Benzodiazepine and β-carboline modulation of GABA-stimulated 36Cl-influx in cultured spinal cord neurons

Paul F. Lehoullier; Maharaj K. Ticku

doi:10.1016/0014-2999(87)90617-0

Benzodiazepine and β-carboline modulation of GABA-stimulated ³⁶Cl-influx in cultured spinal cord neurons

Paul F. Lehoullier, Maharaj K. Ticku

Department of Pharmacology

Research output: Contribution to journal › Article › peer-review

25 Scopus citations

Abstract

GABA_A agonists stimulate ³⁶Cl-influx in spinal cord cultured neurons in a concentration-dependent manner. This effect of GABA_A receptor stimulation is enhanced by benzodiazepines like clonazepam, diazepam and flurazepam and attenuated by (+)bicuculline and picrotoxinin. The β-carbolines, methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM) and propyl-β-carboline-3-carboxylate (β-CCPr) exhibited opposite effects, with DMCM attenuating, while β-CCPr potentiating GABA's effect. These results are consistent with the behavioral and electrophysiological effect of benzodiazepines and β-carbolines with GABA receptor complex.

Original language	English (US)
Pages (from-to)	235-238
Number of pages	4
Journal	European Journal of Pharmacology
Volume	135
Issue number	2
DOIs	https://doi.org/10.1016/0014-2999(87)90617-0
State	Published - Mar 17 1987

Keywords

Cl-influx
Benzodiazepines
GABA
Spinal cord (cultured neurons)
β-Carbolines

ASJC Scopus subject areas

Pharmacology

Access to Document

10.1016/0014-2999(87)90617-0

Cite this

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title = "Benzodiazepine and β-carboline modulation of GABA-stimulated 36Cl-influx in cultured spinal cord neurons",

abstract = "GABAA agonists stimulate 36Cl-influx in spinal cord cultured neurons in a concentration-dependent manner. This effect of GABAA receptor stimulation is enhanced by benzodiazepines like clonazepam, diazepam and flurazepam and attenuated by (+)bicuculline and picrotoxinin. The β-carbolines, methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM) and propyl-β-carboline-3-carboxylate (β-CCPr) exhibited opposite effects, with DMCM attenuating, while β-CCPr potentiating GABA's effect. These results are consistent with the behavioral and electrophysiological effect of benzodiazepines and β-carbolines with GABA receptor complex.",

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N2 - GABAA agonists stimulate 36Cl-influx in spinal cord cultured neurons in a concentration-dependent manner. This effect of GABAA receptor stimulation is enhanced by benzodiazepines like clonazepam, diazepam and flurazepam and attenuated by (+)bicuculline and picrotoxinin. The β-carbolines, methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM) and propyl-β-carboline-3-carboxylate (β-CCPr) exhibited opposite effects, with DMCM attenuating, while β-CCPr potentiating GABA's effect. These results are consistent with the behavioral and electrophysiological effect of benzodiazepines and β-carbolines with GABA receptor complex.

AB - GABAA agonists stimulate 36Cl-influx in spinal cord cultured neurons in a concentration-dependent manner. This effect of GABAA receptor stimulation is enhanced by benzodiazepines like clonazepam, diazepam and flurazepam and attenuated by (+)bicuculline and picrotoxinin. The β-carbolines, methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM) and propyl-β-carboline-3-carboxylate (β-CCPr) exhibited opposite effects, with DMCM attenuating, while β-CCPr potentiating GABA's effect. These results are consistent with the behavioral and electrophysiological effect of benzodiazepines and β-carbolines with GABA receptor complex.

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