Biology & Sustainability
Decreased Sodium Channel Expression During Spinal Cord Regeneration in Lamprey
Document Type
Poster Presentation
Location
Indianapolis, IN
Subject Area
Biology & Sustainability
Start Date
11-4-2014 8:30 AM
End Date
11-4-2014 9:30 AM
Sponsor
Robert Rosenberg (Earlham College)
Description
There are ~273,000 people living with spinal cord injury (SCI) in the US today, with ~12,000 new cases per year. Decreased quality of life, low chances of full recovery, decreased life expectancy, and health care costs of up to $1 million/person/year make SCI a devastating condition. Lampreys are a well-characterized vertebrate model for SCI. Unlike higher vertebrates, lampreys exhibit spinal cord regeneration, allowing them to swim almost normally 10-12 weeks after complete spinal transection. New knowledge on lamprey spinal cord regeneration could help identify targets and mechanisms for improved recovery from SCI in humans.
Voltage-gated sodium channels (NaV) are ion channels that allow neurons to create and propagate action potentials. Although NaV are required for neuronal function, excessive NaV activity after injury could cause hyper-excitability and excitotoxicity that can kill neurons. Lampreys recovering from SCI are resistant to NaV blockers, suggesting that the expression of NaV is decreased. Thus, changes in NaV expression may be involved in the survival and regeneration of spinal neurons following SCI.
This study aims to assess NaV expression in uninjured and transected lamprey spinal cords. We use immunofluorescence microscopy of transverse and longitudinal spinal cord sections to visualize NaV in spinal cords. To quantify expression, we use image analysis of immunofluorescence micrographs and Western blots. We also perform behavioral studies to measure swimming ability and anesthesia susceptibility during recovery. Our preliminary data provide evidence of decreased expression of voltage-gated sodium channels in regenerating lamprey axons.
Decreased Sodium Channel Expression During Spinal Cord Regeneration in Lamprey
Indianapolis, IN
There are ~273,000 people living with spinal cord injury (SCI) in the US today, with ~12,000 new cases per year. Decreased quality of life, low chances of full recovery, decreased life expectancy, and health care costs of up to $1 million/person/year make SCI a devastating condition. Lampreys are a well-characterized vertebrate model for SCI. Unlike higher vertebrates, lampreys exhibit spinal cord regeneration, allowing them to swim almost normally 10-12 weeks after complete spinal transection. New knowledge on lamprey spinal cord regeneration could help identify targets and mechanisms for improved recovery from SCI in humans.
Voltage-gated sodium channels (NaV) are ion channels that allow neurons to create and propagate action potentials. Although NaV are required for neuronal function, excessive NaV activity after injury could cause hyper-excitability and excitotoxicity that can kill neurons. Lampreys recovering from SCI are resistant to NaV blockers, suggesting that the expression of NaV is decreased. Thus, changes in NaV expression may be involved in the survival and regeneration of spinal neurons following SCI.
This study aims to assess NaV expression in uninjured and transected lamprey spinal cords. We use immunofluorescence microscopy of transverse and longitudinal spinal cord sections to visualize NaV in spinal cords. To quantify expression, we use image analysis of immunofluorescence micrographs and Western blots. We also perform behavioral studies to measure swimming ability and anesthesia susceptibility during recovery. Our preliminary data provide evidence of decreased expression of voltage-gated sodium channels in regenerating lamprey axons.