Parul Verma is a postdoctoral scholar at the Brain networks lab at University of California, San Francisco. She holds a PhD from Purdue
University and a bachelor’s degree from IIT Bombay. She currently works on understanding the relationship between the brain anatomical structure and the diverse functions it can exhibit, as well as how this relationship is affected in neurological conditions
such as Alzheimer’s disease. More broadly, Parul is interested in understanding the underlying mechanisms of neural activity ranging from a single neuron to the entire brain using mathematical modeling. Parul's research is generously supported by the Alzheimer's
Association postdoctoral fellowship.
Pain is a common sensation that arises due to injuries as well as various diseases and disorders. In this talk, we will examine the pathophysiology of pain by investigating
the pain-sensing neuron dynamics using an engineering approach. Specifically, we will focus on exploring the following: (i) pain sensation mutations, and (ii) chemotherapy-induced peripheral neuropathy (CIPN) mechanisms.
Pain signaling can be characterized in terms of electrical signaling by a pain-sensing neuron. To investigate this electrical signaling, a mathematical modeling approach
was employed in this work. The pain-sensing neuron membrane was assumed to be an electrical circuit and the potential across the membrane was modeled in terms of the interplay of sodium and potassium ions flowing across it via voltage-gated sodium and potassium
channels, respectively. A bifurcation theory approach was used to explore possible bifurcations to explain the switch from a “no-pain” to a “painful” solution regime.
Using this approach, we firstly detected potential mutation points in specific sodium channels that can alter the pain sensation threshold of an individual. This was
supported by experimental evidence in existing literature. Secondly, we examined the role of voltage-gated ion channels in inducing CIPN. Bifurcation analysis revealed that alterations in specific sodium and potassium channel conductance can induce CIPN. These
findings were supplemented by in vitro recordings of the electrical activity of a sensory neuron culture.
In summary, this talk will outline a framework that (i) can be used to find potential voltage-gated ion channels that can be targeted to control the pain sensation
threshold in individuals and (ii) can be extended to investigate CIPN mechanisms to find therapeutic cures for it.
