A5066269700- Pesticide Exposure and Toxicity
- Cholinesterase and Neurodegenerative Diseases
- Insect and Pesticide Research
- Environmental Toxicology and Ecotoxicology
- Neuroscience and Neuropharmacology Research
- Pesticide and Herbicide Environmental Studies
- Animal testing and alternatives
- Carcinogens and Genotoxicity Assessment
- Nicotinic Acetylcholine Receptors Study
- Neurotransmitter Receptor Influence on Behavior
- Immunotoxicology and immune responses
- Photoreceptor and optogenetics research
- Electrochemical Analysis and Applications
- Infectious Encephalopathies and Encephalitis
- Animal Ecology and Behavior Studies
- Pain Mechanisms and Treatments
- Ion channel regulation and function
- Epilepsy research and treatment
- Vagus Nerve Stimulation Research
- Adenosine and Purinergic Signaling
- Olfactory and Sensory Function Studies
- Pharmacological Effects and Toxicity Studies
- Effects and risks of endocrine disrupting chemicals
- Neurological Disorders and Treatments
- Mosquito-borne diseases and control
United States Army
2005-2024
United States Army Medical Research Institute of Infectious Diseases
1986-2024
DEVCOM Army Research Laboratory
1984-2019
United States Department of the Army
1984-2011
GTx (United States)
2000
Boston Medical Center
1998
Boston University
1998
University of California, Irvine
1998
University of California, Los Angeles
1997
West Los Angeles College
1997
This study examined brain regional neurotransmitter level changes as a function of seizure duration following soman intoxication. Rats, implanted with cortical electrodes and pretreated HI-6, received convulsant dose soman. At selected times after onset the EEG recording were removed animal was killed. Spinal cord cholinesterase (ChE) activity rapidly maximally depressed, while acetylcholine (ACh) levels showed elevations early 3 min treatment reached significantly high at time onset....
Two guinea pig models were used to study the anticonvulsant potency of diazepam, midazolam, and scopolamine against seizures induced by nerve agents tabun, sarin, soman, cyclosarin, O-ethyl S-(2-(diisopropylamino)ethyl)methylphosphonothioate (VX), O-isobutyl S-(2-diethylamino)ethyl)-methyl phosphonothioate (VR). Animals instrumented for electroencephalogram recording pretreated with pyridostigmine bromide (0.026 mg/kg i.m.) 30 min before challenge 2 x LD50 (s.c.) a agent. In model A,...
Near-lethal exposure to nerve agents produces prolonged epileptiform seizures requiring the administration of benzodiazepine anticonvulsant drugs, such as diazepam. Clinically, benzodiazepines are reported lose effectiveness greater delay between seizure onset and treatment. This time-dependent diminished diazepam was tested in present study. Seizures elicited by agent, soman, were produced guinea pigs instrumented record brain electrocorticographic (ECoG) activity. Different groups animals...
The acute effects of the organophosphorus cholinesterase inhibitor soman include hypersecretions, convulsions, and death. purpose this study was to evaluate anticholinergic compounds aprophen, atropine sulfate, azaprophen, benactyzine, benztropine, biperiden, scopolamine HBr, trihexyphenidyl for their efficacy in preventing soman-induced hypersecretions convulsions. Male rats were injected with oxime HI-6 (125 mg/kg, i.p.), increase survival time, along various intramuscular doses...
In atropine-pretreated rats, HI-6 (125 mg/kg i.p.) raised the LD50 of Soman (subcutaneous) 5.7 times. Addition (25 micrograms i.c.v.) failed to enhance this protection further. (intraperitoneal) also protected animals from intracerebroventricular Soman. HI-6, administered intracerebroventricularly either alone or in combination with intraperitoneal increase protection, nor did it reactivate Soman-inhibited acetylcholinesterase (AChE) several brain areas. 62.5 rats Sarin lethality, but only...