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Cytidine (5′) Diphosphocholine Modulates Dopamine K + ‐evoked Release in Striatum Measured by Microdialysis
Author(s) -
AGUT J.,
ORTIZ J. A.,
WURTMAN R. J.
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06944.x
Subject(s) - homovanillic acid , microdialysis , striatum , choline , dopaminergic , chemistry , dopamine , endocrinology , medicine , cytidine , 3,4 dihydroxyphenylacetic acid , depolarization , neurotransmitter , biochemistry , central nervous system , serotonin , enzyme , receptor
A bstract : Experiments were performed to determine whether exogenous cytidine (5′) diphosphocholine (CDP‐choline) could modify the release of dopamine (DA) in the striatum. Rats were divided into two groups, receiving either a standard diet (UAR 004) or the same diet supplemented with CDP‐choline (250 mg/kg day) for 28 days. On the last day the dialysis probes were inserted in the striatum, and DA, homovanillic acid (HVA), and 3,4‐dihydroxyphenylacetic acid (DOPAC) efflux were measured in the dialysis stream basally and during K + depolarization (80 mM K + ). Basal DA, HVA, and DOPAC did not show any difference between treated and untreated groups. Depolarization with K + increased DA levels by up to 3,000% in the control group and by up to 4,770% in the CDP‐choline‐treated group ( p <0.05 ), and reduced extracellular HVA and DOPAC concentration by up to 45 and 35%, respectively, both in the untreated and CDP‐choline‐treated groups. These results show that long‐term treatment with CDP‐choline increases the K + induced release of DA and suggest, in accordance with previous research, that by providing exogenous choline and cytidine, CDP‐choline modulates dopaminergic transmission.