Research Day
EXERCISE TO THE RESCUE: EFFECTS OF AGING AND LONG-TERM EXERCISE ON STRUCTURAL PLASTICITY OF MOTOR NEURONS AND GDNF EXPRESSION IN SPINAL CORD
Document Type
Abstract
Date
2021
Abstract
As age progresses the neuromuscular system weakens. A possible reason for this weakening is the loss of connectivity between motor neuron and muscle. Physical exercise has been linked to neuroprotection by increasing neurotrophic factor (NF) expression. GDNF is a potent NF for somatic motor neurons (MNs) maintenance and survival. The goal of this study was to examine structural neuroplastic changes that occur with age and exercise by examining MN size in the lumbar spinal cord. Spinal tissues were taken from sedentary and exercised Sprague-Dawley rats between 4 weeks and 24 months of age. Exercise groups consisted of 14-week-old rats that had access to running wheels for 10 weeks; and 12-month-old, 18-month-old, and 24-month-old rats that had access to running wheels for 24 weeks. Antibody against choline acetyltransferase (ChAT) was used for detection of motor neurons, anti-GDNF was used for GDNF localization, and DAPI was used for nuclear staining. The results show that MN cell body size increased from 4 weeks of age to 6 months of age then decreased at older ages (12, 18, and 24 months of age) in sedentary, aging rats. Exercise in age-matched groups caused a significant increase in cell bodysize at 12 months of age and had a tendency to towards increase at 18 and 24 months of age. MNs had GDNF co-localized at the cell body at all ages. These findings suggest that exercise plays a role in the structural plasticity of ChAT-positive cells. Understanding the role that NFs play in regulating neural plasticity.