Smiling ear to ear after receiving my NIH/NINDS K99 NOA today!
I look forward to future discoveries about cerebellar signals in dystonia, and I am so grateful for my village of supporters, mentors, and advisors who helped me along the long way here.
For this #FluorescentFriday, I want to share the most festive Purkinje cell of them all: Joy Zhouβs Purkinje cells with Santa hats.
Original image: https://elifesciences.org/articles/55569
#introduction
Hi, #neuroscience community.
I'm an assistant professor at the University of Washington who works at the intersection of engineering and neuroscience. I am excited about using engineering tools like closed-loop motor brain-computer interfaces to probe basic neuroscience questions, and using insights about the brain to improve functionality of BCI applications.
My lab's current work
1) explores using BCIs as tools to begin unravelling how learning computations happen in neural populations
2) studies the interactions between users who learn alongside algorithms ("co-adaptation").
3) investigates how brains build "internal models", with a current interest in how to quantify internal model formation behaviorally.
We use both animal models (non-human primates) and human subject experiments. We also collaborate closely with computational and theoretical neuroscientists.
Trying out this thing as an alternative to Twitter. I'm already intimidated by the space to write and minimal pressure to edit.
Did you know that the beta-blocker propranolol is so effective in reducing tremors that it is banned in the Olympics?
But how does it work?
New paper with wonderful graduate student Joy Zhou now published in Cells:
Tremor is the most common movement disorder. Several drugs reduce tremor severity, but no cures are available. Propranolol, a Ξ²-adrenergic receptor blocker, is the leading treatment for tremor. However, the in vivo circuit mechanisms by which propranolol decreases tremor remain unclear. Here, we test whether propranolol modulates activity in the cerebellum, a key node in the tremor network. We investigated the effects of propranolol in healthy control mice and Car8wdl/wdl mice, which exhibit pathophysiological tremor and ataxia due to cerebellar dysfunction. Propranolol reduced physiological tremor in control mice and reduced pathophysiological tremor in Car8wdl/wdl mice to control levels. Open field and footprinting assays showed that propranolol did not correct ataxia in Car8wdl/wdl mice. In vivo recordings in awake mice revealed that propranolol modulates the spiking activity of control and Car8wdl/wdl Purkinje cells. Recordings in cerebellar nuclei neurons, the targets of Purkinje cells, also revealed altered activity in propranolol-treated control and Car8wdl/wdl mice. Next, we tested whether propranolol reduces tremor through Ξ²1 and Ξ²2 adrenergic receptors. Propranolol did not change tremor amplitude or cerebellar nuclei activity in Ξ²1 and Ξ²2 null mice or Car8wdl/wdl mice lacking Ξ²1 and Ξ²2 receptor function. These data show that propranolol can modulate cerebellar circuit activity through Ξ²-adrenergic receptors and may contribute to tremor therapeutics.
David J Solecki
CLaE
Amy Orsborn