Systemic inflammation enhances stimulant-induced striatal dopamine elevation [2017]
This is a human study with 8 participants to test the effects of inflammation on the dopamine increase produced by Methylphenidate (MP = Ritalin/Concerta), a dopamine reuptake inhibitor. Inflammation was induced in the participants by the injection of Lipopolysaccharide (LPS), a bacteria-derived toxin.
On two separate days, the 8 participants received either MP alone, or LPS+MP, later having a brain scan (fMRI) to test for dopamine levels in the brain. It was found that LPS, the pro-inflammatory compound, significantly increased the dopamine elevation by MP. When LPS was given alone, no increase in dopamine levels was detected.
Why does inflammation potentiate the dopaminergic effects of Methylphenidate (MP)?
A possible mechanism could be through Arachidonic Acid, an Omega 6 polyunsaturated fat, which is a precursor to certain inflammatory signalling molecules. Arachidonic Acid metabolizes into γ-ketoaldehyde, a chemical that blocks the Dopamine Transporter (DAT) - in a similar manner to MP's mechanism of action. Therefore, inflammation may indirectly result in decreased dopamine reuptake, leading to higher levels staying in the synapse.
Systemic inflammation enhances stimulant-induced striatal dopamine elevation
Changes in the mesolimbic dopamine (DA) system are implicated in a range of neuropsychiatric conditions including addiction, depression and schizophrenia. Dysfunction of the neuroimmune system is often comorbid with such conditions and affects similar ...
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