Acetylcholine release from frontal cortex in the waking rat measured by microdialysis without acetylcholinesterase inhibitors: effects of diisopropylfluorophosphate.
Acetylcholine (ACh) release was measured in frontal cortex of awake quietly resting rats by microdialysis without using cholinesterase blockers in the perfusate. Resting release was 16.61 +/- 2.05 fmol/h (+/- S.E.M., n = 18). Injection of sublethal doses of the acetylcholinesterase blocker, diisopropylfluorophosphate produced dose-dependent increases in ACh release, reaching 79.9 fmol/h with a dose of 0.7-times the LD50. Although this irreversible inactivation of acetylcholinesterase increased ACh recovery to more than 700% of control values, levels of ACh in the perfusate never reached those seen in physostigmine-treated animals. The relationship between the amount of acetylcholinesterase inactivation and the quantity of ACh in the perfusate suggests that the extracellular ACh concentrations are controlled by simple enzyme kinetics. Within 2 h after enzyme inactivation, extracellular choline levels fell significantly, suggesting that ACh degradation by acetylcholinesterase plays an important role in regulating the amount of choline in the extracellular space.
Testylier
G
G
Centre de Recherches du Service de Santé des Armées, Grenoble, La Tronche, France.
Dykes
R W
RW
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D005625:Frontal Lobe / Q000187:drug effects* / Q000378:metabolism; D007531:Isoflurophate / Q000494:pharmacology*; D008297:Male; D017551:Microdialysis; D051381:Rats; D017207:Rats, Sprague-Dawley
D007531:Isoflurophate; D000109:Acetylcholine