AI Article Synopsis
- Intermittent hypoxia (IH) from obstructive sleep apnea causes damage to the hippocampus in adult rats, leading to difficulties with spatial learning.
- After initial impairment, there is a partial recovery in spatial learning abilities over time, even with ongoing IH exposure.
- This recovery is linked to changes in neurogenesis, with decreased initial production of new neurons followed by an increase in the presence of neuronal progenitors and mature neurons, while synaptic protein levels remain unchanged.
Article Abstract
Intermittent hypoxia (IH) during sleep, such as occurs in obstructive sleep apnea, leads to degenerative changes in the hippocampus, and is associated with spatial learning deficits in the adult rat. We report that in Sprague-Dawley rats the initial IH-induced impairments in spatial learning are followed by a partial functional recovery over time, despite continuing IH exposure. These functional changes coincide with initial decreases in basal neurogenesis as shown by the number of positively colabelled cells for BrdU and neurofilament in the dentate gyrus of the hippocampus, and are followed by increased expression of neuronal progenitors and mature neurons (nestin and BrdU-neurofilament positively labelled cells, respectively). In contrast, no changes occurred during the course of IH exposures in the expression of the synaptic proteins synaptophysin, SNAP25, and drebrin. Collectively, these findings indicate that the occurrence of IH during the lights on period results in a biphasic pattern of neurogenesis in the hippocampus of adult rats, and may account for the observed partial recovery of spatial function.
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| http://dx.doi.org/10.1046/j.1460-9568.2003.02947.x | DOI Listing |
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