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Project Leaders

The SBC supports four interrelated research projects.

Dr. Jared Bushmanhead shot of Jared Bushman

Assistant Professor of Pharmaceutical Science, School of Pharmacy | (307) 766-4189  | Health Sciences 480


Delineating and Modulating the Gliotic Changes Occurring After Spinal Cord Injury

Project Summary:

Injury to the central nervous system (CNS) by disease or trauma causes a cascade of cellular responses that must occur to restore the delicate microenvironment necessary for function of the CNS. However, the changes caused to CNS tissue by these cellular responses may create an environment that is not permissive to functional regeneration. For patients, this results in permanent loss or aberration of function. In the case of spinal cord injury (SCI), patients often develop allodynia and other pain syndromes in addition to motor impairment. We are seeking to gain a better understanding of the cellular processes that occur following SCI that cause impairment and to develop therapies of small molecules and optogenetically responsive cells to promote functional repair of neural circuits.

We are specifically interested in the changes that occur in activated astrocytes and the alterations in the expression of glycans following SCI that occur during gliosis. We will develop a model of reactive astrogliosis using precursor derived astrocytes that can be used to delineate the signaling mechanisms responsible for astrogliosis. We hypothesize that extensive changes in glycosylation occur during astrogliosis that mediate the injury response after SCI and will test this by characterizing large scale changes in glycosylation after SCI. Glycomics is an advancing field and this would be the first study documenting the changes in glycosylation in the CNS after an injury.

Our second and third aims are more translational in nature and will develop therapeutics that both mitigate inhibitory signals after SCI and provide positive cues to stimulate regeneration. Chondroitin sulfate (ChS) is a glycan known to inhibit regeneration and we hypothesize that compounds can be identified that bind to and mask ChS from inhibitory receptors. To provide positive stimuli, we will develop and test an optogenetic system that we hypothesize can be used to control the behavior of cells (proliferation, gene expression etc) post-implantation by non-invasive means.

Dr. William "Trey" Todd 

Assistant Professor, Department of Zoology and Physiology  william-todd.jpg  |  (307) 314-4207  | Biological Sciences 406  





Project Title: Circadian behavior circuits, Alzheimer’s pathology, chemogenetic output and input

Project Summary:

Aim 1. To examine the relationship between circadian dysfunction of aggression propensity and LMA rhythms to immunohistochemical markers of AD-related neuropathology in the central SCN clock, the SPZ, and their output and input pathways. In tissue from TAPP mice and double WT controls, I will use immunohistochemistry to assess AD neuropathology (a-beta and tau) in the SCN, the SPZ and its major output targets, the VMH and DMH, as well as in regions known to project to the SCN and SPZ. I will also examine cell loss in these brain areas and in RGCs that project to and entrain the SCN. I will use brain tissue and retinas from male mice in which I previously examined aggression and LMA rhythms, and I will add an equal number of additional female mice that will also undergo LMA recordings and aggression tests.

Aim 2. To determine whether chemogenetic activation of the SPZ output pathway, and the RHT input pathway, reduces increased aggression and circadian sleep-wake dysfunction associated with ADrelated neuropathology. Using neural injections of a nonconditional, excitatory chemogenetic viral vector into male and female TAPP mice, I will activate SPZ neurons and RGCs via peripheral injection of the chemogenetic ligand, or its vehicle, at a time of day at which I have shown these cells to normally be active. I will then measure the effects of this phase-dependent neuronal activation on aggression using a resident intruder paradigm, and separately on sleep-wake rhythms using encephalographic (EEG) and electromyographic (EMG) recordings.

Dr. Yun Liyun-li-1.jpeg

Assistant Professor, Department of Zoology and Physiology   | (307) 766-4207 |   Biological Sciences Building 414   |


In Vivo Calcium Imaging at the Frontal Cortex in Mouse Models of Brain Disorders

Project summary:

One of the core missions in neuroscience is to understand how neuronal activities carry information to guide behavior. A direct approach is to simultaneously record large-scale neural activity in vivo while animal freely performs behavioral tasks. Such measurement could establish detailed mechanisms by which activity of individual neurons or neural ensembles codes animal’s behavior. The development of miniature fluorescence microscope (miniScope) opens up new avenues for obtaining large-scale in vivo neural calcium imaging from freely behaving mice, to elucidate the function and dysfunction of neural circuitry in health and diseases. The long-term goal of the proposed work is to develop and to apply cutting-edge miniScope imaging technique to study neural circuit mechanisms of depression, autism, and dementia in the medial prefrontal cortex (mPFC).

We have two specific aims. Our first specific aim is to elucidate how dysfunctional mPFC neural circuits contribute to social behavior deficits in depression, autism, and dementia. Human patients of depression, autism, and dementia all display deficits in social behavior. To unravel the underlying circuit mechanisms leading to social behavior deficits in these brain disorders, miniScope imaging approach will be employed to examine mPFC neural circuitry in mouse models of depression, autism, and frontotemporal dementia.

Our second specific aim is to develop dual-color miniScopes to advance neural circuitry studies. A new version of miniScope with dual LED and a liquid lens will be developed. This new miniScope will enable not only dual-color calcium imaging from both principle neurons and inhibitory interneurons, but also optogenetic manipulation of interneurons and concurrent calcium imaging from principle neurons.


Dr. Karen Mrukmcnair-2019-8479.jpg

Assistant Professor, School of Pharmacy   |    Health and Sciences Center   |


Zebrafish Models of CNS Injury and Locomotor Recovery

Project Summary:

In the central nervous system (CNS), specialized cells work together to differentiate, wire, and later die to form a completely integrated system. Zebrafish have a remarkable ability to regenerative. Our lab is interested in understanding how the zebrafish recovers and regenerates after injury to the central nervous system (CNS). Zebrafish are ideal model to study nervous system development and regeneration because: (1) the zebrafish CNS shares many organizational, cellular and molecular pathways with mammals; (2) they are genetically tractable and amendable to several forward- and reverse-genetic methods; (3) their optical transparency makes allows real-time visualization of the central nervous system, and (4) they have a fixed locomotor repertoire permitting analysis of function and behavior.

My lab is focused on understanding the role bioelectricity plays in locomotor recovery and the genetic factors that govern this process. Bioelectric signals generated by membrane proteins, such as changes in membrane voltage, are required for embryonic patterning, wound healing, and tissue regeneration suggesting a mechanistic link between membrane potential and an individual cell’s behavior as well as cell-cell communication. In addition, recent studies show that an electric field can supersede genetic information or a chemical cue, highlighting the need to focus on ion flow and transmembrane gradients. To gain a systems-level understanding of the bioelectric network we utilize multi-electrode array electrophysiology and ion imaging. By recording the CNS network over time and monitoring swim behavior, we will understand how global changes in bioelectricity contribute to recovery. We aim to combine these studies with traditional cellular biology and genomics in order to identify new therapeutic intervention points.


Contact Us

Dr. Qian-Quan Sun, SBC Director, Professor

Department of Zoology and Physiology

Laramie, WY 82071

Phone: 307-766-5602



1000 E. University Ave. Laramie, WY 82071
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