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Research ArticleArticle

Absence Seizures Decrease Steroid Modulation of t-[35S]Butylbicyclophosphorothionate Binding in Thalamic Relay Nuclei

Pradeep K. Banerjee, Richard W. Olsen, Niranjala J. K. Tillakaratne, Simon Brailowsky, Allan J. Tobin and O. Carter Snead III
Journal of Pharmacology and Experimental Therapeutics November 1998, 287 (2) 766-772;
Pradeep K. Banerjee
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Richard W. Olsen
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Niranjala J. K. Tillakaratne
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Simon Brailowsky
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Allan J. Tobin
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O. Carter Snead III
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Abstract

Interaction of γ-aminobutyric acid (GABA), pentobarbital and two neuroactive steroids on t-butylbicyclophosphorothionate ([35S]TBPS) binding to GABAA receptors in thalamus was studied during absence seizures. In control brain sections, the steroids alphaxalone and tetrahydrodeoxycorticosterone (at low 0.1–1 μM concentrations) increased [35S]TBPS binding in thalamic relay nuclei. Both GABA and pentobarbital dose-dependently decreased [35S]TBPS binding in these nuclei. A significant decrease in the ability of steroids to increase [35S]TBPS binding in thalamic relay nuclei was observed during absence seizures induced by γ-hydroxybutyric acid (GHB). This loss of steroid effect on binding was 1) selective to steroids only as GABA and pentobarbital modulation of [35S]TBPS binding in these nuclei did not change significantly and 2) not causally related to the generation of GHB-induced absence seizures as it was not observed at the onset of GHB-seizures but developed 30 min after the seizure-onset. We tested whether absence seizures were critical for the development of this loss of steroid effect on [35S]TBPS binding in thalamic relay nuclei. The ability of the steroids to increase [35S]TBPS binding in relay nuclei was preserved when GHB-seizures were blocked. When the duration of GHB-seizures was prolonged, the loss of steroid effect on [35S]TBPS binding in thalamus persisted throughout the seizure-duration. These findings suggest that absence seizures cause a rapid loss of steroid effect on [35S]TBPS binding to GABAAreceptors in thalamic relay nuclei.

Footnotes

  • Send reprint requests to: Dr. Pradeep K. Banerjee, Department of Neurology/The Epilepsy Research Program, Hospital for Sick Children, 555 University Ave., Toronto, Ontario M5G 1X8, Canada.

  • ↵1 This work was supported by the Brain and Behavior Program, Division of Neurology, Hospital for Sick Children, Toronto; National Institutes of Health Grants NS 17117 (O.C.S.), NS 28772 (R.W.O.) and NS 22256 (A.J.T.).

  • ↵2 Deceased May 28, 1998: to whom this work is dedicated.

  • Abbreviations:
    GHB
    γ-Hydroxybutyric acid
    GABA
    γ-aminobutyric acid
    THDOC
    tetrahydrodeoxycorticosterone
    TBPS
    t-butylbicyclophosphorothionate
    GBL
    γ-butyrolactone
    EEG
    electroencephalogram
    ROD
    relative optical density
    • Received March 26, 1998.
    • Accepted June 16, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 287, Issue 2
1 Nov 1998
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Research ArticleArticle

Absence Seizures Decrease Steroid Modulation of t-[35S]Butylbicyclophosphorothionate Binding in Thalamic Relay Nuclei

Pradeep K. Banerjee, Richard W. Olsen, Niranjala J. K. Tillakaratne, Simon Brailowsky, Allan J. Tobin and O. Carter Snead
Journal of Pharmacology and Experimental Therapeutics November 1, 1998, 287 (2) 766-772;

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Research ArticleArticle

Absence Seizures Decrease Steroid Modulation of t-[35S]Butylbicyclophosphorothionate Binding in Thalamic Relay Nuclei

Pradeep K. Banerjee, Richard W. Olsen, Niranjala J. K. Tillakaratne, Simon Brailowsky, Allan J. Tobin and O. Carter Snead
Journal of Pharmacology and Experimental Therapeutics November 1, 1998, 287 (2) 766-772;
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