ArticleNeuroscience2008
Novel role of adrenergic neurons in the brain stem in mediating the hypothalamic-pituitary axis hyperactivity caused by prenatal alcohol exposure.
Article in Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Prenatal Alcohol Exposure: Impact on Neuroimmune Function in the Stress Response and Pain.Advances in experimental medicine and biology · 2026Review
- Enhancement of parvalbumin interneuron-mediated neurotransmission in the retrosplenial cortex of adolescent mice following third trimester-equivalent ethanol exposure.Scientific reports · 2021Article
- Exposure to alcohol during adolescence exerts long-term effects on stress response and the adult brain stress circuits.Neuroscience · 2016Article
- Consumption of Substances of Abuse during Pregnancy Increases Consumption in Offspring: Possible Underlying Mechanisms.Frontiers in nutrition · 2016Review
- Adolescent alcohol exposure alters the rat adult hypothalamic-pituitary-adrenal axis responsiveness in a sex-specific manner.Neuroscience · 2013Article
- Influence of lameness on follicular growth, ovulation, reproductive hormone concentrations and estrus behavior in dairy cows.Theriogenology · 2011Article
- Brain stem catecholamines circuitry: activation by alcohol and role in the hypothalamic-pituitary-adrenal response to this drug.Journal of neuroendocrinology · 2011Article
- Adolescent alcohol exposure alters the central brain circuits known to regulate the stress response.Neuroscience · 2011Article
- Corticotropin-releasing factor-1 receptor activation mediates nicotine withdrawal-induced deficit in brain reward function and stress-induced relapse.Biological psychiatry · 2009Article
- Role of various neurotransmitters in mediating the long-term endocrine consequences of prenatal alcohol exposure.Annals of the New York Academy of Sciences · 2008Review
- Translational studies of alcoholism: bridging the gap.Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism · 2008Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Exposure to alcohol during embryonic development leads to changes in the hypothalamic-pituitary-adrenal (HPA) axis such that adult offspring release more adrenocorticotrophic hormone (ACTH) than controls when exposed to stress. In the present work, we tested the hypothesis that changes in the activity of the catecholaminergic system modulate, at least in part, this upregulation of the HPA axis. Pregnant Sprague-Dawley rats were exposed to alcohol 6 h daily during gestation days 7-18 using the vapor chamber model, which generated mean blood alcohol levels of 188.6+/-10 mg/dl. All experiments were performed on 2 to 3-month-old offspring. We first measured the ACTH response to i.c.v. injection of adrenergic receptor agonists. In rats exposed to footshocks, we then investigated the activity of corticotrophin-releasing factor (CRF) as well as indexes of catecholamine ir, namely tyrosine hydroxylase (TH) immunopositive neurons in the paraventricular nucleus (PVN), TH immunopositive neurons in the locus coeruleus, and phenylethanolamine N-methyltransferase (PNMT) immunopositive neurons in the brain stem. While adult females exposed to alcohol during fetal development (FAE) displayed the expected enhanced ACTH response to stress, there were no significant differences in response to adrenergic receptor agonists or in shock-induced CRF/TH ir and neuronal activity, as determined by c-fos colocalization. In contrast, FAE female offspring exposed to footshocks showed a significant increase in the activity of adrenergic neurons in the C1 region of the brain stem, a population of cells that project to the PVN. Collectively, these results suggest that while FAE-induced hyperactivity of the HPA axis is not accompanied by significant changes in PVN CRF or TH-ir neurons, it is characterized by an upregulation of C1 adrenergic neurons of the brain stem. This novel finding should lead to the functional characterization of this brain region in the FAE model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.