Modulation of acetylcholine release in human cortical slices: possible implications for Alzheimer's disease.
Superfused slices of human neocortex, prepared from surgically removed tissue (to gain access to subcortical tumors) and prelabelled with [3H]choline, were stimulated electrically to evoke action potential-induced, exocytotic [3H]acetylcholine release. For comparison, rat cortex slices were also used. [3H]ACh release decreased with the age of the patients and was modulated by muscarinic autoreceptors and by 5-hydroxytryptamine1F, neurokinin1, and kappa-opioid receptors located on cholinergic terminals. In addition, 5-hydroxytryptamine2 and delta-opioid receptors located on interneurons were also involved in the modulation of [3H]ACh release. The present findings might help to explain pathological conditions in Alzheimer's disease.
Feuerstein
T J
TJ
Sektion Klinische Neuropharmakologie der Neurologischen Universitätsklinik, Freiburg, Germany.
Seeger
W
W
D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials / Q000502:physiology; D000375:Aging / Q000378:metabolism; D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology; D000818:Animals; D004558:Electric Stimulation; D006801:Humans; D018727:Muscarinic Antagonists / Q000494:pharmacology; D019579:Neocortex / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D012702:Serotonin Antagonists / Q000494:pharmacology
D018727:Muscarinic Antagonists; D012702:Serotonin Antagonists; D000109:Acetylcholine