Sydney Haselden

Sydney Haselden

What do Parasympathetic Ganglia Neurons have to do with Type 1 Diabetes?

Authors

Sydney Haselden, Dr. Martha Campbell-Thompson

Mentor

Dr. Martha Campbell-Thompson

College

College of Medicine

Abstract

Type 1 Diabetes (T1D), despite ongoing research has no cure, and treatment mainly focuses on management of the disease through insulin replacement therapies. Although many studies have explored beta-cell anatomical and functional pathology, the characterization of features of intrapancreatic ganglia have not been examined. This project aimed to identify and analyze the neurons, synapses, and macrophages within the ganglia between T1D, auto-antibody positive (AAb), and no diabetes (ND) donors. It was hypothesized that the neurodegeneration of the parasympathetic efferent neurons of the autonomic nervous system contributes to the T1D pathogenesis. Each slide was stained using an immunofluorescence multiplex technique with four primary antibodies from different hosts including: HuC/D, Synapsin, and IBA1 to identify neurons, synapses, and macrophages, respectively. Following confocal microscopy, image analysis was performed using Neurolucida360. Data analysis was conducted using Prism with statistical tests between controls and T1D donors as AAb donors data were too small for inclusion. Indeed, the morphological analysis of the intrapancreatic ganglia revealed significant (P ≤ 0.01) enlargement of the neuronal soma in T1D donors. No significant difference was indicated regarding the overall size of the ganglia or numbers and proportional area of macrophages within the ganglia. More studies are needed to determine whether the larger neuronal area can be contributed to over activity of neurons in this region. This indicates that the post-ganglionic neurons, otherwise known as intrapancreatic ganglia, in a T1D pancreas exhibits differences in size that would be expected to have functional effects on the nervous system communication.

Poster

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Research Pitch

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