Feeding behavior in dopamine-deficient mice
نویسندگان
چکیده
منابع مشابه
Feeding behavior in dopamine-deficient mice.
Mice that cannot make dopamine (DA), a condition caused by the selective inactivation of tyrosine hydroxylase in dopaminergic neurons, are born normal but gradually become hypoactive and hypophagic, and die at 3 weeks of age. We characterized the feeding and locomotor responses of these DA-deficient (DA-/-) mice to 3, 4-dihyroxy-L-phenylalanine (L-DOPA) to investigate the relationship between b...
متن کاملDopamine Production in the Caudate Putamen Restores Feeding in Dopamine-Deficient Mice
Dopamine-deficient (DD) mice cannot synthesize dopamine (DA) in dopaminergic neurons due to selective inactivation of the tyrosine hydroxylase gene in those neurons. These mice become hypoactive and hypophagic and die of starvation by 4 weeks of age. We used gene therapy to ascertain where DA replacement in the brain restores feeding and other behaviors in DD mice. Restoration of DA production ...
متن کاملInteraction of dopamine and adenosine receptor function in behavior: studies with dopamine-deficient mice.
The interactive effects of dopamine and adenosine on various behaviors in mammals have been studied extensively. The observation that dopamine and adenosine receptors are expressed together in neurons of the striatum has been a major impetus for studying these neurotransmitters because the striatum has been implicated in regulating motor and reward-related behaviors. This article reviews recent...
متن کاملViral Gene Delivery Selectively Restores Feeding and Prevents Lethality of Dopamine-Deficient Mice
Dopamine-deficient mice (DA-/- ), lacking tyrosine hydroxylase (TH) in dopaminergic neurons, become hypoactive and aphagic and die by 4 weeks of age. They are rescued by daily treatment with L-3,4-dihydroxyphenylalanine (L-DOPA); each dose restores dopamine (DA) and feeding for less than 24 hr. Recombinant adeno-associated viruses expressing human TH or GTP cyclohydrolase 1 (GTPCH1) were inject...
متن کاملDopamine-deficient mice are hypersensitive to dopamine receptor agonists.
Dopamine-deficient (DA-/-) mice were created by targeted inactivation of the tyrosine hydroxylase gene in dopaminergic neurons. The locomotor activity response of these mutants to dopamine D1 or D2 receptor agonists and l-3,4-dihydroxyphenylalanine (l-DOPA) was 3- to 13-fold greater than the response elicited from wild-type mice. The enhanced sensitivity of DA-/- mice to agonists was independen...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Proceedings of the National Academy of Sciences
سال: 1999
ISSN: 0027-8424,1091-6490
DOI: 10.1073/pnas.96.21.12138