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Moderate Prenatal Alcohol Exposure and Quantification of Social Behavior in Adult Rats
Published on: December 14, 2014
Impaired arousal in rat pups with prenatal alcohol exposure is modulated by GABAergic mechanisms
Chrystelle M Sirieix1, Christine M Tobia2, Robert W Schneider2
1Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire chrystelle.sirieix@gmail.com.
Insights
Prenatal alcohol exposure (PAE) impairs arousal responses to hypoxia in rat pups. This impairment is linked to increased brainstem GABA levels and enhanced GABAergic activity, potentially increasing Sudden Infant Death Syndrome (SIDS) risk.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Prenatal alcohol exposure (PAE) is a known risk factor for Sudden Infant Death Syndrome (SIDS).
- Arousal from hypoxia is crucial for survival and is modulated by GABAergic mechanisms in the brainstem.
- The specific impact of PAE on hypoxia-induced arousal and its underlying neurochemical basis remains unclear.
Purpose of the Study:
- To investigate the effect of PAE on arousal responses to hypoxia in developing rat pups.
- To determine if PAE alters brainstem GABA concentrations and GABAergic activity.
- To elucidate the role of medullary GABAergic mechanisms in PAE-induced deficits in arousal.
Main Methods:
- Rat dams were exposed to ethanol (ETOH), pair-fed (PF), or control (CHOW) diets during gestation.
- Arousal latency to hypoxia was measured in pups at postnatal days 5, 15, and 21.
- Brainstem GABA concentrations were measured, and medullary raphe injections of GABAergic agents (nipecotic acid, gabazine) or artificial cerebrospinal fluid were performed.
Main Results:
- ETOH pups exhibited significantly increased arousal latency to hypoxia at P15 and P21 compared to controls.
- Brainstem GABA concentration was elevated in ETOH pups at P21.
- Pharmacological enhancement of GABAergic activity (nipecotic acid) in control pups mimicked the impaired arousal seen in ETOH pups, while it did not further impair ETOH pups.
Conclusions:
- PAE significantly impairs the arousal response to hypoxia in developing rats.
- This impairment is associated with increased brainstem GABA levels and enhanced GABAergic neurotransmission.
- Medullary GABAergic mechanisms play a critical role in mediating or modulating the effects of PAE on hypoxia-induced arousal, with implications for SIDS risk.
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.
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