Intermittent hypoxia induces neuroplasticity changes in the nucleus of the solitary tract (1132.1)

Abstract

Intermittent hypoxia (IH) is known to alter responses of neurons in NTS to cardiovascular afferent inputs. The mechanisms related for these IH effects in NTS may involve pre‐ or post‐synaptic neuroplasticity changes. To investigate this possibility, adult male Sprague‐Dawley rats were exposed to either 1‐, 7‐ or 95‐days of IH (8 h/day) or normoxia. Protein was extracted from NTS in each group of rats and analyzed by western blot for expression of brain‐derived neurotrophic factor (BDNF), tropomyosin kinase B (TrkB), synaptophysin and growth‐associated protein‐43 (GAP‐43). Arterial pressure (AP) and heart rate were not different between the IH and normoxic animals at 1‐ or 7‐days, but AP was elevated after 95‐days of chronic IH. After 1‐day IH, TrkB protein expression was higher and synaptophysin was lower than normoxic controls. After 7‐days of IH, BDNF and TrkB protein expression was higher in NTS. After 95‐days of chronic IH exposure, BDNF, synaptophysin, and GAP‐43 protein expression was lower in NTS. These results suggest that neuroplasticity changes occurring within NTS may be associated with the elevated AP induced by chronic IH activation of chemoreceptor afferents. Additionally, these data suggest that changes in neuroplasticity within NTS may contribute to the development of autonomic dysregulation often seen in patients with chronic obstructive sleep apnea. Supported by HSFO.Grant Funding Source: Heart and Stroke Foundation of Ontario