Major
Biological Sciences
Minor(s)
Chemistry
Advisor
Quinlan, Katharina, A
Advisor Department
Biomedical and Pharmaceutical Sciences
Date
5-2020
Keywords
Hypoxia-Ischemia; Cerebral Palsy; 5HT
Abstract
Cerebral palsy (CP) is a motor deficit disorder affecting 1 in 400 live births with over 90% of cases presenting some degree of muscle stiffness and spasticity. Despite this high prevalence, the neuronal mechanisms of spasticity are still not well understood, putting restrictions on the kinds and abilities of therapeutics available. In an effort to advance understanding of how changes in spinal motoneurons contribute to motor deficits we used the rabbit hypoxia-ischemia (HI) model of developmental injury at 79% pregnancy (E25). This study aimed to look at the effects injury had on changes in the number, physical structure, and expression of serotonergic receptors on spinal motoneurons during development. To quantify any structural changes we imaged spinal cord tissue using a 2- photon microscope and then converted the images into a digital 3D reconstruction. Serotonin, a neurotransmitter, has been shown to play a role in rhythmic movement as well as motoneuron excitability and muscle stiffness associated with spasticity. Immunohistochemistry of 5-HTr7, a serotonin subtype receptor, was performed to showcase any changes in serotonergic receptor expression that could possibly be playing a role in motor deficits. Nissl staining of embryonic tissue and postnatal tissue was also performed and imaged to track the location of motoneuron pools, specifically lamina 9; to measure neuron migration and cell death throughout development of typical and affected individuals. The purpose of this study is to further understand contributions of spinal motor circuits to movement deficits in cerebral palsy in hopes for therapeutic advancements.