Diversity supplement for the SC2 parent grant

University Of Puerto Rico At Aguadilla, Aguadilla PR

Investigators

Linked publications & trials

Abstract

This is a diversity supplement to an SC2 Score grant parent grant entitled: “Hippocampal astrocytic Kir4.1 channel function in Type 2 diabetic mice: impact on neuronal hyperexcitability”. The purpose of this request is to provide supplemental funding to support and enhance the training of Ph.D. candidate, Mr. Luis A. Rojas-Colón. The recruitment of Mr. Luis A. Rojas-Colón will allow our laboratory to incorporate neuroinflammation studies that will substantially add to the parent grant and to the laboratory team. With his neuroinflammation Ph.D. training, he will assess if pro-inflammatory mediators could be affecting the ability of astrocytes to buffer potassium ions in the hippocampus and if those pro-inflammatory mediators affect neuronal epileptiform activity. Having Mr. Luis A. Rojas-Colón in the laboratory for the next 2 years would be fitting because of Luis’ research, talent, and interest in neuroinflammation. Since he would share his knowledge with our laboratory members, he will be directly enhancing the diversity environment in our workroom facilitating the qualification of this appointment for a diversity supplement. Through focused discussions, Dr. Miguel P. Méndez-González (PI of the parent grant) and Mr. Luis A. Rojas-Colón, together, have developed new specific aims that will take advantage of our recent published findings and of the parent grant specific aims. In 2020, we published that diabetic male mice display neuronal hyperexcitability and decreased astrocytic K+ conductance. Also, it has been shown that TNF-a reduces astroglia potassium conductance (Köller et al., 1998), while neuronal exposure to IL-1b results in neuronal seizure like activity (Schäfers & Sorkin, 2008). By using Electrophysiology, they will determine the astrocytic and neuronal electrophysiological properties in diabetic and non-diabetic female (control) mice. Overall, the developed experiments in this supplement will provide insight of additional mechanism of how hyperglycemia contributes to epileptiform activity.