Premium
Impaired arousal associated with prenatal alcohol exposure in rat pups is related to an increase in brainstem GABA (1177.5)
Author(s) -
Sirieix Chrystelle,
Wrocklage James,
Schneider Robert,
Darnall Robert
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.1177.5
Subject(s) - endocrinology , arousal , medicine , serotonergic , brainstem , hypoxia (environmental) , dorsal raphe nucleus , raphe , serotonin , chemistry , psychology , neuroscience , receptor , organic chemistry , oxygen
Prenatal alcohol exposure (PAE) increases the risk for The Sudden Infant Death Syndrome (SIDS). Many SIDS infants are exposed to repeated hypoxia before death. Arousal in response to hypoxia is impaired after PAE and is modulated by medullary raphe GABAergic mechanisms. We therefore hypothesized that arousal impairment after PAE would be associated with increases in medullary GABA. Pregnant dams received an ethanol liquid diet (ETOH), an iso‐caloric pair fed diet (PF) or a standard chow diet (CHOW). Artificial cerebrospinal fluid (ACSF) or nipecotic acid (NIP), a GABA reuptake inhibitor, was microinjected (50 nL) into the raphe magnus (RMg) of P15 and P21 pups from each diet group. After recovery, pups were exposed to 4 episodes of hypoxia and the time to arousal (latency) was determined behaviorally. Brainstem GABA concentration was measured (HPLC) in P5, P15 and P21 pups from each diet group. At P21, ACSF injected pups in the ETOH group had longer arousal latencies than those in the PF and CHOW pups combined (CON group) (P<0.001). ETOH pups also had higher brainstem GABA concentrations (P=0.013). Moreover, CON pups injected with NIP had arousal latencies similar to those in ETOH pups after ACSF injection and NIP injected ETOH pups had no further increases in arousal latency. Our results show that the effects of PAE on arousal are associated increases in brainstem GABA and that RMg GABA reuptake mechanisms may be involved. Grant Funding Source : Supported by NIH PO1 HD36379 and R21 AA020279