Watson Lab
Cortical circuits and Psychiatry
Brendon Watson M.D., Ph.D.
University of Michigan
Focus: Brain and cortical network dynamics
Basic function in normal brain and role in psychiatric disease
We use electrophysiology and behavioral methods to understand brain-behavior linkages in rodents. We aim to answer questions aimed both at fundamental neurobiological questions as well as the role of neural circuit electrophysiology in disease.
We use an approach informed by an understanding of neuronal microcircuit dynamics, macrocircuit connectivity and organism-level behavior to connect between the level of single neurons, networks of those neurons and animal behavior.
See further details in Research.
Lab life: Lunch after the Silverman Conference
Thanks for the photo, David :)
Recent work
Bueno et al use the social neuroscience model, the prairie vole to extend prior studies of how an autism-like model impacts adult social behavior. Deeplabcut was used to quantify male and female social behavior during co-housing separated by a divider. We found that especially males with early life sleep deprivation but also females show lasting deficits relative to control voles.
Yi*, Hartner* et al have developed systems for replacing the top of the rat skull that can be customized to allow flexible implantation designs. They have also generated inexpensive and efficient methods for lab-based production of arrays. These developments lead the way to inexpensive and flexible implantations in rats.
Tsimpanouli et al ask how neural circuits function differenetly during sleep in a model of SCA3-type spinocerebellar ataxia? Tia Tsimpanouli finds increased REM sleep duration and increased beta oscillatory power. This may mechanistically link SCA3 to other neurodegenerative diseases including Alzheimer's and Parkinson's diseases that show REM pathology.
Bueno et al discovered that REM sleep is structured into cycles between a "phasic REM"-like pole and a "tonic-REM" like pole, showing that the classical phasic/tonic dichotomy is actually a fluctuation at the infraslow timescale (minutes). These fluctuations affect a variety of physiologic features ranging from breathing, to eye movements to neural firing and neural assembly activity.
We propose that the neocortical populations have a constant "backbone" element to their sequence as well as a proportion of neurons with maleable timing. These stable and maleable aspects may have differential roles. The stable firing sequence may play a role in network homeostasis while the variable element may related to information "coding".
Why and how is the field of rodent ketamine research yielding such variable results. How can we interpret that variance?
Only stressed mice show antidepressant-like response to ketamine. Unestressed ones actually show an opposite response. See Paul Fitzgerald and Jessica Yen's paper here: Link
How neuronal activity changes during sleep and wake: An integrative and statistically-controlled re-analysis of data from neocortex and hippocampus
What we know about how antidepressants work at an electrophysiologic level
A minutes-timescale rhythm of the brain that dictates brain function and performance: What do we know about it already?
Might gamma oscillations be biomarkers for depression? What is the current state of the field in both patients and rodent models.
How field potential oscillations and neuronal firing rates are correlated time in the frontal cortex in rodent recordings.
Review article putting forward novel ideas about the role of learning rules in sculpting activity of cortical neuronal populations over wake-sleep cycles
Cortical neuronal firing rates are dynamically modulated over sleep wake cycles without novel learning tasks.