Maria Munoz

UC Davis

“Effects of acute organophosphate intoxication on neurodegeneration and an immunohistochemical biomarker of neuronal activity in the juvenile rat brain”

Acute intoxication with cholinesterase-inhibiting organophosphates (OP) triggers a cholinergic crisis that can progress to status epilepticus (SE). Many labs have reported that adult animals acutely exposed to OPs exhibit persistent neuroinflammation and neurodegeneration up to 6 months after exposure; however, few studies have characterized chronic OP-associated neuropathology in juveniles. Here, our goal is to quantify neuropathology and the development of acquired epilepsy in juvenile rats 3 months after acute intoxication with the OP pesticide, diisopropylfluorophosphate (DFP). We quantified active neurodegeneration using FJC-labeling and neuronal excitability via c-FOS immunoreactivity in the DG and piriform cortex of juvenile rats at this chronic time point. Our studies confirm that juveniles experience SE and developed spontaneous recurrent seizures (SRS) following acute OP intoxication. Further, we found no significant differences in our measures of active neurodegeneration or neuronal excitability at 3 months post-exposure. These observations suggest that neuropathology may be resolving and these animals may not be experiencing SRS at this timepoint. Future experiments will assess neuroinflammation, which is another neuropathological hallmark observed in adult animals exposed to OP pesticides.

ABSTRACT

Individuals acutely intoxicated with cholinesterase-inhibiting organophosphates (OP) exhibit persistent neuroinflammation and neurodegeneration and develop chronic neurological consequences including acquired epilepsy and cognitive impairment. Historically, study of acute OP intoxication has focused on adults, and little is known about how the developing brain may respond to such an exposure. The goal of this research is to address this gap by characterizing a juvenile rat model of acute OP intoxication.
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