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Minocycline prevents the attenuated acute hypoxic ventilatory response and changes in brainstem neurochemistry following neonatal sustained hypoxia exposure (1092.11)
Author(s) -
MacFarlane Peter,
Mayer Catherine
Publication year - 2014
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.28.1_supplement.1092.11
Subject(s) - neurochemistry , brainstem , hypoxia (environmental) , serotonergic , microglia , medicine , endocrinology , sudden infant death syndrome , anesthesia , neurology , serotonin , inflammation , chemistry , receptor , pediatrics , organic chemistry , psychiatry , oxygen
Sustained hypoxia (SH) exposure uniquely during the end of the second postnatal week of life (postnatal (P) age 11‐15) attenuates the acute hypoxic ventilatory response (HVR) in rats. In the current study, we investigated whether the microglia inhibitor minocycline would be protective against the SH‐induced attenuation of the HVR and changes in brainstem neurochemistry. Neonatal rats were exposed to SH (11% O 2 , 5 days) starting at P11 and received an i.p. injection of minocycline (25mg/kg) or saline midway into the exposure period; plethysmography and measurements of brainstem immunoreactivity for Iba1 and 5‐HT were performed the day after SH ended (P16). SH exposure attenuated the HVR, increased Iba1 and decreased 5‐HT immunoreactivity in the nTS compared normoxia raised rats. Minocycline prevented the SH‐induced attenuated HVR including the changes in nTS Iba1 and 5‐HT immunoreactivity. We speculate that brainstem microglia may be involved in SH‐induced changes in brainstem neurochemistry leading to a 5‐HT‐induced modification of the mechanisms mediating the acute HVR. These data share several similarities to Sudden Infant Death Syndrome victims including evidence of impaired (cardio)‐respiratory control, brainstem gliosis, and serotonergic deficits associated with a vulnerability to an environmental stressor.