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Mechanisms of allosteric modulation ...
~
Beckstead, Michael John.
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Mechanisms of allosteric modulation of GABA(A) and glycine receptors.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Mechanisms of allosteric modulation of GABA(A) and glycine receptors./
作者:
Beckstead, Michael John.
面頁冊數:
138 p.
附註:
Adviser: S. John Mihic.
Contained By:
Dissertation Abstracts International63-02B.
標題:
Chemistry, Biochemistry. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3043094
ISBN:
0493566384
Mechanisms of allosteric modulation of GABA(A) and glycine receptors.
Beckstead, Michael John.
Mechanisms of allosteric modulation of GABA(A) and glycine receptors.
- 138 p.
Adviser: S. John Mihic.
Thesis (Ph.D.)--Wake Forest University, The Bowman Gray School of Medicine, 2002.
Inhalable solvents possess abuse liability and produce many neurobehavioral effects typically associated with central nervous system - depressant agents, such as ethanol (EtOH) and volatile anesthetics. We first tested the hypothesis that commonly abused solvents toluene (TOL), 1,1,1-trichloroethane (TCE), and trichloroethylene (TCY) affect ligand-gated ion channel activity, as do other classes of central nervous system-depressive agents. All three inhalants reversibly enhanced neurotransmitter-activated currents at GABA<sub>A</sub> and glycine receptors expressed in <italic>Xenopus laevis</italic> oocytes. TOL, TCE and TCY were tested on several glycine receptor mutants, some of which were insensitive to ethanol and/or the anesthetic enflurane (ENF). TCE effects were abolished in three mutants and enhanced in two, a pattern strikingly similar to that seen with ENF.
ISBN: 0493566384Subjects--Topical Terms:
1017722
Chemistry, Biochemistry.
Mechanisms of allosteric modulation of GABA(A) and glycine receptors.
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Thesis (Ph.D.)--Wake Forest University, The Bowman Gray School of Medicine, 2002.
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Inhalable solvents possess abuse liability and produce many neurobehavioral effects typically associated with central nervous system - depressant agents, such as ethanol (EtOH) and volatile anesthetics. We first tested the hypothesis that commonly abused solvents toluene (TOL), 1,1,1-trichloroethane (TCE), and trichloroethylene (TCY) affect ligand-gated ion channel activity, as do other classes of central nervous system-depressive agents. All three inhalants reversibly enhanced neurotransmitter-activated currents at GABA<sub>A</sub> and glycine receptors expressed in <italic>Xenopus laevis</italic> oocytes. TOL, TCE and TCY were tested on several glycine receptor mutants, some of which were insensitive to ethanol and/or the anesthetic enflurane (ENF). TCE effects were abolished in three mutants and enhanced in two, a pattern strikingly similar to that seen with ENF.
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We next hypothesized that alcohols, anesthetics and inhalants share common or overlapping molecular sites of action on glycine receptors. To investigate this possibility, these compounds were applied singly and in combination to wild-type glycine receptors. A mutant glycine receptor (S267I), insensitive to ethanol but not anesthetics, was used to demonstrate antagonism of anesthetic and inhalant effects. EtOH had no effect on its own in S267I receptors and reversibly inhibited the enhancing effect of ENF and CHCl<sub>3</sub>. ENF also antagonized the direct activating effect of CHCl<sub>3</sub> on a glycine receptor mutant (S267L) that demonstrated constitutive activity. These data suggest the existence of overlapping molecular sites of action for ethanol, inhalants, and volatile anesthetics on glycine receptors and demonstrate the possibility of pharmacological antagonism of volatile anesthetic effects.
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A complication in studying allosteric actions on ligand-gated ion channels is in the dissection of modulator effects on neurotransmitter binding from their effects on channel opening. A mutant glycine receptor (D97R) that exhibits constitutive activity was used to investigate the hypothesis that alcohols, anesthetics and inhalants directly affect channel opening in the absence of glycine. In these receptors, EtOH, ENF, CHCl<sub>3</sub>, halothane, TCE and TOL elicited currents in the absence of glycine. Double mutant (D97R-S267I) receptors were constitutively active <italic>and</italic> insensitive to the direct enhancing effects of modulators. These data demonstrate that ethanol, volatile anesthetics and inhalants can affect glycine receptor channel opening independently of their effects on enhancing neurotransmitter binding.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3043094
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