Long-term cognitive deficits accompanied by reduced neurogenesis after soman poisoning.

  title={Long-term cognitive deficits accompanied by reduced neurogenesis after soman poisoning.},
  author={Marloes J. A. Joosen and Edwin Jousma and Tom M van den Boom and Willem C. Kuijpers and August Benjamin Smit and Paul J. Lucassen and Herman P. M. van Helden},
  volume={30 1},

Potential pharmacological strategies for the improved treatment of organophosphate-induced neurotoxicity.

These neuroprotective strategies may prevent secondary neuronal damage in both early and late stages of OP poisoning, and thus may be a beneficial approach to treating the neuropsychological and neuronal impairments resulting from OP toxicity.

Alpha-Linolenic Acid-Induced Increase in Neurogenesis is a Key Factor in the Improvement in the Passive Avoidance Task After Soman Exposure

The results suggest that alpha-linolenic acid induces a long-lasting neurorestorative effect that involves activation of mTORC1 possibly via a BDNF-TrkB-mediated mechanism.

Treatment efficacy in a soman-poisoned guinea pig model: added value of physostigmine?

Combined treatment of obidoxime and physostigmine shortened the duration of seizures, if present, from up to 80 min to ~10–15 min, and treatment of OP poisoning with a carbamate, such as physostIGmine should be carefully re-evaluated.

Long‐term neuropathological and behavioral impairments after exposure to nerve agents

The basolateral amygdala (BLA), which appears to be a key site for seizure initiation upon exposure, suffers severe neuronal loss; however, GABAergic BLA interneurons display a delayed death, perhaps providing a window of opportunity for rescuing intervention.

(-)-Phenserine Attenuates Soman-Induced Neuropathology

It is demonstrated that (-)-phenserine protects neurons against soman-induced neuronal cell death in rats when administered either as a pretreatment or post-treatment paradigm, improves motoric movement in soman -exposed animals and reduces mortality when given as a Pretreatment.



Differential effects of chronic haloperidol and olanzapine exposure on brain cholinergic markers and spatial learning in rats

The results in the rat suggest that OLZ (relative to HAL) may be more desirable as an antipsychotic for patients suffering from memory dysfunction especially for those in which cholinergic deficits may already be present.

Sarin-induced neuropathology in rats

Sarin has a potent acute and long-term central neurotoxicity, which must be considered in the design of therapeutic regimes, and frontal cortex damage was specific to soman poisoning.

Neurochemical Mechanisms in Soman‐induced Seizures

Findings are consistent with the notion that inhibition of ChE and elevation of ACh initiate the seizure process, resulting in secondary changes in DA turnover and release of NE, and later changes in excitatory (aspartate, glutamate) and inhibitory (GABA) amino acid transmitters.

Effects of atropine sulphate on seizure activity and brain damage produced by soman in guinea-pigs: ECoG correlates of neuropathology.

Data confirm the tight relationships which exist between seizure activity and neuropathology in soman poisoning, and suggest that refined, standardized analysis of electrographic parameters drawn from ECoG tracings and power spectrum might serve as a useful tool to predict the presence, localization, and severity of soman-induced brain damage.

Changes of acetylcholinesterase activity in various parts of brain following nontreated and treated soman poisoning in rats.

Despite its limited effectiveness in the brain, HI-6 seems to be the most effective oxime yet found against soman poisoning because of its high reactivating effect in the peripheral compartment and other beneficial effects.

Effects of Antipsychotic Drugs on Neurogenesis in the Forebrain of the Adult Rat

Despite the significant increase in newlygenerated cells in the PFC of olanzapine-treated rats, the total number of these cells is low, suggesting that the therapeutic effects of atypical APD treatment may not be due to the presence of newly generated cells that have migrated to the cortex.

Anticonvulsants for soman-induced seizure activity.

This report describes studies of anticonvulsants for the organophosphorus (OP) nerve agent soman: a basic research effort to understand how different pharmacological classes of compounds influence