The effects of hyperglycaemia on neuronal mitochondria

Neurons depend on mitochondria more than any other cell type for their growth and survival. Mitochondria are known as the main powerhouse of the cell because of their important metabolic functions. Through the processes of the electron transport chain (ETC) and oxidative phosphorylation, mitochondria convert pyruvate into adenosine triphosphate(ATP), a primary energy carrier. Mitochondria play an essential role in providing cellular energy by manufacturing ATP, buffering calcium and partaking in metabolic pathways. We hypothesised that high extracellular glucose concentration inhibits mitochondrial motility inmature primary hippocampal neurons. We did primary hippocampal cell culture, imaging and image analysis with KymoAnalyzer software to evaluate the proposed hypothesis. Neuronal cells were grown in high glucose (25 mM) or low glucose (1 mM) concentration and analysed for various parameters of mitochondrial characteristics.;When mitochondria are exposed to various concentrations of glucose, it provides more insights about their normal functions and mechanism in the cells and how dysfunction of mitochondria leads to neuron death and degeneration. Importantly, our results demonstrated that the fraction of stationary mitochondria increased and the fraction of mitochondria travelling uni-directionally either anterograde or retrograde decreased. Our study also revealed that the density of mitochondria travelling retrograde or reversing decreased and the density of stationary mitochondria increased in high glucose compared to lower glucose media. That means there was significantly difference between the parameters analysed in 25 mM and 1 mM glucose. Our findings suggest that mature primary hippocampal neurons cultured in hyperglycemic condition (25 mM) for acute period does affect mitochondrial transport.

Name dc:type.qualificationname

mres

Level dc:type.qualificationlevel

masters-pg

Grantor dc:publisher.institution

University of Strathclyde

Year dc:date.issued

2020

Author dc:creator

• Arabi, Ayesha Binte Abdus Salam

Advisor dc:contributor.advisor

• Chalmers, Susan

DOI

10.48730/phtc-cn12

Identifier

T15736

Author Identifier

201878915

OAI identifier oai:identifier

oai:strathclyde:2v23vt426