Amitriptyline increases GABA-stimulated 36Cl- influx by recombinant (alpha 1 gamma 2) GABAA receptors
| Autor: | Nancy L. Schindler, Glenda Crites, Angela Knapp, Howell W. Rogers, Ewa Malatynska, Alicia Cecil, Cortland Miller |
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| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
Amitriptyline Drug action Pharmacology Antidepressive Agents Tricyclic Kidney chemistry.chemical_compound Chloride Channels Internal medicine medicine Animals Humans Neurotransmitter Receptor GABA Modulators Molecular Biology Cells Cultured gamma-Aminobutyric Acid Diazepam Chemistry GABAA receptor General Neuroscience Receptors GABA-A Rats Endocrinology Flumazenil Antidepressant Neurology (clinical) Developmental Biology medicine.drug |
| Zdroj: | Brain research. 851(1-2) |
| ISSN: | 0006-8993 |
| Popis: | WSS-1 cells expressing (α1γ2)GABAA receptors show an augmented 36 Cl − response to GABA in the presence of amitriptyline that is increased by flumazenil, unlike augmentation by diazepam which is blocked by flumazenil. This amitriptyline effect is opposite to the inhibition of GABA-stimulated 36 Cl influx manifested in membrane vesicles prepared from drug-naive rats or submissive rats (a model of depression) but is similar to that seen in tissue from amitriptyline-treated rats or dominant rats. The results suggest a novel mechanism of antidepressant drug action having a delayed onset. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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