Use of neuronal mitochondrial isolation to assess NDUFS4 levels in GABAergic neuron

Location

Poster #3

Start Date

2-5-2025 10:00 AM

Department

Biology

Abstract

GABAergic neurons play a crucial role in the functioning of the central nervous system. GABAergic neurons balance excitation and inhibition in the brain and require proper mitochondrial function to sustain neural circuitry. The NDUFS4 protein is one of the 45 subunits in mitochondrial Complex I of the electron transport chain (ETC). The ETC is responsible for energy production, yet in mice deletion of the NDUFS4 subunit in the brain is sufficient to impair neural control and disrupt cognitive and motor function. More specifically, studies have shown that selective deletion of NDUFS4 restricted to GABAergic neurons causes impaired inhibitory control and widespread neuronal dysfunction resulting in seizures in mice. However, the mechanisms that allow NDUFS4 deletion to alter mitochondrial function in GABAergic neurons are unclear. One possibility is that the absence of NDUFS4 causes compensatory changes in the protein structure of mitochondrial Complex I or in other mitochondrial compartments. By using novel mitochondrial isolation techniques from the brain, the project aims to compare mitochondrial protein composition from GABAergic neurons in the presence and absence of NDUFS4. The study will advance our understanding of mitochondria in GABAergic neurons and potentially lead to the development of biomarkers, targeted therapies, and personalized treatments for mitochondrial diseases.

Faculty Sponsor

Cindy Voisine

Faculty Sponsor

Divakar Mithal

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May 2nd, 10:00 AM

Use of neuronal mitochondrial isolation to assess NDUFS4 levels in GABAergic neuron

Poster #3

GABAergic neurons play a crucial role in the functioning of the central nervous system. GABAergic neurons balance excitation and inhibition in the brain and require proper mitochondrial function to sustain neural circuitry. The NDUFS4 protein is one of the 45 subunits in mitochondrial Complex I of the electron transport chain (ETC). The ETC is responsible for energy production, yet in mice deletion of the NDUFS4 subunit in the brain is sufficient to impair neural control and disrupt cognitive and motor function. More specifically, studies have shown that selective deletion of NDUFS4 restricted to GABAergic neurons causes impaired inhibitory control and widespread neuronal dysfunction resulting in seizures in mice. However, the mechanisms that allow NDUFS4 deletion to alter mitochondrial function in GABAergic neurons are unclear. One possibility is that the absence of NDUFS4 causes compensatory changes in the protein structure of mitochondrial Complex I or in other mitochondrial compartments. By using novel mitochondrial isolation techniques from the brain, the project aims to compare mitochondrial protein composition from GABAergic neurons in the presence and absence of NDUFS4. The study will advance our understanding of mitochondria in GABAergic neurons and potentially lead to the development of biomarkers, targeted therapies, and personalized treatments for mitochondrial diseases.