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• W2023608415 endingPage "676" @default.
• W2023608415 startingPage "669" @default.
• W2023608415 abstract "The consequences of a reduction in the presynaptic protein, SNAP-25, were investigated to determine the neurochemical basis of the marked hyperlocomotor activity in coloboma (Cm/+) mice. SNAP-25 is part of the minimal presynaptic machinery necessary for exocytotic neurotransmitter release. Reserpine treatment was used to deplete vesicular stores of catecholamines. Coloboma mice were more sensitive to the effects of reserpine than control mice. However, presynaptic regulation of dopamine (DA) release, as assessed by low-dose apomorphine challenge, was intact. There were region-specific reductions in in vivo tyrosine hydroxylation and the DA metabolites homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum and nucleus accumbens of Cm/+ mice. While hyperactivity is often associated with changes in DA concentration, norepinephrine (NE) concentration was significantly increased in the striatum and nucleus accumbens of the hyperactive mutant. The increase in NE may regulate the hyperactivity in these mice, as suggested by current hypotheses of the mechanisms underlying attention-deficit hyperactivity disorder (ADHD) and Tourette's syndrome." @default.
• W2023608415 created "2016-06-24" @default.
• W2023608415 creator A5027829280 @default.
• W2023608415 creator A5059346486 @default.
• W2023608415 creator A5069832636 @default.
• W2023608415 date "2001-04-01" @default.
• W2023608415 modified "2023-10-13" @default.
• W2023608415 title "Abnormal presynaptic catecholamine regulation in a hyperactive SNAP-25-deficient mouse mutant" @default.
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• W2023608415 doi "https://doi.org/10.1016/s0091-3057(01)00481-6" @default.
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