Methylphenidate (Ritalin), the first-line drug for treating ADHD, works by increasing dopamine, however the animal-models for ADHD are hyperdopaminergic rats/mice.
How can we explain this?
Hi, Aussan. This is actually a current approach I am doing. I think it is because an excess of dopamine (hyperdopaminergic), both in terms of biosynthesis and degradation, can lead to oxidative stress that can destroy dopaminergic (DA) neurons. This dopamine-induced toxicity would lead to less neurons that make dopamine, and eventually to less dopamine.
This is a way to specifically destroy DA neurons, say by over-expressing the enzymes that catalyze dopamine synthesis (say tyrosine hydroxylase). Now, we can either find a drug that replaces dopamine once the DA neurons are already degenerating (L-DOPA, etc), or we can find drugs that can salvage these neurons from dopamine-induced neurotoxicity.
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