Neurology Central

#NCintroduces… Going through the motions: how modern techniques have changed the face of Parkinson’s research

For most of us, the ability to make smooth, coordinated movements is as easy as breathing in and out. We do it automatically, without thinking. But for the time being, let’s do the opposite of that – let’s break down the process.

When we make a movement, first we have to do a survey. We have to absorb the complexities of our environment, and we have to align our intentions with our perceptions. We have to select the appropriate actions to carry out what we want to achieve. Not only that, we have to engage the right muscle groups, make the correct movements, and then reassess. To do this, our brain is carrying out a series of complex computations, and all of that processing requires power. And that’s why we owe a lot to James Parkinson. Because he made us think about what happens when the circuitry breaks down.

Paralysis and tremor

Neurodegenerative disorders like Parkinson’s disease (PD) have given us a valuable insight into the way the brain is wired. PD, among other things, causes acute neuronal death in a major circuit associated with movement, leaving patients with muscle rigidity, inability to initiate movements and a resting tremor. Although it’s not one of the most emotive symptoms of PD, a large amount of research has focused on the brain’s capacity to initiate and coordinate movements.

At the center of this process is a circuit of interconnected neurons located deep within the mammalian brain, collectively known as the basal ganglia. These ganglia are arranged into a straightforward network. Diagrammatically, this network is made up of multiple loops, or circuits, which take in information from the cerebral cortex, process the signal, and feed forward to areas associated with motor output. In other words, it acts as an interface between your perception and how you respond to what you perceive. The activity of this network is modulated by a tiny, darkly-pigmented region, known as the substantia nigra pars compacta [1]. For simplicity’s sake, let’s call it the SNc.

To view restricted content, please:

Liked this article? Read our previous instalments of “#NCintroduces…” here


  1. Albin RL, Young AB, Penney JB. The functional anatomy of basal ganglia disorders. Trends Neurosci. 12(10), 366–75 (1989).
  2. Gingrich JA, Caron MG. Recent advances in the molecular biology of dopamine receptors. Rev. Neurosci. 16, 299–321 (1993).
  3. Gerfen CR, Engber TM, Mahan LC et al. D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons. Science 250(4986), 1429–1432 (1990).
  4. Kravitz AV, Freeze BS, Parker PRL et al. Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia circuitry. Nature 466(7306), 622–626 (2010).
  5. Tecuapetla F, Jin X, Lima SQ, Costa RM. Complementary contributions of striatal projection pathways to action initiation and execution. Cell 166(3), 703–715 (2016).
  6. Fahn S. The medical treatment of Parkinson disease from James Parkinson to George Cotzias. Disord. 30(1), 4–18 (2015).
  7. Smith Y, Wichmann T, Factor SA, DeLong MR. Parkinson’s disease therapeutics: new developments and challenges since the introduction of levodopa. Neuropsychopharmacology 37(1), 213–246 (2012).
  8. Bergman H, Wichmann T, DeLong MR. Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science 249(4975), 1436–1438 (1990).
  9. de Hemptinne C, Swann NC, Ostrem JL et al. Therapeutic deep brain stimulation reduces cortical phase-amplitude coupling in Parkinson’s disease. Neurosci. 18(5), 779–786 (2015).
  10. Rosin B, Slovik M, Mitelman R et al. Closed-loop deep brain stimulation is superior in ameliorating parkinsonism. Neuron 72(2), 370–384 (2011).

Leave A Comment