title: Increased calcium influx through acetylcholine receptors in dunce neurons.
abstract: Calcium homeostasis was studied in dunce, a Drosophila mutant that is defective in learning and memory. Fura 2-AM fluorescence photometry was used to measure the intracellular calcium concentration in wild type and dunce cleavage-arrested neurons under resting conditions and in response to neurotransmitters. After acetylcholine application, the peak [Ca2+]i was greater in dunce (693 +/- 125 nM) than in wild type neurons (464 +/- 154 nM), but half decay time was shorter in dunce (66 +/- 15 s) than in wild type neurons (104 +/- 40 s). In contrast, the application of glutamate, NMDA, dopamine, and serotonin had no effect on [Ca2+]i. These results indicate that calcium influx through acetylcholine receptors is increased in dunce, compared to wild type neurons. The results also suggest that calcium extrusion to the outside and/or calcium buffering are enhanced in dunce, compared to wild type neurons. This disturbance in the homeostasis of cytosolic calcium concentration in dunce may be implicated in defective associative learning in Drosophila, and may play a role in acute and chronic neurodegenerative disorders in the mammalian brain.
authors.affiliation: Department of Physiology, Faculty of Medicine, Kuwait University, Safat, Kuwait. Waleed@hsc.Kuniv.edu.Kw
authors.forename: Waleed B
authors.initials: WB
authors.lastname: Alshuaib
authors.forename: Mohamed
authors.initials: M
authors.lastname: Hasan
authors.forename: Susan P
authors.initials: SP
authors.lastname: Cherian
authors.forename: Mohamed A
authors.initials: MA
authors.lastname: Fahim
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D019256:Cadmium Chloride / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D003472:Curare / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology; D004330:Drosophila; D004347:Drug Interactions; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D016257:Fura-2 / Q000031:analogs & derivatives* / Q000378:metabolism; D018698:Glutamic Acid / Q000494:pharmacology; D009154:Mutation; D016202:N-Methylaspartate / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000378:metabolism*; D012701:Serotonin / Q000494:pharmacology; D013997:Time Factors; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D018690:Excitatory Amino Acid Agonists; D018733:Nicotinic Antagonists; D011950:Receptors, Cholinergic; D014665:Vasodilator Agents; C049925:fura-2-am; D012701:Serotonin; D018698:Glutamic Acid; D016202:N-Methylaspartate; D011189:Potassium Chloride; D003472:Curare; D019256:Cadmium Chloride; D000109:Acetylcholine; D002118:Calcium; D016257:Fura-2; D004298:Dopamine