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      During Anesthetic-Induced Activation of Hypothalamic Pituitary Adrenal Axis, Blood-Borne Steroids Fail to Contribute to the Anesthetic Effect

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          Abstract

          Anesthetic doses of ethanol (100 mmol/kg p.o.), chloral hydrate (2 mmol/kg i.p.), and urethane (9 mmol/kg i.p.) induce sharp and sustained (6- to 10-fold) dose-dependent increase in rat brain pregnenolone and progesterone content. In contrast, other general anesthetics such as ketamine (0.7 mmol/kg i.p.) and pentobarbital (0.2 mmol/kg i.p.), and the sedative/hypnotic clonazepam (17 µmol/kg i.p.) decrease brain pregnenolone and progesterone content. The increase in brain pregnenolone and progesterone content fails to occur if ethanol, chloral hydrate, and urethane are administered to hypophysectomized-adrenalectomized rats suggesting that the increase of brain steroids requires the hypophysis and probably originates in peripheral tissues and not in brain. The administration to hypophysectomized rats of 5 IU/kg of ACTH produces a brain pregnenolone and progesterone accumulation by an extent comparable to that elicited by anesthetic doses of ethanol, chloral hydrate, or urethane in intact animals. However, the increase in brain pregnenolone and progesterone content induced by ACTH is devoid of anesthetic or sedative effects and does not appear to change central GABAergic tone. In fact, ACTH, unlike allopregnanolone and allodeoxicorticosterone, failed to delay the onset of isoniazid-induced seizures, to reduce the fear of novelty in the elevated plus maze test as inferred by the increase in the number of entries or the time spent in the open arm. Thus, the data suggest that blood-borne steroids cannot function as precursors of brain neurosteroid modulators acting on GABAa receptor.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1993
          1993
          08 April 2008
          : 57
          : 3
          : 559-565
          Affiliations
          Fidia-Georgetown, Institute for the Neurosciences, Washington, D.C, USA
          Article
          126405 Neuroendocrinology 1993;57:559–565
          10.1159/000126405
          8391666
          © 1992 S. Karger AG, Basel

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          Page count
          Pages: 7
          Categories
          Original Paper

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