PMID- 30999061 OWN - NLM STAT- MEDLINE DCOM- 20191212 LR - 20220716 IS - 1878-1519 (Electronic) IS - 1569-9048 (Print) IS - 1569-9048 (Linking) VI - 264 DP - 2019 Jun TI - Mechanisms underlying a critical period of respiratory development in the rat. PG - 40-50 LID - S1569-9048(18)30321-5 [pii] LID - 10.1016/j.resp.2019.04.006 [doi] AB - Twenty-five years ago, Filiano and Kinney (1994) proposed that a critical period of postnatal development constitutes one of the three risk factors for sudden infant death syndrome (SIDS). The underlying mechanism was poorly understood. In the last 17 years, much has been uncovered on this period in the rat. Against several expected trends of development, abrupt neurochemical, metabolic, ventilatory, and electrophysiological changes occur in the respiratory system at P12-13. This results in a transient synaptic imbalance with suppressed excitation and enhanced inhibition, and the response to acute hypoxia is the weakest at this time, both at the cellular and system's levels. The basis for the synaptic imbalance is likely to be contributed by a reduced expression of brain-derived neurotrophic factor (BDNF) and its TrkB receptors in multiple brain stem respiratory-related nuclei during the critical period. Exogenous BDNF or a TrkB agonist partially reverses the synaptic imbalance, whereas a TrkB antagonist accentuates the imbalance. A transient down-regulation of pituitary adenylate cyclase-activating polypeptide (PACAP) at P12 in respiratory-related nuclei also contributes to the vulnerability of this period. Carotid body denervation during this time or perinatal hyperoxia merely delays and sometimes prolongs, but not eliminate the critical period. The rationale for the necessity of the critical period in postnatal development is discussed. CI - Copyright (c) 2019 Elsevier B.V. All rights reserved. FAU - Wong-Riley, Margaret T T AU - Wong-Riley MTT AD - Department of Cell Biology, Neurobiology and Anatomy, USA. Electronic address: mwr@mcw.edu. FAU - Liu, Qiuli AU - Liu Q AD - Department of Pediatrics, Medical College of Wisconsin, 8701 Watertown, Plank Road, Milwaukee, WI 53226, USA. FAU - Gao, Xiuping AU - Gao X AD - Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive, SE, Albuquerque, New Mexico 87108, USA. LA - eng GR - R01 HD048954/HD/NICHD NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20190415 PL - Netherlands TA - Respir Physiol Neurobiol JT - Respiratory physiology & neurobiology JID - 101140022 RN - 0 (Bdnf protein, rat) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Pituitary Adenylate Cyclase-Activating Polypeptide) RN - 0 (Slc12a2 protein, rat) RN - 0 (Solute Carrier Family 12, Member 2) RN - EC 2.7.10.1 (Ntrk2 protein, rat) RN - EC 2.7.10.1 (Receptor, trkB) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Hypoxia/*metabolism MH - Pituitary Adenylate Cyclase-Activating Polypeptide/*metabolism MH - Rats MH - Receptor, trkB/agonists/antagonists & inhibitors/*metabolism MH - *Respiratory Physiological Phenomena MH - Solute Carrier Family 12, Member 2/*metabolism PMC - PMC6564680 MID - NIHMS1527492 OTO - NOTNLM OT - BDNF OT - Hypoxia OT - KCC2 OT - NKCC1 OT - PACAP OT - Synaptic imbalance EDAT- 2019/04/19 06:00 MHDA- 2019/12/18 06:00 PMCR- 2020/06/01 CRDT- 2019/04/19 06:00 PHST- 2019/01/30 00:00 [received] PHST- 2019/04/05 00:00 [revised] PHST- 2019/04/10 00:00 [accepted] PHST- 2019/04/19 06:00 [pubmed] PHST- 2019/12/18 06:00 [medline] PHST- 2019/04/19 06:00 [entrez] PHST- 2020/06/01 00:00 [pmc-release] AID - S1569-9048(18)30321-5 [pii] AID - 10.1016/j.resp.2019.04.006 [doi] PST - ppublish SO - Respir Physiol Neurobiol. 2019 Jun;264:40-50. doi: 10.1016/j.resp.2019.04.006. Epub 2019 Apr 15.