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-hydroxytryptamine 1F, neurokinin 1 and κ-opioid receptors located on cholinergic terminals. In addition, 5-hydroxytryptamine 2 and δ-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.