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Capsaicin이 성숙한 흰쥐의 통각반응과 open-field 행동에 미치는 영향
박순권,김현택,나흥식,홍승길 한국심리학회 한국심리학회지 생물 및 생리 Vol.7 No.1
성숙한 흰쥐에게 전신계로 투여한 capsaicin(150㎎/㎏)이 개방장(open-field)행동과 통각반응의 역치 및 반응잠재기에 미치는 효과를 알아보았다. 첫째, open-field행동에는 capsaicin의 효과가 관찰되지 않았는데 이것은 capsaicin이 흰쥐의 정서반응성과 운동기능에는 영향을 미치지 않음을 의미하는 것이다. 둘째, capsaicin 투여에 의해 열자극에 대한 앞발 및 뒷발핥기의 역치는 변화되지 않았으나, 뛰어오르기의 역치는 증가되었다. 또한 역치 이상의 열자극에 대한 뒷발핥기 반응의 잠재기도 capsaicin 투여에 의해 증가되었다. 이 결과는 비교적 약한 열자극에 대한 적응반응에는 capsaicin이 영향을 미치지 않으나 강한 열자극에 대한 대처반응에는 영향을 미치는 것으로 해석된다. We investigated the effects of capsaicin(s.c. 150㎎/㎏) on the open-field behaviors and the thresholds and latency of nociceptive responses in adult rats. Results are as follows. 1) Capsaicin did not affect open-field behaviors. It hints that capsaicin did not alter the emotionality and motor function of rats. 2) Whereas the threshold of jumping was elevated, those of fore and hind paw licking were not in animals treated with capsaicin. Capsaicin also enhanced hind paw licking latency to thermal stimulus over thershold in hot plate test. These results suggest that capsaicin affects the coping reaction to strong thermal stimulus, but not adaptive reaction to mild stimulus, in adult rats.
Capsaicin 사전 투여에 의한 흰쥐의 공격성 감소 및 자율적 체온조절의 결손
박순권,홍승길,나흥식,김현택 한국심리학회 한국심리학회지 생물 및 생리 Vol.7 No.1
capsaicin 사전 처치가 흰쥐의 공격성과 체온조절에 미치는 영향을 알아보았다. 생후 6주경에 capsaicin을 피하주사하였고, 완전히 성숙한 후에 공격성 및 체온조절 기능을 검사하였다. 실험 1의 공격성 검사 결과 capsaicin 처치동물들의 공격성은 통제동물보다 낮았는데, 이것은 선행 연구의 결과와 상반된다. 체온조절 기능을 알아본 실험 2에서는 capsaicin 처치동물들이 37℃ 및 40℃ 조건에서 과체온과 빠른 체온증가를 보여주었다. 이것은 출생 직후 또는 성숙한 후에 약물을 투여한 선행연구들과 일치되는 결과이다. 따라서 capsaicin이 체온조절에 미치는 영향은 투여 시기와 무관한 것 같다. 논의에서는 본 연구의 두 가지 결과를 시상하부와 관련시켜 해석하였다. The present study was designed to examine effects of capsaicin administration on aggressive behaviors and autonomic thermoregulation in rats. In six-week-old rat, capsaicin was injected subcutaneously on 4 consecutive days in increasing doses(20㎎/㎏, 30㎎/㎏, 30㎎/㎏, 50㎎/㎏) to total of 150㎎/㎏ of the drug. The controls were treated in the same way with vehicle alone. Two experments began six or eight weeks after the treatment. In experiment 1, isolation-induced agressive behaviors, scored a 10-min session in the dyadic situation, were significantly decreased by capsaicin pretreatment. This result was not in accord with the previous findings. In experiment 2, body temperature of the capsaicin-treated rats increased more than the control's at two amibient temperatures studied(37℃ and 40℃). Our result concerning thermoregulation supports the preceding studies that applied to the capsaicin-treated animals as neonate or adult. Thus, it is likely that the effect of capsaicin treatment on thermoregulation has nothing to do with the age of capsaicin injection. The capsaicin effects from this study were compared with hypothalamic lesion effects in the discussion part.
국소성 뇌경색에 미치는 고혈당의 영향에 대한 실험적 연구
권택현,박윤관,정용구,정흥섭,서중근,이훈갑,주정화,이기찬 대한신경외과학회 1992 Journal of Korean neurosurgical society Vol.21 No.1
The present study was undertaken to investigate the influence of hyperglycemia on focal cerebral ischemia in view of morphometric assay and neuropathological examination. Forty Sprague-Dawley rats were divided into two groups of 20 each Rat MCA occlusion model was used for induction of focal ischemia. Hyperglycemia(20 rats, mean±SEM plasma glucose concentration 378±97.6㎎/㎗) was established 30 minutes before MCA occlusion by intraperitoneal injection of 50% dextrose in water ; the control group(20 rats, mean±SEM plasma glucose concentration 121±24.9㎎/㎗) received normal saline only. Twenty-four hours after MCA occlusion neutral red staining and perfusion fixation was performed and ischemic area were measured using computerized image analysis on cortical surface and coronal cut surface. There was no signifcant difference on coronal cut surface, but on cortical surface showed increase of non-stained area(infarct core) and decrease of lightly stained area(transitional zone) in hyperglycemic rats(p<0.05) and the sum of two area was not different between two groups. Pathological findings were evaluated under light microscopy, in which the field scanning was carried out from the midline by 0.5㎜ interval at cortical and basal ganglia level. There showed no significant difference at basal ganglia level, but at cortical level ischemic transitional zone was decreased in hyperglycemic rats(p<0.05). We conclude that hyperglycemia may worsen the brain from severe, focal ischemic neuronal damage.
뇌경색후 Lipid Peroxidation에 미치는 Allopurinol 및 Deferoxamine의 효과에 대한 실험적 연구
권택현,박윤관,정용구,정흥섭,서중근,이훈갑,주정화,이기찬 대한신경외과학회 1992 Journal of Korean neurosurgical society Vol.21 No.1
It has been hypothesized that ischemia, followed by reperfusion, facilitates peroxidative free radical chain process in brain. This study was undertaken to investigate the effect of allopurinol and deferoxamine on cerebral lipid peroxidation, estimated by a thiobarbituric acid test, following transient bilateral forebrain ischemia in the rat model of four vessel occlusion. Sprague-Dawley rats fed ad libitum were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 48 hours later temporarily occluding the common carotid arteries for 20minutes. Carotid artery blood flow was restored and rats were decapitated after 48 hours. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from hippocampus, basal ganglia, cortex and thalamus. The homogenates were subjected to 30 minutes of aerobic incubation. The production of lipid peroxides were decreased in all sampled area in the treated groups compared with the control group. Allopurinol and deferoxamine-treated groups showed decreased lipid peroxide levels in all the sampled area, but especially more in the hippocampus, (p=0.02), (p<0.01) repecxtively. Combined group (allopurinol and deferoxamine) showed decreased lipid peroxide levels in all the sampled area, but was not statistcally significant(p>0.05). The results suggest that allopurinol and deferoxamine play a role in protecting ischemic cellular damages by scavenging free radicals and subsequently lipid peroxides formed by oxygen supply through blood reperfusion.