2011
DOI: 10.1016/j.neuroscience.2010.12.031
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Repeated, intermittent exposures to diisopropylfluorophosphate in rats: protracted effects on cholinergic markers, nerve growth factor-related proteins, and cognitive function

Abstract: Organophosphates (OPs) pose a constant threat to human health due to their widespread use as pesticides and their potential employment in military and terrorist attacks. The acute toxicity of OPs has been extensively studied; however, the consequences of prolonged or repeated exposure to levels of OPs that produce no overt signs of acute toxicity (i.e., subthreshold levels) are poorly understood. Further, there is clinical evidence that such repeated exposures to OPs lead to prolonged deficits in cognition, al… Show more

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Cited by 27 publications
(24 citation statements)
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“…The figure above represents biofunction categories regulated in response to GW agent exposure at postexposure day 150, after a timepoint when cognitive impairment was observed et al 2008). Hence, our data support a psychomotor-related dysfunction rather than fine motor coordination problems, observations that are similar to that reported for another organophosphate AChE inhibitor pesticide, diisopropylfluorophosphate (Terry et al 2011). It is also possible that these GW-agent-induced neurobehavioral changes may be a consequence of circadian abnormalities, often reported by veterans with GWI (Haley et al 2004;Peacock et al 1997), and as such, likely to be a consequence of GW agent exposure.…”
Section: Discussionsupporting
confidence: 89%
See 1 more Smart Citation
“…The figure above represents biofunction categories regulated in response to GW agent exposure at postexposure day 150, after a timepoint when cognitive impairment was observed et al 2008). Hence, our data support a psychomotor-related dysfunction rather than fine motor coordination problems, observations that are similar to that reported for another organophosphate AChE inhibitor pesticide, diisopropylfluorophosphate (Terry et al 2011). It is also possible that these GW-agent-induced neurobehavioral changes may be a consequence of circadian abnormalities, often reported by veterans with GWI (Haley et al 2004;Peacock et al 1997), and as such, likely to be a consequence of GW agent exposure.…”
Section: Discussionsupporting
confidence: 89%
“…This may also suggest that the delayed memory problems in exposed mice might be a consequence of impaired learning. Although the biochemical mechanism of this delayed cognitive impairment in response to PB and PER exposure is unknown, the mechanism may be similar to that proposed for exposure to other AChE inhibitors (Terry et al 2011). For instance, it is suggested that there might be a compensatory increase in AChE after prolonged exposure to AChE inhibitors, as a Representative images of GW agent-exposed (n = 5) and control mice (n = 5), taken with a 209objective providing a 2009 magnification.…”
Section: Discussionmentioning
confidence: 78%
“…The doses evaluated in this study were identified in previous studies (Terry et al, 2003(Terry et al, , 2011Middlemore-Risher et al, 2010) and operationally defined as doses not associated with acute signs of cholinergic toxicity (e.g., fasciculations, seizures, diarrhea, excessive urination, salivation, etc., see reviews, Rusyniak and Nanagas, 2004;Sungurtekin et al, 2006).…”
Section: Chlorpyrifosmentioning
confidence: 99%
“…These animal tasks include delayed matching (working memory), water maze (spatial learning and memory) novel object recognition (recognition memory), and the performance of the five-choice serial reaction time task (sustained attention) (Bushnell et al, 1991;Terry et al, 2003Terry et al, , 2007Terry et al, , 2011Middlemore-Risher et al, 2010;Yan et al, 2012;Terry et al, 2014).…”
mentioning
confidence: 99%
“…OPs that inhibit acetylcholinesterase (AChE) (Pope et al, 2005) or the neuropathy target esterase (Damodaran et al, 2011) pose a threat to human life and health. Chronic exposure to low quantities of these compounds produces pathologies that appear to be less dependent on AChE inhibition than acute poisoning (Ray and Richards, 2001, Terry et al, 2011, Terry, 2012). In the case of acute OP poisoning, most, but not all, neurological damage caused by these compounds can be accounted for by inhibition of AChE, accumulation of acetylcholine, and the ensuing cholinergic crisis.…”
Section: Introductionmentioning
confidence: 99%