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

Joosen, Marloes J.A.; Jousma, E.; Boom, Tom M. van den; Kuijpers, Willem C.; Smit, August B.; Lucassen, Paul J.; Helden, H.P.M. van

doi:10.1016/j.neuro.2008.11.010

Cited by 40 publications

(38 citation statements)

References 57 publications

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“…The findings of the study show that memory test conducted on adolescent rats when atropine was administered demonstrated deficit in cognition, particularly recognition memory in animals as compared with the control from the NOR result. The findings of the present study were strengthened from the earlier reports of Joels et al (2004) and Joosen et al (2009) that show that atropine impairs learning abilities and neurodegeneration. However, the spatial memory was not affected in the treated animal when compared with those of the control.…”

Section: Discussionsupporting

confidence: 83%

“…Tropane is believed to alter neurogenesis (Joels et al, 2004;Joosen, 2009), but little knowledge is known as to the mechanisms of it actions. However, it was thought to exert its activities by either involved in the destruction of the neural precursor cells thus limiting their survival rate.…”

Section: Discussionmentioning

confidence: 99%

“…Many drugs have been used for recreation purposes among adolescent and this includes the likes of atropine (anticholinergic agent) which is commonly found in some plants like Datura metel (Griffin and Lin, 2000). Atropine, an extract from Soma plant has been shown to impair learning ability and neurogenesis (Joosen et al, 2009). Datura metel which contains tropane alkaloids induces hallucinations and metabolic disorder in rats (Abubakar et al, 2010;Damilare et al, 2010;Richard et al, 2011;Tijani et al, 2012), and have also been implicated in the disorders of hippocampal development in rats (Ishola and Adeniyi, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Atropine exposure in adolescence predispose to adult memory loss in Wistar rats

Olawepo¹,

Ishola²,

Ajao³

et al. 2018

Int. J. Bio. Chem. Sci

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Some of the brain malfunctions in adulthoods have been linked to the developmental process in their childhood, especially in most adolescent who have been exposed to one form of drug abuse or another. This study investigated the effect of atropine exposure at adolescence on the memory and histology of the frontal cortex of Wistar rats and its effects on adult memory. 20 male adolescent Wistar rats were used for the study. The rats were divided into two groups of 10 rats each. The first group were administered with100 mg/kg body weight of atropine (Atr), and the other 10 rats were given 10 mL/kg body weight of normal saline (NS) for 7 days at adolescence. On 8 th day, the rats were subjected to novel object recognition test (NOR) and 'Y' maze test to assess their memory function, 5 rats from each group were euthanized using ketamine and were perfused transcardially with 4% paraformaldehyde. Thereafter, the brains were removed and processed for histology using H&E and Giemsa stain. The remaining 5 rats from each group were reared till adult (65 days postpartum) without treatment denoted as Atr-I and NS-I respectively. The same memory tests and histology study were conducted on the rats at adulthood. Data were analysed using Student t test and P<0.05 was set as significant level. Atr and Atr-1showed decline in memory neither index from NOR compared with NS and NS-I respectively. Atr-I shows decline in Y maze compared to NS-I. The study concludes that atropine exposed rats show significant signs of neural cell death in the frontal cortex which progresses into adulthood as evidence from the histological findings.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Atropine exposure in adolescence predispose to adult memory loss in Wistar rats

Olawepo¹,

Ishola²,

Ajao³

et al. 2018

Int. J. Bio. Chem. Sci

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“…Muscarinic antagonists, benzodiazepines, and glutamate receptor antagonists have been tested, showing varying efficacies that depend on several factors, such as the timing of administration after exposure, dose, or drug treatment combinations. All of the animal models used in these experiments involve a pretreatment (Shih et al, 2003;Capacio et al, 2004;Joosen et al, 2009;Figueiredo et al, 2011), or, when no pretreatment is given, oximes and atropine are administered together within 1 minute after exposure (e.g., Moffett et al, 2011). Such protocols of drug administration increase survival rate and allow studies of other parameters but do not mimic a real-life situation in which exposure can be unexpected and pretreatment is not an option, and medical assistance may not be available within a minute after exposure.…”

