ArticleJournal of neurophysiology2017
Fetal alcohol exposure reduces responsiveness of taste nerves and trigeminal chemosensory neurons to ethanol and its flavor components.
Article in Journal of neurophysiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Mixtures of Sweeteners and Maltodextrin Enhance Flavor and Intake of Alcohol in Adolescent Rats.Chemical senses · 2020Article
- Fetal Alcohol Programming of Subsequent Alcohol Affinity: A Review Based on Preclinical, Clinical and Epidemiological Studies.Frontiers in behavioral neuroscience · 2020Review
- Lingering Effects of Prenatal Alcohol Exposure on Basal and Ethanol-Evoked Expression of Inflammatory-Related Genes in the CNS of Adolescent and Adult Rats.Frontiers in behavioral neuroscience · 2020Article
- Clinical presentation, diagnosis, and management of fetal alcohol spectrum disorder.The Lancet. Neurology · 2019Review
- Differentially sensitive neuronal subpopulations in the central nervous system and the formation of hindbrain heterotopias in ethanol-exposed zebrafish.Birth defects research · 2019Article
- Postnatal Exposure to Ethanol Increases Its Oral Acceptability to Adolescent Rats.Chemical senses · 2018Article
- Myrtle berries seeds aqueous extract abrogates chronic alcohol consumption-induced erythrocytes osmotic stability disturbance, haematological and biochemical toxicity.Lipids in health and disease · 2018Article
- Brief Exposures to the Taste of Ethanol (EtOH) and Quinine Promote Subsequent Acceptance of EtOH in a Paradigm that Minimizes Postingestive Consequences.Alcoholism, clinical and experimental research · 2018Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Fetal alcohol exposure (FAE) leads to increased intake of ethanol in adolescent rats and humans. We asked whether these behavioral changes may be mediated in part by changes in responsiveness of the peripheral taste and oral trigeminal systems. We exposed the experimental rats to ethanol in utero by administering ethanol to dams through a liquid diet; we exposed the control rats to an isocaloric and isonutritive liquid diet. To assess taste responsiveness, we recorded responses of the chorda tympani (CT) and glossopharyngeal (GL) nerves to lingual stimulation with ethanol, quinine, sucrose, and NaCl. To assess trigeminal responsiveness, we measured changes in calcium levels of isolated trigeminal ganglion (TG) neurons during stimulation with ethanol, capsaicin, mustard oil, and KCl. Compared with adolescent control rats, the adolescent experimental rats exhibited diminished CT nerve responses to ethanol, quinine, and sucrose and GL nerve responses to quinine and sucrose. The reductions in taste responsiveness persisted into adulthood for quinine but not for any of the other stimuli. Adolescent experimental rats also exhibited reduced TG neuron responses to ethanol, capsaicin, and mustard oil. The lack of change in responsiveness of the taste nerves to NaCl and the TG neurons to KCl indicates that FAE altered only a subset of the response pathways within each chemosensory system. We propose that FAE reprograms development of the peripheral taste and trigeminal systems in ways that reduce their responsiveness to ethanol and surrogates for its pleasant (i.e., sweet) and unpleasant (i.e., bitterness, oral burning) flavor attributes.
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