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- Title
Single cocaine exposure does not alter striatal pre-synaptic dopamine function in mice: an [<sup>18</sup>F]- FDOPA PET study.
- Authors
Bonsall, David R; Kokkinou, Michelle; Veronese, Mattia; Coello, Christopher; Wells, Lisa A.; Howes, Oliver D.
- Abstract
Cocaine is a recreational drug of abuse that binds to the dopamine transporter, preventing reuptake of dopamine into pre-synaptic terminals. The increased presence of synaptic dopamine results in stimulation of both pre- and post-synaptic dopamine receptors, considered an important mechanism by which cocaine elicits its reinforcing properties. However, the effects of acute cocaine administration on pre-synaptic dopamine function remain unclear. Non-invasive imaging techniques such as positron emission tomography have revealed impaired pre-synaptic dopamine function in chronic cocaine users. Similar impairments have been seen in animal studies, with microdialysis experiments indicating decreased basal dopamine release. Here we use micro positron emission tomography imaging techniques in mice to measure dopamine synthesis capacity and determine the effect of acute cocaine administration of pre-synaptic dopamine function. We show that a dose of 20 mg/kg cocaine is sufficient to elicit hyperlocomotor activity, peaking 15-20 min post treatment ( p < 0.001). However, dopamine synthesis capacity in the striatum was not significantly altered by acute cocaine treatment (
- Subjects
DOPAMINE; POSITRON emission tomography; BIOGENIC amines; DRUGS of abuse; MICRODIALYSIS
- Publication
Journal of Neurochemistry, 2017, Vol 143, Issue 5, p551
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/jnc.14223