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Effects of NADH on dopamine release in rat striatum
Author(s) -
Pearl Sandra M.,
Antion Marcia D.,
Stanwood Gregg D.,
Jaumotte Juliann D.,
Kapatos Gregory,
Zigmond Michael J.
Publication year - 2000
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(200005)36:2<95::aid-syn2>3.0.co;2-u
Subject(s) - dopamine , striatum , dopaminergic , tetrahydrobiopterin , chemistry , nad+ kinase , nicotinamide adenine dinucleotide , biochemistry , tyrosine hydroxylase , in vivo , extracellular , basal ganglia , cofactor , medicine , endocrinology , enzyme , biology , central nervous system , microbiology and biotechnology
Nicotinamide adenine dinucleotide (NADH) may be utilized for the synthesis and regeneration of tetrahydrobiopterin (BH 4 ), which in turn is an essential cofactor for tyrosine hydroxylase, the rate‐limiting enzyme in the synthesis of dopamine (DA). NADH has been reported to relieve some of the symptoms of Parkinson's disease, presumably by altering dopaminergic function. The present study examines the efficacy of NADH in influencing DA activity in the rat striatum. In striatal slices, NADH (350 μM) significantly increased basal DA and DOPAC efflux and caused a 2‐fold increase in the DA overflow evoked by high KCl (25 mM). Tissue levels of BH 4 , basal BH 4 efflux, and KCl‐evoked BH 4 overflow were unaffected by NADH, as was [ 3 H]DA uptake into striatal synaptosomes. In contrast to the effects of NADH on DA function in vitro, no effects were observed when NADH was administered systemically. NADH (10 or 100 mg/kg, s.c.) did not influence the tissue content of DA, 5‐HT, or their metabolites in the midbrain or striatum, nor did it alter DA extracellular concentrations. These results indicate that NADH can increase DA release from striatal slices, although we are as yet unable to detect this effect in vivo. Synapse 36:95–101, 2000. © 2000 Wiley‐Liss, Inc.