• Title/Summary/Keyword: Posterior hypothalamus

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Brain Benzodiazepine-like Molecules and Stress-anxiety Response (뇌조직내 Benzodiazepine 유사물질과 스트레스-불안 반응)

  • Ha, Jeoung-Hee
    • Journal of Yeungnam Medical Science
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    • v.16 no.1
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    • pp.25-33
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    • 1999
  • Benzodiazepines(BZDs) are among the most widely prescribed drugs in the world. They are potent anxiolytic, antiepileptic, hypnotic, and muscle relaxing agents. There is an emerging model of the role of several neural systems in anxiety and their relation to the mechanism of action of BZDs. It has been postulated that BZD drugs exert their anxiolytic action by regulating GABAergic transmission in limbic areas such as the amygdala, in the posterior hypothalamus, and in the raphe nuclei. The involvement of the amygdala in the behaviors triggered by fear and stress has been suggested by many previous studies. In this review, reports about regulatory effects of endogenous BZD receptor ligands on the perception of anxiety and memory consolidation were summerized. These findings further support the contention that BZD receptor ligands modulate memory consolidation of averse learning tasks by influencing the level of stress and/or anxiety that accompanies a learning experience. The findings suggest that the decrease in the limbic levels of BZD-like molecules seen after the various behavioral procedures represent a general response to stress and/or anxiety, since it occurs in proportion to the level of stress and/or anxiety that accompany these tasks. In addition, these findings further support the hypothesis that the $GABA_A$/BZD receptor complex in limbic structures plays a pivotal role in the stress and anxiety.

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The influence of ginseng, reserpine, and chlorpromazine on epinephrine-induced and morphine induced hyperglycemiae (인삼(人蔘), reserpine, 및 chlorpromazine이 epinephrine 및 morphine 과혈당(過血糖)에 미치는 영향(影響))

  • Cheong, Dong-Kyun
    • The Korean Journal of Pharmacology
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    • v.1 no.1 s.1
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    • pp.17-36
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    • 1965
  • Besides it's all important analgesic action, morphine has, among others, hyperglycemic effect, though not important clinically, which is believed to be resulted from augmented glycogenolysis in the liver and muscles due to the increased liberation of epinephrine from the adrenal medulla upon the stimulation of the posterior part of hypothalamus. It is known that adrenergic blocking agents are acting inhibitory to this sort of hyperglycemia. Much, however, should as yet be studied for the drugs which affect central nervous system and release of endogenous catecholamine as far as their effects on hyperglycemia are concerned. Much is still not known about the effect of ginseng, which has been highly regarded in the Herb Medicine, as far as it's influence on the blood sugar is concerned. Author investigated the effects of chlorpromazine, reserpine and ginseng on epinephrine induced, and morphine-induced hyperglycemiae. Animals used in this experiment were healthy albino rabbits weighing approximately 2.0 kg of body weight and were all fasted for 24 hours, before the experiment undertaken. Blood sugar determination was carried out by Nelson-Somogy method. Results obtained are summarized as follows; 1. The groups of rabbits administered intravenously with epinephrine 0.02 mg/kg, and 0.05 mg/kg, showed marked and transient hyperglycemia within 15 minutes after injection. The maximal rate of elevation in blood sugar to the control level, were 28% and 57% respectively. The blood sugar returned to the control level within 3 hours. Thus, the hyperglycemic responses were paralleled with epinephrine doses. 2. The hyperglycemic responses by morphine were different according to the doses. The groups of rabbits in which 4 mg/kg of morphine was administered, did not show any hyperglycemic effect, but, in which 10 mg/kg of morphine administered, showed severe hyperglycemic effect, resulting in the maximal level within 2 hours after injection. The maximal rate of increasing in blood sugar ,level was 88%. Compared .with epinephrine-injected groups, morphjne-injected groups showed more persistent hyperglycemic effect, but returned to control blood sugar .level in 6 hours after injection. 3. The intravenous injection of chlorpromazine 2 mg/kg and 8 mg/kg evoked a slight, and persistent hyperglycemia. The maximal rate of increasing in blood sugar level were 15% and 23% respectively. These hyperglycemia gradually returned to the normal level in 5 or 6 hours after injection. Thus, the intensity of response was paralleled with the dose of chlorpromazine. 4. The intravenous injection of reserpine 0.2 mg/kg and 0.5mg/kg, showed the most persistent but steady elevation of blood sugar level in this experiments, resulting in the maximal level in 5 hours after injection. The maximal rate of increasing of blood sugar level were 18% and 39% respectively. 5. The blood sugar level from 24 hours to 30 hours after intraperitoneal administration of reserpine 1.0mg/kg, did not show statistically significant difference, compared with control groups. 6. The oral administration of ginseng extract 15 ml/kg did not. show any :change in blood sugar level. 7. The intravenous administration of epinephrine 0.05 mg/kg or morphine 4 mg/kg to the group pretreated with ginseng extract 15 ml/kg $20{\sim}30$ minutes before the experiment, evoked more marked hyperglycemic effect than the non-pretreated group. 8. The intravenous administration of epinephrine 0.02 mg/kg, morphine 4 mg/kg, or morphine 10 mg/kg to the groups pretreated with reserpine 0.2 mg/kg or 0.5 mg/kg $20{\sim}30$ minutes before experiment, produced more marked and persistent hyperglycemic effects than the groups injected with single epinephrine or morphine injection. 9. When epinephrine 0.05 mg/kg or morphine 10 mg/kg administered intravenously to the groups pretreated with the intraperitoneal administration of reserpine 1 mg/kg 24 hours before experiment morphine-induced hyperglycemia was inbibited, but epinephrine-induced hyperglycemia was augmented. 10. When epinephrine 0.05mg/kg or morphine 10 mg/kg administered intravenously to the groups pretreated with chlorpromazine, 2 mg/kg, 4 mg/kg, and 8 mg/kg $20{\sim}30$ minutes before the experiment, morphine-induced hyperglycemia was inbibited, but epinephrine-induced hyperglycemia was more persistent.

