Inhibitory effect of new quinolones on GABA(A) receptor-mediated response and its potentiation with felbinac in Xenopus oocytes injected with mouse-brain mRNA: correlation with convulsive potency in vivo.

@article{Kawakami1997InhibitoryEO,
  title={Inhibitory effect of new quinolones on GABA(A) receptor-mediated response and its potentiation with felbinac in Xenopus oocytes injected with mouse-brain mRNA: correlation with convulsive potency in vivo.},
  author={Junichi Kawakami and K Yamamoto and Atsushi Asanuma and Keiji Yanagisawa and Yasufumi Sawada and Tatsuji Iga},
  journal={Toxicology and applied pharmacology},
  year={1997},
  volume={145 2},
  pages={
          246-54
        }
}
Convulsions induced by the interaction of new quinolone antimicrobial agents (NQs) and nonsteroidal anti-inflammatory drugs (NSAIDs) were previously reported, and blockade of GABA(A) receptor by NQs and its potentiation with NSAIDs were considered as one of its possible mechanisms. However, useful methodology for prediction of convulsive potencies of NQs with or without NSAIDs in vivo based on in vitro screening was not established. Therefore, we applied the Xenopus oocytes translation system… Expand
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Inhibition of GABAA receptor-mediated current responses by enoxacin (new quinolone) and felbinac (non-steroidal anti-inflammatory drug) in Xenopus oocytes injected with mouse-brain messenger RNA.
The convulsant interaction between enoxacin (ENX), a new quinolone antibacterial agent (NQ), and felbinac (FLB), a non-steroidal anti-inflammatory drug (NSAID), in vivo was reproduced as the changeExpand
The effects of quinolones and NSAIDs upon GABA-evoked currents recorded from rat dorsal root ganglion neurones.
TLDR
The present results support earlier binding studies and extend them by demonstrating electrophysiologically a potent quinolone/NSAID drug interaction at the GABAA receptor, commensurate with clinical observations of an increased risk of fits in patients prescribed certain quinols together with certain NSAIDs. Expand
Inhibitory effects of quinolone antibacterial agents on gamma-aminobutyric acid binding to receptor sites in rat brain membranes
TLDR
The findings suggest that the inhibition of GABA binding to receptors (including uptake sites) in the brain may be involved in the induction of epileptogenic neurotoxicities by quinolones. Expand
Neurochemical studies on quinolone antibiotics: effects on glutamate, GABA and adenosine systems in mammalian CNS.
Quinolone antibiotics, which can be proconvulsant in susceptible patients, were found to inhibit the specific binding of the adenosine receptor ligands L-3H-N6-phenylisopropyladenosine (L-3H-PIA) andExpand
Quinolones and fenbufen interact with GABAA receptor in dissociated hippocampal cells of rat.
TLDR
It was concluded that, in the presence of an anti-inflammatory agent, the quinolone antibiotics decrease the affinity of GABAA receptors, the result being induction of epileptogenic neurotoxicities. Expand
[Adverse drug interactions between pyridonecarboxylic acids and nonsteroidal antiinflammatory drugs: convulsion after oral or intracerebral administration in mice].
TLDR
The intracerebral injection of drugs alone to mice revealed that both FBF and 4-biphenylacetic acid (BPAA), which is principally responsible for FBF's antiinflammatory action, scarcely had convulsant activity. Expand
Structure-epileptogenicity relationship of quinolones with special reference to their interaction with gamma-aminobutyric acid receptor sites
TLDR
The results indicate that the epileptogenic activity of quinolones possibly relates to the GABA-like structures of substituents at their 7 positions, which act as antagonists of GABA receptors. Expand
Modulation of the seizure threshold for excitatory amino acids in mice by antiepileptic drugs and chemoconvulsants.
TLDR
A novel method for the assessment of the threshold for clonic seizures induced by excitatory amino acids based on continuous infusion of the glutamate agonists into the lateral brain ventricle of unrestrained mice is reported, it was found that systemically administered diphenylhydantoin and carbamazepine elevated thereshold for ATPA and had negligible effects on the thresholds for kainate and NMDA. Expand
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TLDR
Low-dose quinolones (administered as an intravenous bolus) cause pronounced but transient systolic hypotension in dogs and cats; cardiovascular effects may be mediated by histamine release and mutagenicity studies have been performed. Expand
Minimal model to account for the membrane conductance increase and desensitization of gamma-aminobutyric acid receptors synthesized in the Xenopus oocytes injected with rat brain mRNA.
TLDR
Estimated equilibrium and rate constants in the model for GABA receptors could successfully explain the results of the five measurements made to establish the relationship between GABA concentration and the electrical responses. Expand
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