Hypoxia-Induced Activation of Respiratory Nuclei in the Ventral Brainstem of the Streptozotocin-Induced Rat Model of Alzheimer’s Disease
Besides memory impairment, patients with Alzheimer's disease (AD) also develop cardiorespiratory problems and brainstem pathology. Using the streptozotocin (STZ)-induced model of AD, we found decreased hypoxia-induced cell activation in the nucleus tractus solitarii, a dorsal brainstem area integral for respiratory control. Here we concentrate on the activation of other brainstem nuclei relevant for chemoreflex function.
Sporadic AD was induced (1.5 mg/kg STZ, twice) and peripheral chemoreflex function tested with two hours of hypoxia (10% O2) using plethysmography. Immediately following hypoxia, brains were fixed and analyzed for cell activation (c-Fos).
Although not significant (4 rats/group), this ongoing study shows trends for decreased cell activation in the rostral ventral respiratory group, pre-Bötzinger complex, and the Bötzinger complex of AD rats when compared to vehicle control.
Decreased cell activation is consistent with decreased chemoreflex function in the STZ-rat model of AD. This finding may help explain the respiratory symptoms developed in AD patients.
Keywords: Alzheimer's Disease, Rat model, Streptozotocin, Cell activation, c-Fos, Respiration, Hypoxia, Brain Nuclei
Topic(s):Biology
Presentation Type: Oral Paper
Session: 105-2
Location: MG 2001
Time: 8:15