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Evaluation of Multiple System Atrophy and Early Parkinson's Disease Using $^{123)I$-FP-CIT SPECT ($^{123)I$-FP-CIT SPECT를 이용한 다중계위축증 및 조기 파킨슨병에서의 평가)

  • Oh, So-Won;Kim, Yu-Kyeong;Lee, Byung-Chul;Kim, Bom-Sahn;Kim, Ji-Sun;Kim, Jong-Min;Kim, Sang-Eun
    • Nuclear Medicine and Molecular Imaging
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    • v.43 no.1
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    • pp.10-18
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    • 2009
  • Purpose: We investigated quantification of dopaminergic transporter (DAT) and serotonergic transporter (SERT) on $^{123}I$-FP-CIT SPECT for differentiating between multiple systemic atrophy (MSA) and idiopathic Parkinson's disease (IPD). Materials and Methods: N-fluoropropyl-$2{\beta}$-carbomethoxy-$3{\beta}$-4-[$^{123}I$]-iodophenylnortropane SPECT ($^{123}I$-FP-CIT SPECT) was performed in 8 patients with MSA (mean age: $64.0{\pm}4.5yrs$, m:f=6:2), 13 with early IPD (mean age: $65.5{\pm}5.3yrs$, m:f=9:4), and 12 healthy controls (mean age: $63.3{\pm}5.7yrs$, m:f=8:4). Standard regions of interests (ROls) of striatum to evaluate DAT, and hypothalamus and midbrain for SERT were drawn on standard template images and applied to each image taken 4 hours after radiotracer injection. Striatal specific binding for DAT and hypothalamic and midbrain specific binding for SERT were calculated using region/reference ratio based on the transient equilibrium method. Group differences were tested using ANOVA with the postHoc analysis. Results: DAT in the whole striatum and striatal subregions were significantly decreased in both patient groups with MSA and early IPD, compared with healthy control (p<0.05 in all). In early IPD, a significant increase in the uptake ratio in anterior and posterior putamen and a trend of increase in caudate to putamen ratio was observed. In MSA, the decrease of DAT was accompanied with no difference in the striatal uptake pattern compared with healthy controls. Regarding the brain regions where $^{123}I$-FP-CIT binding was predominant by SERT, MSA patients showed a decrease in the binding of $^{123}I$-FP-CIT in the pons compared with controls as well as early IPD patients (MSA: $0.22{\pm}0.1$ healthy controls: $0.33{\pm}0.19$, IPD: $0.29{\pm}0.19$), however, it did not reach the statistical significance. Conclusion: In this study, the differential patterns in the reduction of DAT in the striatum and the reduction of pontine $^{123}I$-FP-CIT binding predominant by SERT could be observed in MSA patients on $^{123}I$-FP-CIT SPECT. We suggest that the quantification of SERT as well as DAT using $^{123}I$-FP-CIT SPECT is helpful to differentiate parkinsonian disorders in early stage.