Punam Pokam, PhD

Research Interests

• Our team investigated how traumatic brain injury (TBI) affects neuronal intrinsic and synaptic mechanisms, and how those factors influence dysfunctional brain excitability, such as epilepsy and spreading depolarization, after a TBI. Large numbers of the US population, including civilians and the military, suffer from brain injuries, making the impact of TBI research tremendous. Notably, edema is one of the most prominent secondary injuries associated with TBI, one that can be observed within minutes and persist for days; because it is the principal cause of death following TBI, it is a crucially important target for intervention and unfortunately is still confronted with decades-old primary treatments that yield little success. Our recently published work in the Journal of Clinical Investigations shows that neuronal edema after TBI may not be harmful under all circumstances and can actually increase excitability when suppressed at certain time points. This has potentially major clinical implications, as the current clinical priority still centers around eliminating edema at all costs. Currently, we are examining sex-based physiological differences in neuronal edema that may contribute to the greater burden of brain excitability after traumatic brain injury in females.
• In addition, we are interested in understanding the cellular mechanisms of spreading depolarization (SD; also known as cortical spreading depression), a massive excitable event that is recognized as the pathological correlate of neurologic diseases such as TBI and subarachnoid haemorrhage. Notably, SDs have emerged not only as a pathological target for therapies but also as a potentially useful biomarker for brain injuries. We investigate how SDs ignite and how different cell types (neurons and astrocytes) are involved in this process. By determining the mechanisms driving SD initiation, we can target upstream pathways to mitigate the occurrence of SDs.
• We leverage a multifaceted approach to our research in the laboratory, including in vivo whole-cell electrophysiology, two-photon microscopy, and brain slice electrophysiology. Our lab is the first ever to deploy in vivo whole-cell recording following a brain injury, enabling a mechanistic assessment of intrinsic, synaptic, and network behaviors in intact animals—work that was previously impossible in TBI models.
• I take the training of undergraduate, graduate, and postdoctoral students seriously. I am highly committed to helping provide the mentorship and training environment they need to be successful.
• Research in my lab is supported by the NIH R01 and R21 grants.