at both 60 and 120 minutes after widespread destruction of the hippocampus, while some cases, MV decreased at 10 minutes.
13. MV decreased at 10 minutes after damage of the ventrolateral nucleus of the thalamus, whereas it increased at both 60 and 120 minutes after destruction.
14. Destruction of the internal capsule resulted in different effects on MV at 10 minutes, though MV tended to decrease at both 60 and 120 minutes.
15. Intravenous injection of barbiturate (5mg/kg) markedly suppressed MV.
16. The effect of electrical stimulation of the subcortical structures was frequently reversed by the prior application of barbiturate.

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It has been reported that electrical stimulation or destruction of the subcortical structures influences the photo-evoked eyelid microvibration (MV) in rabbits.
The author stuied the effect of electrical stimulation of the basal ganglia (caudate nucleus, globus pallidus) and amygdaloid nucleus on the muscular discharge evoked by stimulation of cerebral cortex or hippocampus, and on MV in the attempt to clarify the relation between MV and the subcortical strucutures.
1. Evoked muscular discharge of the fore and himd limbs elicited by 100 Hz stimulation of the cerebral cortex was frequently inhibited by simultaneous 100 Hz stimulation of th e caudate nucleus.
2. Evoked musclar discharge, induced by stimulation of the cerebral cortex, was frequently potentiated by simultaneous 100 Hz stimulation of the globus palliodus.
3. Evoked muscular discharge, elicited by stimulation of the cerebral cortex, was usually inhibited by the simultaneous stimulation of the anteromedial division of the amyg d aloid nucleus, whereas it was rather potentiated by stimulation of the basolateral d ivision of the amygdaloid nucleus.
4. Muscular discharge of the fore and hind limbs, evoked by 100 Hz stimulation of hippocampus, was markedly inhibited by the simultaneous 100 Hz stimulation of the ca u date nucleus.
5. Evoked muscular discharge, elecited by stimulation of the hippocampus, was markedly suppressed by simultaneous stimulation of the globus pallidus.
6. Evoked muscular discharge, elicited by stimulation of the hippocampus, was somewhat potentiated by the simultaneous stimuiation of the anteromedial divizion of the am ygdaloid nucleus, while it was strongly inhibited by stimulation of the basolateral divisi o n of the amygdaloid nucleus.
7. Muscular discharge, evoked by stimuration of cerebral cortex or hippocamus, was classified into tonic, tonic phasic and phasic types. Generally the tonic type and tonic phas i c type were observed in the fore limb and the phasic type in the hind limb.
8. Stimulation of the anteromedial division of amygdaloid nucleus with 100 Hz facilitated not only MV but also muscular discharge evoked by 100 Hz stimulation of the hippocampus. Inversely, stimulation of the basolateral division of the amygdaloid nucleus su p pressed both MV and evoked muscular discharge.

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Influences of the tissue fixation and the existence of either calcium ion or DMSO in the reaction medium on the enzymic digestive methods for fat granules were observed under a light microscope.
Tiss ue samples: (1) The hepatic tissues of Sprague-Dawley female rats, either 20 hrfasting condition,12 hr after a single intraperitoneal injection of ethionine,1 g/Kg, or 7days after daily feeding of Coralgil (Torii),70 mg/Kg, (2) The cerebellar tissue of 20 hrfasted rats, (3) The epididymal fat tissue and interscapular brown fat of suckling rats aged 7 days.
Tissue sections: (1) Fresh unfixed criostat section, (2) Similar criostat section fixed in 3% formal saline for 10 min.
Enzyme preparation (Bo erhinger-Mannheim): (1) Lipase from Rhizopus arrhizus (50,000U/ml), (2) Phospholipase A₂ from Crotalus durissus terrficus (1,600 U/ml).
Reaction Media: (1) 0.05 M Tris buffer (pH 7.5); 4 ml + 2 % calc ium chloride; 1 ml+ enzyme preparation; 0.25 ml, (2) Tris buffer 4.25 ml + CaCl₂ 1 ml, (3) Tris buffer 5 ml + enzyme preparation 0.25 ml, (4) Tris buffer including DMSO, 0.13,0.26 or O.52 ml; 4 ml + CaCl₂ 1 ml + enzyme preparation 0.25 ml.
Histochemical demonstration of the rea ction products (newly detected fatty acids after the digestion) was performed by Holczinger's method.
As shown in Table 1, unfixed criostat s ection of Coralgil phospholipid fatty livers revealed much more intensive positivity than fixed ones by phospholipase-digestive method, but such an influence of fixation was not marked in lipase-digestive method. Unfixed criostat sections of triglyceride fatty livers digested by the reaction medium containing no calcium ion revealed a litte less amounts of bigger reaction products than those digested by the reaction medium containing calcium ion. As shown in Table 2, the reaction media containing 5% DMSO gave the best demonstration of hydrophobic fat granules, and 10% DMSO inhibited all tested enzymatic digestions.

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