Dysregulation of striatal dopamine signaling by amphetamine inhibits feeding by hungry mice.

Abstract:

:Amphetamine (AMPH) releases monoamines, transiently stimulates locomotion, and inhibits feeding. Using a genetic approach, we show that mice lacking dopamine (DA-deficient, or DD, mice) are resistant to the hypophagic effects of a moderate dose of AMPH (2 microg/g) but manifest normal AMPH-induced hypophagia after restoration of DA signaling in the caudate putamen by viral gene therapy. By contrast, AMPH-induced hypophagia in response to the same dose of AMPH is not blunted in mice lacking the ability to make norepinephrine and epinephrine (Dbh(-/-)), dopamine D(2) receptors (D2r(-/-)), dopamine D(1) receptors (D1r(-/-)), serotonin 2C receptors (Htr2c(-/Y)), neuropeptide Y (Npy(-/-)), and in mice with compromised melanocortin signaling (A(y)). We suggest that, at this moderate dose of AMPH, dysregulation of striatal DA is the primary cause of AMPH-induced hypophagia and that regulated striatal dopaminergic signaling may be necessary for normal feeding behaviors.

journal_name

Neuron

journal_title

Neuron

authors

Cannon CM,Abdallah L,Tecott LH,During MJ,Palmiter RD

doi

10.1016/j.neuron.2004.10.009

subject

Has Abstract

pub_date

2004-10-28 00:00:00

pages

509-20

issue

3

eissn

0896-6273

issn

1097-4199

pii

S0896627304006774

journal_volume

44

pub_type

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