Teresa Ann Murray, PhD

Director, Principal Investigator

Integrated Neuroscience and Imaging Lab

We identify mechanisms of and test therapies for brain injuries, neurological disorders, and neuro-cardiovascular diseases with emphases on changes in cellular morphology, network function, and inflammation over time in the same rodents. In doing so, we have developed novel tools for in vivo, longitudinal imaging, neurochemical recording, and behavioral analysis. Using our longitudinal approach, we normalize measurements to preinjury baseline data, which reduces experimental variability and the numbers of animals required for a study; it also permits unparalleled comparisons between treatment conditions, the elucidation of time windows for the sequelae of pathological processes, and the timing of therapeutic effects over weeks or months.

 

Our research includes longitudinal studies of:

  • inflammation and microcirculation in secondary injury associated with traumatic brain injury and stroke and the effects of novel therapies,

  • the connection between nicotinic acetylcholine receptors and Alzheimer's disease,

  • design and testing of novel neurochemical probes for chronic use, and

  • continuous intracortical and subcortical EEG recordings in epileptic rats to predict seizures and explain the network mechanisms of memory loss.

 

We are funded by the National Institutes of Health, National Science Foundation (BRAIN Initiative), and private foundations.


Murray lab publications and grants: click here for ORCID list.

Area for images (yellow box) has resting microglia.

Affect of GRIN lens implant on microglia morphology. An thin layer of inflammation exists under the GRIN lens, but does not extend into the imaged tissue. A) Lens track is the dark area at the top of image. The yellow box is the area imaged with the GRIN lens (working distance is 150 μm). Several microglial cells had de-ramified or amoeboid morphology, which is typical of activated microglia, in the non-imaging area immediately under the lens. The mean distance of activated microglia from the end of the lens was 46 μm (dotted blue line, n = 3 mice). This was also the mean thickness of the glial scar (image shown in paper). One such activated cell, identified by the top arrow, is enlarged in C). Only a few activated microglia (cell identified by lower arrow is enlarged in D) were observed in the imaging area. Most microglia had a ramified morphology which is indicative of the resting state (arrow in E points to ramified process). B. Similar to the region under the lens, the control areas had very few microglia with activated morphology (cells identified by arrows are enlarged in F and G). Scale bars are 50 μm. Lee et al., 2016, PLoS ONE.

Tel. 1-318-257-5237  I  Fax: 1-318-257-4000 tmurray@latech.edu | bioengineer1@hotmail.com

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