冬眠の薬理 : 冬眠導入・覚醒に関与する中枢因子  [in Japanese] Pharmacological aspects of mammalian hibernation: Central thermoregulation factors in hibernation cycle  [in Japanese]

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Author(s)

    • 塩見 浩人 SHIOMI Hirohito
    • 福山大学薬学部薬理教室 Department of Pharmacology, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University
    • 田村 豊 TAMURA Yutaka
    • 福山大学薬学部薬理教室 Department of Pharmacology, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University

Abstract

冬季,環境温度の低下への適応として,一部の哺乳動物では体温を低下させ,非活動の状態で冬期を過ごす冬眠行動をとる.哺乳動物の冬眠は,気温が上昇する春季まで持続するのではなく,冬眠-覚醒のサイクルを何度も繰り返す.しかし,冬眠への導入と維持ならびに冬眠からの覚醒における生理機構はほとんど解明されていない.我々は,冬眠への移行期の体温下降ならびに冬眠状態から覚醒への移行期の体温上昇に関与する中枢機構を検討し,以下の知見を得ている. (1)非冬眠ハムスターの体温(37°C)は,アデノシンA<SUB>1</SUB>受容体作用薬,N<SUP>6</SUP>-cyclohexyladenosine(CHA) の側脳室内投与により用量依存性に下降する. (2)冬眠初期の低体温(6°C)は,アデノシンA<SUB>1</SUB>受容体拮抗薬,8-cyclopentyl-theophylline (CPT) の側脳室内投与により活動期正常体温へ急激に上昇する. (3)A<SUB>1</SUB>受容体を介するアデノシンの体温下降作用は,視床下部後野の熱産生中枢の抑制作用による. (4)深冬眠期にはCPT処置によって体温上昇が起こらないことから,アデノシンとは異なる系が熱産生中枢を抑制している可能性がある. (5)冬眠初期,深冬眠期のいずれにおいても, TRH (thyrotropin releasing hormone)の側脳室内投与は活動期正常体温へと急激に体温を上昇させる. (6)非冬眠ハムスターの体温をCHA投与により急性的に15°C以下に低下させると, CPTの拮抗作用は発現せず, TRH の体温上昇作用も現れない.これらの結果から,冬眠導入期には中枢アデノシンが,冬眠からの覚醒には,中枢TRHが重要な役割を演じていることが示唆される.また,自然冬眠時には低温時でも作動する非冬眠時とは異なる熱産生系の存在が示唆される.

Hibernation in mammalians such as hamsters is a physiological state characterized by an extreme reduction of various functions such as body temperature and metabolism. Under such severe conditions, the central nervous system (CNS) activity is maintained at a functionally responsive level. Although hibernation is an interesting behavioral state, the physiological mechanisms of the introduction to and/or the arousal from hibernation have not been clearly defined. Intracerebroventricularly (i.c.v.) injected adenosine produces hypothermia in various animals. The effect of adenosine is generated by A1-receptors and is caused by the suppression of the thermogenesis center of the posterior hypothalamus. At on ambient temperature of 5, i.c.v. injected <I>N</I><SUP>6</SUP>-cyclohexyladenosine (CHA) adenosine A1-receptor agonist induces profound hypothermia in hamsters. Although the time course of the descent of body temperature coincided with that of entry into natural hibernation, the effect was not antagonized by 8-cyclopentyltheophyllin (CPT), an adenosine A1-receptor antagonist. However, i.c.v. injection of CPT elevated the body temperature and interrupted hibernation, albeit the deep-phase (post-entry 30 h) was unaffected. This result suggests that a different system may suppress the thermogenesis center in the deep hibernation phase. Interestingly, i.c.v. injected thyrotropin releasing hormone (TRH) elevated the body temperature in both hibernation phases in hamsters. These findings suggest that the central adenosine and TRH play important roles in thermoregulation and that the new thermogenesis system, activating in low-body temperature, is induced in naturally hibernating animals.

Journal

  • Folia Pharmacologica Japonica

    Folia Pharmacologica Japonica 116(5), 304-312, 2000-11-01

    The Japanese Pharmacological Society

References:  25

Cited by:  4

Codes

  • NII Article ID (NAID)
    10008181315
  • NII NACSIS-CAT ID (NCID)
    AN00198335
  • Text Lang
    JPN
  • Article Type
    Journal Article
  • ISSN
    00155691
  • NDL Article ID
    5539915
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z19-247
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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