PMID- 29516654
OWN - NLM
STAT- MEDLINE
DCOM- 20190221
LR  - 20240314
IS  - 2051-817X (Electronic)
IS  - 2051-817X (Linking)
VI  - 6
IP  - 5
DP  - 2018 Mar
TI  - Effects of neonatal hyperoxia on the critical period of postnatal development of 
      neurochemical expressions in brain stem respiratory-related nuclei in the rat.
LID - 10.14814/phy2.13627 [doi]
LID - e13627
AB  - We have identified a critical period of respiratory development in rats at 
      postnatal days P12-13, when inhibitory influence dominates and when the response 
      to hypoxia is at its weakest. This critical period has significant implications 
      for Sudden Infant Death Syndrome (SIDS), the cause of which remains elusive. One 
      of the known risk factors for SIDS is prematurity. A common intervention used in 
      premature infants is hyperoxic therapy, which, if prolonged, can alter the 
      ventilatory response to hypoxia and induce sustained inhibition of lung alveolar 
      growth and pulmonary remodeling. The goal of this study was to test our 
      hypothesis that neonatal hyperoxia from postnatal day (P) 0 to P10 in rat pups 
      perturbs the critical period by altering the normal progression of neurochemical 
      development in brain stem respiratory-related nuclei. An in-depth, 
      semiquantitative immunohistochemical study was undertaken at P10 (immediately 
      after hyperoxia and before the critical period), P12 (during the critical 
      period), P14 (immediately after the critical period), and P17 (a week after the 
      cessation of hyperoxia). In agreement with our previous findings, levels of 
      cytochrome oxidase, brain-derived neurotrophic factor (BDNF), TrkB (BDNF 
      receptor), and several serotonergic proteins (5-HT(1A) and (2A) receptors, 5-HT 
      synthesizing enzyme tryptophan hydroxylase [TPH], and serotonin transporter 
      [SERT]) all fell in several brain stem respiratory-related nuclei during the 
      critical period (P12) in control animals. However, in hyperoxic animals, these 
      neurochemicals exhibited a significant fall at P14 instead. Thus, neonatal 
      hyperoxia delayed but did not eliminate the critical period of postnatal 
      development in multiple brain stem respiratory-related nuclei, with little effect 
      on the nonrespiratory cuneate nucleus.
CI  - (c) 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on 
      behalf of The Physiological Society and the American Physiological Society.
FAU - Mu, Lianwei
AU  - Mu L
AD  - Departments of Cell Biology, Neurobiology and Anatomy, Medical College of 
      Wisconsin, Milwaukee, Wisconsin.
FAU - Xia, Dong Dong
AU  - Xia DD
AD  - Departments of Cell Biology, Neurobiology and Anatomy, Medical College of 
      Wisconsin, Milwaukee, Wisconsin.
FAU - Michalkiewicz, Teresa
AU  - Michalkiewicz T
AD  - Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
FAU - Hodges, Matthew
AU  - Hodges M
AD  - Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
FAU - Mouradian, Gary
AU  - Mouradian G
AD  - Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
FAU - Konduri, Girija G
AU  - Konduri GG
AD  - Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
FAU - Wong-Riley, Margaret T T
AU  - Wong-Riley MTT
AD  - Departments of Cell Biology, Neurobiology and Anatomy, Medical College of 
      Wisconsin, Milwaukee, Wisconsin.
LA  - eng
GR  - R01 HL122358/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Physiol Rep
JT  - Physiological reports
JID - 101607800
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Receptors, Serotonin)
RN  - 0 (Serotonin Plasma Membrane Transport Proteins)
RN  - EC 1.14.16.4 (Tryptophan Hydroxylase)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain Stem/growth & development/*metabolism/physiology
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - Electron Transport Complex IV/genetics/metabolism
MH  - Female
MH  - Hyperoxia/etiology/*metabolism
MH  - Male
MH  - Oxygen Inhalation Therapy/adverse effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/genetics/metabolism
MH  - Receptors, Serotonin/genetics/metabolism
MH  - *Respiration
MH  - Serotonin Plasma Membrane Transport Proteins/genetics/metabolism
MH  - Tryptophan Hydroxylase/genetics/metabolism
PMC - PMC5842315
OTO - NOTNLM
OT  - BDNF
OT  - brain stem
OT  - critical period
OT  - cytochrome oxidase
OT  - respiratory development
OT  - serotonin
EDAT- 2018/03/09 06:00
MHDA- 2019/02/23 06:00
PMCR- 2018/03/08
CRDT- 2018/03/09 06:00
PHST- 2018/01/06 00:00 [received]
PHST- 2018/02/01 00:00 [revised]
PHST- 2018/02/02 00:00 [accepted]
PHST- 2018/03/09 06:00 [entrez]
PHST- 2018/03/09 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2018/03/08 00:00 [pmc-release]
AID - PHY213627 [pii]
AID - 10.14814/phy2.13627 [doi]
PST - ppublish
SO  - Physiol Rep. 2018 Mar;6(5):e13627. doi: 10.14814/phy2.13627.