The presence of atropinesterase activity in animal plasma.

The enzyme atropinesterase (EC 3.1.1.

Effects of anticonvulsants on soman-induced epileptiform activity in the guinea-pig in vitro hippocampus.

Seizures arising from acetylcholinesterase inhibition are a feature of organophosphate anticholinesterase intoxication. Although benzodiazepines are effective against these seizures, alternative anticonvulsant drugs may possess greater efficacy and fewer side-effects. We have investigated in the guinea-pig hippocampal slice preparation the ability of a series of anticonvulsants to suppress epileptiform bursting induced by the irreversible organophosphate anticholinesterase, soman (100 nM).

Inhibiting MAP kinase activity prevents calcium transients and mitosis entry in early sea urchin embryos.

A transient calcium increase triggers nuclear envelope breakdown (mitosis entry) in sea urchin embryos. Cdk1/cyclin B kinase activation is also known to be required for mitosis entry. More recently, MAP kinase activity has also been shown to increase during mitosis.

A guinea pig hippocampal slice model of organophosphate-induced seizure activity.

Extracellular recording techniques have been used in the guinea pig hippocampal slice preparation to investigate the electrophysiological actions of the organophosphate (OP) anticholinesterase soman. When applied at a concentration of 100 nM, soman induced epileptiform activity in the CA1 region in approximately 75% of slices. This effect was mimicked by the anticholinesterases paraoxon (1 and 3 microM), physostigmine (30 microM), and neostigmine (30 microM), thus providing indirect evidence that the epileptiform response was mediated by elevated acetylcholine levels.

Periodic orbit analysis reveals subtle effects of atropine on epileptiform activity in the guinea-pig hippocampal slice.

Epileptiform activity is a state often induced in vitro in order to study seizures and antiepileptic/anticonvulsant drugs. Traditional methods of evaluating drug effects have commonly relied upon measuring changes in the frequency and duration of such events. We have used a recently developed mathematical technique based on periodic orbit analysis to investigate the effect of atropine (a muscarinic antagonist) on epileptiform activity induced by soman (an irreversible acetylcholinesterase inhibitor), 4-aminopyridine (a K+ channel blocker) and 8-cyclopentyl-1,3-dipropylxanthine (an adenosine A1 receptor antagonist) in the guinea-pig hippocampal slice.

Partial adenosine A(1) receptor agonists inhibit sarin-induced epileptiform activity in the hippocampal slice.

Organophosphate poisoning can result in seizures and subsequent neuropathology. One possible therapeutic approach would be to employ adenosine A(1) receptor agonists, which have already been shown to have protective effects against organophosphate poisoning. Using an in vitro model of organophosphate-induced seizures, we have investigated the ability of several adenosine A(1) receptor agonists to inhibit epileptiform activity induced by the organophosphate sarin, in the CA1 stratum pyramidale of the guinea pig hippocampal slice.