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Time Course of Brainstem Glial Activation Following Exposure to Chronic Sustained Hypoxia
Author(s) -
Arbogast Tara Elizabeth,
Stokes Jennifer Ann,
Powell Frank L
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1262.1
Subject(s) - brainstem , microglia , astrocyte , hypoxia (environmental) , central nervous system , neuroscience , chemistry , perfusion , chemoreceptor , medicine , biology , pathology , endocrinology , inflammation , oxygen , receptor , organic chemistry
Neuron‐glia communication in the central nervous system (CNS) is proving to be an important component of neuronal signaling and recently we showed that glial activation in the brainstem plays a role in neural plasticity that increases ventilation following chronic sustained hypoxia (CSH) in rats (Stokes JA et al., 2015). In this study we measured the time course of activation of microglia and astrocytes following different lengths of exposure to CSH (10% O 2 ). Rats were exposed to CSH followed by immediate tissue perfusion and brainstem collection at the following time points: 15‐, 30‐ and 60‐minutes, 4‐, 12‐ and 24‐hours, 2‐, 4‐ and 7‐days. We measured activation of glial cells using immunohistochemistry, focusing on respiratory control centers: the nucleus tractus solitarius (NTS) and the retrotrapezoidal nucleus (RTN). Initial results show that microglia (Iba1‐positive cells) display an active morphology at 60 minutes, but are less active in appearance at 24 hours and return to the resting state (as determined by morphology) at 7 days. In contrast, astrocytes progressively increased in GFAP expression over the same time points of 1 hour, 24 hours, and 7 days. The results show that there is an order to glial activation, which we previously showed was necessary for ventilatory acclimatization to hypoxia: microglia are activated first, followed by astrocytes during CSH exposure. Support or Funding Information NIH RO1 HL‐081823