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Respir Physiol Neurobiol. 2015 Jan 1;205:28-36. doi: 10.1016/j.resp.2014.09.015. Epub 2014 Sep 26.

Changes in carotid body and nTS neuronal excitability following neonatal sustained and chronic intermittent hypoxia exposure.

Author information

1
Department of Pediatrics, Case Western Reserve University, Rainbow Babies & Children's Hospital, Cleveland, OH 44106, USA.
2
Center for Perinatal Biology, Loma Linda University, Loma Linda, CA 92350, USA.
3
Department of Pediatrics, Case Western Reserve University, Rainbow Babies & Children's Hospital, Cleveland, OH 44106, USA. Electronic address: pmm71@case.edu.

Abstract

We investigated whether pre-treatment with neonatal sustained hypoxia (SH) prior to chronic intermittent hypoxia (SH+CIH) would modify in vitro carotid body (CB) chemoreceptor activity and the excitability of neurons in the caudal nucleus of the solitary tract (nTS). Sustained hypoxia followed by CIH exposure simulates an oxygen paradigm experienced by extremely premature infants who developed persistent apnea. Rat pups were treated with 5 days of SH (11% O2) from postnatal age 1 (P1) followed by 10 days of subsequent chronic intermittent hypoxia (CIH, 5% O2/5 min, 8 h/day, between P6 and P15) as described previously (Mayer et al., Respir. Physiol. Neurobiol. 187(2): 167-75, 2013). At the end of SH+CIH exposure (P16), basal firing frequency was enhanced, and the hypoxic sensory response of single unit CB chemoafferents was attenuated. Further, basal firing frequency and the amplitude of evoked excitatory post-synaptic currents (ESPC's) of nTS neurons was augmented compared to age-matched rats raised in normoxia. These effects were unique to SH+CIH exposure as neither SH or CIH alone elicited any comparable effect on chemoafferent activity or nTS function. These data indicated that pre-treatment with neonatal SH prior to CIH exposure uniquely modified mechanisms of peripheral (CB) and central (nTS) neural function in a way that would be expected to disturb the ventilatory response to acute hypoxia.

KEYWORDS:

Carotid body; Chronic intermittent hypoxia; nTS

PMID:
25266393
DOI:
10.1016/j.resp.2014.09.015
[Indexed for MEDLINE]

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