Cortical Inputs and GABA Interneurons Imbalance Projection Neurons in the Striatum of Parkinsonian Rats
Nicolas Mallet, Berangere Ballion, Catherine Le Moine, and Francois Gonon
The Journal of Neuroscience (2006)
DOI:10.1523/JNEUROSCI.4439-05.2006
The gap/question: how the activities of the striatonigral (D1-MSNs direct pathway) and striatopallidal pathways (D2-MSNs indirect pathway) were modulated in Parkinsonian animal models?
How the authors proposed the question: classic models proposed that (The functional anatomy of basal ganglia disorders,1989) the death of dopamine neurons in Parkinson’s patients led to the imbalanced activity of the direct- and indirect- pathways. Limited by the experimental tools to specifically target these different pathways, no studies had directly test this hypothesis. Thanks to a recent anatomical study (Evidence for differential cortical input to direct pathway versus indirect pathway striatal projection neurons in rats. J Neurosci, 2004), it renders the experiments doable.
Three points are crucial to this study: be familiar with the old and classic hypotheses; be sensitive to the cutting-edge progress in the field; and pay attention to the connections between the above two.
Brief summary: with the dopamine-depletion Parkinson’s rat models, Mallet and colleagues found that both the activities of the D2-MSNs and their cortical inputs were enhanced. And the spiking window of D2-MSNs was significantly increased while the D1-MSNs’ spiking window was narrowed after dopamine depletion through pavalbumin fast-spiking interneurons.
This is a good case showing a successful application of new experimental approach to the old scientific questions. The lesson is investigators can not only read the most recent or the old papers. A better strategy may be keep jumping around the old to the most recent papers back and forth. Let’s try it.
