| Affiliations: | Neuroscience Research Leadership |
| Project Leader: | Michaela Edmond, Ph.D.
medmond@tamu.edu Neuroscience & Experimental Therapeutics |
| Faculty Mentor: | Punam Pokam |
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Meeting Times:
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TBA |
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Team Size:
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6 |
| Open Spots: | 0 |
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Special Opportunities:
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Mentored research program focused on animal models of brain injury, neural-glial interactions and cell edema in the CNS, and sex-differences in brain excitability. If the candidate is highly motivated, he/she will learn two-photon imaging techniques to measure neuronal intracellular calcium and extracellular glutamate activity in awake, behaving mice. The candidate will learn 2-photon imaging data processing and analysis using MATLAB, Fiji/ImageJ, and Excel software. In addition, there is an opportunity to become a full member of the lab, learning a plethora of experimental and analytical techniques/skills, guided through professional development, attending conferences, and authorship on publications.
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Team Needs:
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Prior experience in neuroscience and animal handling is preferred but not required. |
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Description:
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Cerebral edema, or swelling, is one of the major causes of death and morbidity following traumatic brain injury (TBI). Edema is an important therapeutic target, yet its treatment has not significantly advanced in decades, and outcomes are often unsatisfactory. A potential reason is that the edema process is complex – involving multiple mechanisms and affecting different cell types in distinct ways. Astrocytic edema and vascular response have been well documented after TBI, but there has been little examination of neuronal contributions. Our recently published work revealed that the shape of the neuron influences its intrinsic and network excitability in males after TBI – i.e., membranes of swollen neurons are less excitable and network activity is dampened 48 hours after TBI. In contrast to males, our recent preliminary findings show no evidence of neuronal edema in female mice 48h after TBI. This is consistent with prior studies that show a lack of brain edema at 24h post-TBI when the injury is induced during the proestrus stage of the estrous cycle. Importantly, if less edema is observed after TBI in females, we predict less protection against excitability and an earlier transition to the ‘excitable window.’ This is noteworthy since clinical outcomes are worse in females after mild and moderate TBI. This striking difference in severity is poorly understood. Our goal is to systematically examine whether (and how) sex-based physiological differences in neuronal edema contribute to the greater burden of TBI in females. In addition, we will examine the progression of changes in cortical excitability in females, as well as the underlying mechanisms responsible for those changes over weeks and months after TBI. |