Diisopropylfluorophosphate and GABA synaptic function: effect on levels, enzymes, release and uptake in the rat striatum.
The present study revealed that diisopropylfluorophosphate increased the GABA and glutamate levels, decreased the uptake of GABA, decreased the spontaneous release of GABA and did not exhibit its effects on the metabolic enzymes of GABA, glutamic acid decarboxylase and GABA-transaminase. These results, together with our previous finding that the postsynaptic GABA receptor population is increased by DFP treatment, indicate that GABA transmission is affected by DFP. An overall enhancement of GABA function appears to be involved in DFP poisoning; it is suggested that this may be a compensatory mechanism to counteract the cholinergic hyperactivity.
D000612:4-Aminobutyrate Transaminase / Q000378:metabolism; D000818:Animals; D003342:Corpus Striatum / Q000378:metabolism*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism; D007531:Isoflurophate / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D017981:Receptors, Neurotransmitter / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005971:Glutamates; D017981:Receptors, Neurotransmitter; D007531:Isoflurophate; D005680:gamma-Aminobutyric Acid; D000612:4-Aminobutyrate Transaminase; D005968:Glutamate Decarboxylase