James Conner

Laboratory for the Analysis of Brain Circuits Mediating Behavior

Our lab is interested in brain circuitry mediating skilled motor learning.  We want to know how motor circuitry is assembled, how it is activated during motor learning, how it contributes to specific aspects of behavior, and how it is modified by experience.  To address these questions, we use an array of viral and genetic tools to examine and manipulate brain circuitry with a high degree of spatial and temporal precision. A variety of targeted viral tracers allow us to trace projections of functionally-defined cell populations and then characterize both pre- and post-synaptic connections.  Targeted neuronal silencing (using DREADDs or PSAM systems), activation (channelrhodopsin-2), along with targeted neuronal ablation (using diphtheria toxin system) are used to dissect the functional contribution of distinct aspects of motor circuitry to the acquisition and performance of skilled motor behavior.  Finally, in vitro whole cell approaches are used to explore more subtle details regarding how brain circuitry becomes modified by experience and learning.
  1. Wang L, Conner JM, Rickert J, Tuszynski MH (2011) Structural plasticity within highly specific neuronal populations identifies a unique parcellation of motor learning in the adult brain. Proc Natl Acad Sci U S A 108:2545-2550.
  2. Biane JS, Scanziani M, Tuszynski MH, Conner JM. (2015) Motor cortex maturation is associated with reductions in recurrent connectivity among functional subpopulations and increases in intrinsic excitability. J Neurosci. 35(11):4719-28.
  3. Biane JS, Takashima, Y., Scanziani M, Conner, JM, Tuszynski MH (2015) Thalamocortical Projections Exhibit Plasticity Onto Behaviorally-Relevant Neurons During Adult Motor Learning. Neuron (in press).
  4. Wang, L., Conner, J.M., and M.H. Tuszynski (2015) Rehabilitation Drives Enhancement of Neuronal Structure in Functionally Relevant Neuronal Subsets: Cholinergic Dependence. PNAS (in press).
We are also interested in underlying mechanisms that enable experience-dependent plasticity.  Prior studies by our group have demonstrated the critical role of the basal forebrain cholinergic system for permitting experience dependent plasticity in the context of behavior.  Highly specific lesions of cholinergic forebrain systems abolish plasticity mediated by a learning experience.  Both brain map reorganization and structural modifications normally driven by experience are completely abolished following targeted removal of cortical cholinergic afferents and behavior is markedly compromised.  Future studies will examine the cellular and synaptic basis for cholinergic actions in mediating experience-dependent plasticity.
  1. Conner, J.M., A.C. Culberson. C. Packowski, A. Chiba and M.H. Tuszynski (2003) Lesions of the basal forebrain cholinergic system impair task acquisition and abolish cortical plasticity associated with motor skill learning. Neuron 38:819-829.
  2. Conner, J.M., A. Chiba and M.H. Tuszynski (2005) The basal forebrain cholinergic system is essential for cortical plasticity and functional recovery following brain injury.  Neuron 46: 173-179.
  3. Ramanathan, D.R, M.H. Tuszynski and J.M. Conner. (2009) The basal forebrain cholinergic system required specifically for behaviorally mediated cortical map plasticity. J. Neuroscience 29: 5992-6000. A complete bibliography of past work can be found here.

James Conner 
James Conner, PhD
Project Scientist