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Witten et al. in 2011 used optogenetic tools to clarify the relationship between dopamine (DA) neuron firing and positive reinforcement in genetically modified rats. They observed that optical stimulation of DA neurons in the ventral tegmental area of these rats led to vigorous intracranial self-stimulation.
Tsai et al. in 2009 demonstrated that phasic dopaminergic activity is sufficient to mediate mammalian behavioral conditioning, by using an optogenetic approach. They emphasize that integrating optogenetics with other approaches (e.g., electrophysiological, behavioral and electrochemical methods) will reveal relevant interactions of DA neurons with other neuromodulatory circuits (e.g., monoaminergic and opioid circuits).
The use of optogenetics further revealed opposite roles of D1+ and D2+ neurons (in the nucleus accumbens) in processing cocaine reward (Lobo et al., 2010). In this study the firing rate of D1+ and D2+ neurons was selectively controlled to investigate the resulting effects on cocaine reward. It was found that activation of D2+ neurons suppresses cocaine reward, while activation of D1+ neurons shows the opposite pattern.
Another example of optogenetic neuromodulation shows how symptoms of Parkinson's disease can be either aggravated or improved (Kravitz et al., 2010). Kravitz et al. (2010) modulated the firing activity of single neurons, manipulating either direct or indirect pathways in the basal ganglia.
Another study (Bass et al., 2010) showed how neuronal dopamine release patterns could be evoked in the dorsal part of the striatum in living rats. Results like these show that the use of optogenetics can lead to a better understanding of cause-effect relationships, for example in dopamine-based disorders.
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