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Caramiphen edisylate as adjunct to standard therapy attenuates soman-induced seizures and cognitive deficits in rats.
TLDR
It is shown that physiological, behavioral, and neuropathological effects of GD exposure can be attenuated by treatment with caramiphen as an adjunct to therapy, even if administration is delayed to 30min after seizure onset.
Pharmacogenetic neuronal stimulation increases human tau pathology and trans-synaptic spread of tau to distal brain regions in mice
TLDR
This model underscores the propensity of non-mutant hTau to undergo neuronal spreading, as seen in AD, and can translate to other preclinical species and be used to evaluate modes of tau transmission and test the efficacy of therapeutic approaches that target tau or hyperexcitability.
Impaired auditory and contextual fear conditioning in soman-exposed rats
TLDR
The present study suggests that contextual and auditory fear conditioning is impaired in GD-exposed rats possibly due to neuropathology observed in the hippocampus, amygdala and thalamus.
The anticholinergic and antiglutamatergic drug caramiphen reduces seizure duration in soman-exposed rats: synergism with the benzodiazepine diazepam.
TLDR
It is concluded that CED and DZP treatment offers considerable protection against the effects of GD and PHY is a potential therapeutic option following GD exposure, albeit with a limited window of opportunity.
Rational polytherapy in the treatment of cholinergic seizures
TLDR
Treatment of RSE with combinations of the GABAAR agonists midazolam or diazepam and the NMDAR antagonists MK-801 or ketamine terminated RSE unresponsive to high-dose monotherapy with benzodiazepines, ketamine or other antiepileptic drugs (AEDs), and this drug combination based on the receptor trafficking hypothesis is effective in terminating RSE.
Early polytherapy for benzodiazepine-refractory status epilepticus
TLDR
Treating RSE with combinations of the GABAAR allosteric modulators midazolam or diazepam and the NMDAR antagonists dizocilpine or ketamine terminated RSE unresponsive to high-dose monotherapy, suggesting that treatment of RSE should be based at least in part on its pathophysiology.
Treatment of acetylcholinesterase inhibitor-induced seizures with polytherapy targeting GABA and glutamate receptors
TLDR
It is suggested that future clinical trials should treat both the lack of sufficient inhibition and the excess excitation that characterize RSE, and include early combination drug therapies, as well as the therapeutic index of drug combinations.
Dataset of EEG power integral, spontaneous recurrent seizure and behavioral responses following combination drug therapy in soman-exposed rats
This article investigated the efficacy of the combination of antiepileptic drug therapy in protecting against soman-induced seizure severity, epileptogenesis and performance deficits. Adult male rats