Section: Discussionmentioning

confidence: 99%

“…Research aimed at developing effective medical countermeasures to terminate seizure activity and prevent brain damage by nerve agent exposure has traditionally used models in which the animal is pretreated with an oxime or pyridostigmine. Usually, pretreatment is administered 30 minutes before nerve agent exposure, followed by atropine administration within 1 minute after exposure (e.g., Shih et al, 2003;Capacio et al, 2004;Joosen et al, 2009;Figueiredo et al, 2011). The reactivation of inhibited acetylcholinesterase by the oxime and the blockade of muscarinic receptors by atropine prevent acute death from cardiorespiratory depression and allow the subsequent testing of anticonvulsant compounds.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of the GluK1/AMPA Receptor Antagonist LY293558 against Seizures and Neuropathology in a Soman-Exposure Model without Pretreatment and its Pharmacokinetics after Intramuscular Administration

Apland

Aroniadou‐Anderjaska

Figueiredo

et al. 2012

J Pharmacol Exp Ther

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Control of brain seizures after exposure to nerve agents is imperative for the prevention of brain damage and death. Animal models of nerve agent exposure make use of pretreatments, or medication administered within 1 minute after exposure, in order to prevent rapid death from peripheral toxic effects and respiratory failure, which then allows the testing of anticonvulsant compounds. However, in a real-case scenario of an unexpected attack with nerve agents, pretreatment would not be possible, and medical assistance may not be available immediately. To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the GluK1 (GluR5)/ a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl) ethyl]decahydroisoquinoline-3-carboxylic acid (LY293558) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman. We injected LY293558 intramuscularly, as this would be the most likely route of administration to humans. LY293558 (15 mg/kg), injected along with atropine and the oxime HI-6 at 20 minutes after soman exposure, stopped seizures and increased survival rate from 64% to 100%. LY293558 also prevented neuronal loss in the amygdala and hippocampus, and reduced neurodegeneration in a number of brain regions studied 7 days after soman exposure. Analysis of the LY293558 pharmacokinetics after intramuscular administration showed that this compound readily crosses the blood-brain barrier. There was good correspondence between the time course of seizure suppression by LY293558 and the brain levels of the compound.

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Chemical Terrorism

Ballantyne¹

2009

General, Applied and Systems Toxicology

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Terrorism has a very long history. Terrorism has been defined terrorism as deliberately and violently targeting civilians for political purposes. One of the objectives of terrorism may be to generate a disproportionate response and thereby alienate the population against the state. The range of weaponry potentially available to terrorists is wide and variable: weapons used may include guns or explosive devices, radioactive/nuclear sources, biological organisms and toxins (bioterrorism) or xenobiotic chemicals (chemical terrorism). Chemicals that might be used include irritant and/or disorienting materials, nauseating materials, psychogenic materials and severely toxic and lethal agents. The only major chemical terrorist action to date was the two instances of use in Japan of sarin, an organophosphorus ester G‐agents, where there was large‐scale mass casualties. While many other compounds could be used in chemical terrorism (eg cyanide, arsine), the only other mass casualty situation to date involving terrorism was the death of many innocent citizens in an anti‐hostage situation in Moscow; this appears to have caused by the authorities' response, rather than the action of the terrorists.

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

Cited by 40 publications

References 57 publications

Atropine exposure in adolescence predispose to adult memory loss in Wistar rats

Atropine exposure in adolescence predispose to adult memory loss in Wistar rats

Efficacy of the GluK1/AMPA Receptor Antagonist LY293558 against Seizures and Neuropathology in a Soman-Exposure Model without Pretreatment and its Pharmacokinetics after Intramuscular Administration

Chemical Terrorism

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