title: Role of calcium on the modulation of spontaneous acetylcholine efflux by the D2 dopamine receptor subtype in rat striatal synaptosomes.
abstract: The role of calcium in the modulation of spontaneous [3H]acetylcholine ([3H]ACh) efflux through presynaptic D2 dopamine hetero-receptors was investigated in rat striatal synaptosomes. The kinetic studies of [3H]ACh efflux in the presence or absence of Ca2+ were carried out in nonstimulating conditions. When Ca2+ was omitted from the superfusion medium, a notable and significant (P<0.001) decrease of tritium efflux (39%) was obtained. While [3H]ACh efflux was insensitive to tetrodotoxin (TTX) 1 microM, cadmium (10 microM), a nonselective antagonist of calcium channels, significantly reduced the tritium efflux by 24% (P<0.001), while the L-type calcium antagonist, nifedipine, (30 microM) inhibited the tritium efflux by only 10% (P<0.02). 2-(4-Fenylpiperidine)cyclohexanol (vesamicol), an inhibitor of the vesicular [3H]ACh carrier, significantly depressed the spontaneous tritium efflux in the presence of Ca2+ (60%; P<0.001) and in a low-calcium medium (20%; P<0.001). Although 1 microM of 7-hydroxy-N,N-di-n-propyl-2-aminotetraline (7-OH-DPAT) inhibited spontaneous [3H]ACh efflux in the presence of calcium, this dopaminergic agonist did not modify the neurotransmitter release in either the low-Ca2+ medium or in the presence of vesamicol. These results suggest that the spontaneous [3H]ACh efflux is a process involving a Ca2+-dependent component (39%), sensitive to calcium channel-blockers and vesamicol, in rat striatal synaptosomes. In addition, activation of the D2 dopamine hetero-receptor only modulates the calcium-dependent component of spontaneous [3H]ACh efflux.
authors.affiliation: Departament de Farmacologia i Terapèutica, Facultat de Medicina, Universitat Autònoma de Barcelona, Spain.
authors.forename: A G
authors.initials: AG
authors.lastname: Sanz
authors.forename: A
authors.initials: A
authors.lastname: Badia
authors.forename: M V
authors.initials: MV
authors.lastname: Clos
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D003342:Corpus Striatum / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D008297:Male; D010830:Physostigmine / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017448:Receptors, Dopamine D2 / Q000502:physiology*; D013574:Synaptosomes / Q000378:metabolism*; D013764:Tetrahydronaphthalenes / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D014316:Tritium / Q000493:pharmacokinetics
chemical_list: D002121:Calcium Channel Blockers; D002800:Cholinesterase Inhibitors; D018491:Dopamine Agonists; D010880:Piperidines; D017448:Receptors, Dopamine D2; D013764:Tetrahydronaphthalenes; D014316:Tritium; C006189:vesamicol; D013779:Tetrodotoxin; D010830:Physostigmine; D000109:Acetylcholine; C031349:7-hydroxy-2-N,N-dipropylaminotetralin; D002118:Calcium