• The korean journal of orthodontics
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• v.28 no.3 s.68
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• pp.441-452
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• 1998

The c-fos is known as neuronal marker of second neurons which is activated by noxious peripheral stimulation. To investigate the changes of c-fos el(pression in the trigeminal nucleus complex during tooth movement, immunohistochemical study was performed. Experimental rats(9 weeks old, 210 gm 21 rats) were divided into seven groups(normal, 1 hour group, 3 hour group, 6 hour group, 12 hour group, 1 day group,3 day group). Rats in the normal group were anesthesized without orthodontic force. Rats in the experimental groups were applied orthodontic force (approximately 30 gm) to upper right maxillary molar. Frozen sections of brain stem were immunostained using rabbit antisera. The changes of c-fos expression were observed with respect to rostrocaudal distribution, laminar organization, md duration of orthodontic force application. The study results were as follows $\cdot$The c-fos nuclei in the dorsal part were observed from ipsilateral transition zone of subnucleus interpolaris and subnucleus caudalis to $C_1$ cervical dorsal horn rostrocaudally. The maximal peak point was the rostral part of subnucleus caudalis. The greatest proportion of c-fos cells were located within lamina I and II. $\cdot$The c-fos nuclei in the dorsal Part were observed from the most caudal part of subnucleus interpolaris to the middle part of the subnucleus caudalis. $\cdot$The number of c-fos immunoreactive dot increased at 1 hour group, reached its maximum at the 3 and 6 hour groups, and showed a decreasing trend after 12 hours. These results imply that nociceptive stimulation caused by continuous orthodontic force might be modulated by transition zone of subnucleus interpolaris and subnucleus caudalis, subnucleus caudalis, $C_1$ spinal dorsal hem.

• The Korean Journal of Pharmacology
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• v.11 no.2
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• pp.29-40
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• 1975

1. Sites of the cardioaccelerating action of nicotine, DMPP, McN-A-343, AHR-602, tyramine, angiotensin and neostigmine were investigated in spinal rabbits. 2. The cardioaccelerating action of the above substances was substantially weak in reserpine-pretreated rabbits. The accelerating action was scarcely observed after propranolol administration. 3. Tetrodotoxin and guanethidine did not affect the cardioacceleration due to nicotine, DMPP, tyramine and isoproterenol, but they markedly weakened that due to McN-A-343, AHR-602, angiotensin and neostigmine. 4. Chlorisondamine blocked the cardioacceleration by nicotine and DMPP; atropine that by McN-A-343 and AHR-602. 5. Appropriate doses of isoproterenol, nicotine, DMPP, McN-A-343, tyramine, angiotensin and neostigmine, when administered into the right auricle, produced almost the same degree of cadia acceleration as when they were given to the right ear vein. AHR-602 did not produce significant cardioacceleration through this route. 6. Nicotine, DMPP and neostigmine when injected into the right auricle produced marked cardioacceleration, whereas they produced little action when injected into the left ventricle. Isoproterenol and tyramine produced more marked effect by the intraauricular route than the intraventricular one. 7. McN-A-343, AHR-602 and angiotensin produced more marked cardioacceleration by the intraventricular administration than the intraauricular one. The intraventricular AHR-602 produced marked cardioacceleration. 8. It is inferred that the sites of cardioaccelerating action of nicotine, DMPP, and tyramine will be either the terminals of the adrenergic nerves or the extraneuronal stores of norepinephrine and that of McN-A-343, AHR-602, angiotensin and neostigmine will be the adrenergic neurons in the heart. The sites on which nicotine, DMPP, tyramine and neostigmine will act are chiefly distributed in the auricular tissues and those on which McN-A-343, AHR-602, and angiotensin act chiefly in the ventricular tissues.