anticholinergic/seizures

A total of eight anticholinergic drugs (aprophen, atropine, azaprophen, benactyzine, biperiden, procyclidine, scopolamine, trihexyphenidyl) were tested in parallel with diazepam for the ability to terminate seizure activity induced by the nerve agent soman. Guinea pigs, implanted with electrodes to

Severe preeclampsia is a pathophysiological disorder specific to pregnancy and characterized by vasoconstriction and hypercoagulability. Eclampsia (convulsion associated with preeclampsia) and hemolysis, elevated liver enzymes, and low platelet count associated with preeclampsia (HELLP syndrome) are

We recently reported that systemic administration of the anticholinesterase, soman, caused rapid depletion of forebrain norepinephrine (NE) in convulsive but not in nonconvulsive rats. As neurons in nucleus locus coeruleus (LC) provide the bulk of NE innervation to most of the forebrain and the sole

Rats were given daily injections of atropine, mecamylamine or both drugs in combination, 1 h prior to daily electrical amygdaloid kindling stimulation. Neither drug was effective alone, but the two drugs in combination significantly increased the latency to develop stage 5 kindled seizures.

Therapy of seizure activity following exposure to the nerve agent soman (GD) includes treatment with the anticonvulsant diazepam (DZP), an allosteric modulator of γ-aminobutyric acid A (GABA(A)) receptors. However, seizure activity itself causes the endocytosis of GABA(A) receptors and diminishes

In an attempt to know the relation of seizure and gastric mucosal damage, we challenged arecoline (ACL) centrally to induce seizure and investigated gastric hemorrhagic injury in acid-irrigated stomachs of rats. The protective effects of several drugs also were evaluated. After deprivation of food

Organophosphorus nerve agents (NAs) irreversibly inhibit acetylcholinesterase, which results in the accumulation of acetylcholine and widespread excitotoxic seizure activity. Because current medical countermeasures (anticholinergics, AChE reactivators, and benzodiazepines) lack sufficient

The nature of the antagonism by anticholinergic compounds of nicotine-induced convulsion in mice has not been defined clearly. Although, because they do not compete effectively for agonist binding to brain tissue in-vitro, these compounds are thought to be non-competitive antagonists in the brain,

Tricyclopinate hydrochloride(TCPN.HCl) and methiodide(TCPN.CH3I) have been identified as new chemical entities. The effects of these two compounds on central and peripheral nicotinic and muscarinic cholinergic receptor activities were investigated. Excitation of the central nicotinic receptors by

Organophosphate poisoning is associated with adverse effects on the central nervous system such as seizure/convulsive activity and long term changes in neuronal networks. This study reports on investigations designed to assess the consequences of soman exposure on excitatory amino acids receptors in