Release of acetylcholine from tissue slices of the rat nucleus basalis magnocellularis.
We investigated the release of acetylcholine (ACh) from tissue slices obtained from the nucleus basalis magnocellularis (nbM) of the rat brain. Potassium (35 mM) depolarization produced a 10- to 12-fold increase in the release of endogenous ACh above spontaneous release. Potassium-evoked ACh release was Ca2+ dependent. Injection of the excitotoxin quinolinic acid into the nbM produced a 72.8 +/- 13.0% decrease in spontaneous ACh release and a 60.4 +/- 8.2% decrease in potassium-evoked release. A fourfold increase in ACh release was observed following perfusion of the tissue with 1 mM 3,4-diaminopyridine (3,4-DAP) whereas 10 mM 3,4-DAP caused a sevenfold increase. The increase in ACh release caused by 3,4-DAP was inhibited by tetrodotoxin. Tissue slices accumulated [3H]choline by high-affinity choline uptake and this could be inhibited by hemicholinium-3. These results indicate that ACh can be released from tissue slices of the nbM by a calcium-dependent process and that a part of this release appears to be from the cholinergic neurons of the nbM.
Metcalf
R H
RH
Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.
Boegman
R J
RJ
D015761:4-Aminopyridine / Q000031:analogs & derivatives*; D000109:Acetylcholine / Q000378:metabolism*; D000077770:Amifampridine; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D011188:Potassium / Q000494:pharmacology; D017378:Quinolinic Acid; D011805:Quinolinic Acids / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013116:Spinal Cord / Q000201:enzymology / Q000378:metabolism*
D000631:Aminopyridines; D011805:Quinolinic Acids; D015761:4-Aminopyridine; D002795:Choline O-Acetyltransferase; D017378:Quinolinic Acid; D000109:Acetylcholine; D000077770:Amifampridine; D011188:Potassium; D002118:Calcium