Determining Sensory Plasticity and Developing Recovery for Sexual Dysfunction in Chronic Spinal Cord-Injured Male Rats
Abstract
In the current proposal, the hypothesis will be tested that chronic SCI causes long term deficits in transmission of sensory inputs related to sexual activity to the spinal ejaculation generator. It is hypothesized that chronic spinal injury causes reorganization of the sensory fibers that relay sensory information from the sexual organs to the spinal ejaculation generator. In the first aim, tract tracing injections are utilized to identify changes in Group A nerve fibers in the main sensory nerve that relays sensory information related to sexual activity. Significant progress has been made towards this aim and further analysis is ongoing. Secondly, the hypothesis is tested that chronic contusion injury alters glutamate inputs to and expression of glutamate receptors in the spinal ejaculation generator. Confocal microscopy analysis was used to investigate changes in glutamatergic inputs to spinal neurons in the ejaculation generator using immunolabeling for vesicular glutamate transporters 1 and 2 and galanin for LSt cells. Indeed, it was demonstrated that chronic contusion injury caused a significant reduction of glutamatergic axon inputs to the spinal ejaculation generator, which may in turn contribute to ejaculatory dysfunction following spinal cord injury. Finally, studies will aim to test effectiveness of glutamate receptor agonists on recovery and restoration of ejaculatory function following spinal cord injury.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2023
- Accession Number
- AD1224433
Entities
People
- Eric N Brown
- Lique M. Coolen
- Thywill Ettey
Organizations
- Kent State University