Abstract:
:Pitrazepin is a potent new GABA antagonist which differs from bicuculline in its chemical structure and its interaction with both [3H]muscimol and [3H]flunitrazepam binding sites, whereby the potency of pitrazepin in displacing [3H]muscimol exceeds that of bicuculline by at least a factor of 10. In physiological experiments, blockade of synaptically released GABA by pitrazepin was shown to reduce inhibitory postsynaptic potentials and resulted in the onset of bursting activity which persisted for hours following drug application. The effect of pitrazepin was not tissue specific since it induced a bursting discharge pattern in cultures derived from hippocampus and hypothalamus. Bursting activity was abolished by GABA, baclofen and pentobarbital, but only weakly reduced by midazolam. Pitrazepin also antagonized the action of exogenous GABA, but failed to influence the action of baclofen, an effect which was associated with a decreased membrane input resistance and which was blocked by barium. These results indicate that pitrazepin selectively interacts with the putative GABAA site, thereby antagonizing the chloride-dependent GABA response.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Gähwiler BH,Maurer R,Wüthrich HJdoi
10.1016/0304-3940(84)90244-1subject
Has Abstractpub_date
1984-04-06 00:00:00pages
311-6issue
3eissn
0304-3940issn
1872-7972pii
0304-3940(84)90244-1journal_volume
45pub_type
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