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Sirieix CM, Tobia CM, Schneider RW, et al. Impaired arousal in rat pups with prenatal alcohol exposure is modulated by GABAergic mechanisms. Physiol Rep. 2015;3(6)doi: 10.14814/phy2.12424.
Sirieix, C. M., Tobia, C. M., Schneider, R. W., & Darnall, R. A. (2015). Impaired arousal in rat pups with prenatal alcohol exposure is modulated by GABAergic mechanisms. Physiological reports, 3(6), . https://doi.org/10.14814/phy2.12424
Sirieix, Chrystelle M, et al. "Impaired arousal in rat pups with prenatal alcohol exposure is modulated by GABAergic mechanisms." Physiological reports vol. 3,6 (2015). doi: https://doi.org/10.14814/phy2.12424
Sirieix CM, Tobia CM, Schneider RW, Darnall RA. Impaired arousal in rat pups with prenatal alcohol exposure is modulated by GABAergic mechanisms. Physiol Rep. 2015 Jun;3(6). doi: 10.14814/phy2.12424. PMID: 26059034; PMCID: PMC4510626.
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Physiol Rep. 2015 Jun;3(6). doi: 10.14814/phy2.12424.

Impaired arousal in rat pups with prenatal alcohol exposure is modulated by GABAergic mechanisms.

Physiological reports

Chrystelle M Sirieix, Christine M Tobia, Robert W Schneider, Robert A Darnall

Affiliations

  1. Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire [email protected].
  2. Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire.
  3. Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire Department of Pediatrics, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire.

PMID: 26059034 PMCID: PMC4510626 DOI: 10.14814/phy2.12424

Abstract

Prenatal alcohol exposure (PAE) increases the risk for The Sudden Infant Death Syndrome (SIDS) in human infants. In rat pups, the arousal response to hypoxia is modulated by medullary raphe GABAergic mechanisms. We hypothesized that arousal to hypoxia is impaired by PAE, and is associated with an increase in medullary GABA and enhanced GABAergic activity. Pregnant dams received an ethanol liquid diet (ETOH), an iso-caloric pair fed diet (PF) or a standard chow diet (CHOW). We first measured the time to arousal (latency), during four episodes of hypoxia in P5, P15, and P21 CHOW, PF, and ETOH pups. We also measured brainstem GABA concentration in the same groups of pups. Finally, we injected artificial cerebrospinal fluid (aCSF), nipecotic acid (NIP) or gabazine into the medullary raphe of P15 and P21 pups receiving the three diets. For statistical analysis, the PF and CHOW groups were combined into a single CONTROL group. Our main finding was that compared to CONTROL, arousal latency to hypoxia is increased in ETOH pups at P15 and P21, and the concentration of brainstem GABA is elevated at P21. NIP administration in CONTROL pups led to arousal latencies similar in magnitude to those in ETOH pups after aCSF injection. NIP injected ETOH pups had no further increases in arousal latency. We conclude that PAE impairs arousal latency and this is mediated or modulated by medullary GABAergic mechanisms.

© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

Keywords: Arousal; GABA; hypoxia; prenatal alcohol exposure

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