Effect of chronic imipramine or baclofen on GABA-B binding and cyclic AMP production in cerebral cortex |
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| Authors: | P D Suzdak G Gianutsos |
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| Affiliation: | 1. Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan;2. Department of Pharmacy Practice, Tri-Service General Hospital, Taipei, Taiwan;3. Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan;4. Department of Otorhinolaryngology-Head and Neck Surgery, Tri-Service General Hospital, Taipei, Taiwan;5. Department of Otorhinolaryngology, Taichung Armed Forces General Hospital, Taichung, Taiwan;6. Department of Nuclear Medicine, Tri-Service General Hospital, Taipei, Taiwan;7. School of Pharmacy, National Defense Medical Center, Taipei, Taiwan;8. Universal Eye Center, Taipei, Taiwan |
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| Abstract: | ![]()
Long-term (14 days) treatment of mice with the antidepressant drug imipramine increased the number of GABA-B receptors in the cerebral cortex and also led to an increase in the potentiation of norepinephrine-induced cAMP accumulation by baclofen (a GABA-B agonist) in cortical slices. Chronic baclofen treatment decreased both of these measures. These results suggest that previous evidence of increased GABA-B binding by antidepressants is coupled to a functional increase in adenylate cyclase activity, but that the mechanism responsible for this effect is not due simply to direct GABA-B receptor stimulation. |
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