ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Nicotine self-administration differentially regulates hypothalamic corticotropin-releasing factor and arginine vasopressin mRNAs and facilitates stress-induced neuronal activation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Hyponatremia in patients with arterial hypertension: pathophysiology and management.Archives of medical science : AMS · 2023Article
- Multidimensional Intersection of Nicotine, Gene Expression, and Behavior.Frontiers in behavioral neuroscience · 2021Article
- Role of corticotropin-releasing factor in alcohol and nicotine addiction.Brain research · 2020Review
- Anatomical Markers of Activity in Hypothalamic Neurons.Comprehensive Physiology · 2020Review
- Nicotinic Cholinergic System in the Hypothalamus Modulates the Activity of the Hypothalamic Neuropeptides During the Stress Response.Current neuropharmacology · 2018Review
- The influence of adolescent nicotine exposure on ethanol intake and brain gene expression.PloS one · 2018Article
- Substance use modulates stress reactivity: Behavioral and physiological outcomes.Physiology & behavior · 2016Review
- The Sociopharmacology of Tobacco Addiction: Implications for Understanding Health Disparities.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2016Review
- Sex-influence of nicotine and nitric oxide on motor coordination and anxiety-related neurophysiological responses.Psychopharmacology · 2014Article
- Altered hypothalamic response to food in smokers.The American journal of clinical nutrition · 2013Article
- Nicotine modulates multiple regions in the limbic stress network regulating activation of hypophysiotrophic neurons in hypothalamic paraventricular nucleus.Journal of neurochemistry · 2012Article
- Sexually diergic hypothalamic-pituitary-adrenal (HPA) responses to single-dose nicotine, continuous nicotine infusion, and nicotine withdrawal by mecamylamine in rats.Brain research bulletin · 2011Article
- Nicotine self-administration differentially modulates glutamate and GABA transmission in hypothalamic paraventricular nucleus to enhance the hypothalamic-pituitary-adrenal response to stress.Journal of neurochemistry · 2010Article
- Venous plasma nicotine correlates of hormonal effects of tobacco smoking.Pharmacology, biochemistry, and behavior · 2010Article
- Nicotine self-administration diminishes stress-induced norepinephrine secretion but augments adrenergic-responsiveness in the hypothalamic paraventricular nucleus and enhances adrenocorticotropic hormone and corticosterone release.Journal of neurochemistry · 2010Article
- Subtypes of nicotinic acetylcholine receptors in nicotine reward, dependence, and withdrawal: evidence from genetically modified mice.Behavioural pharmacology · 2008Review
- Sexually diergic, dose-dependent hypothalamic-pituitary-adrenal axis responses to nicotine in a dynamic in vitro perfusion system.Journal of pharmacological and toxicological methodsArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Acute nicotine is a potent stimulus for activation of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis, while chronic nicotine self-administration (SA) desensitizes the ACTH response to self-administered nicotine but cross-sensitizes to mild footshock stress (mFSS). To identify underlying mechanisms, we investigated (1) the effects of chronic nicotine SA on the coexpression of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) mRNAs, the primary hypothalamic neuropeptides regulating ACTH release, in the parvocellular division of paraventricular nucleus (pcPVN), and (2) mFSS-induced activation of these neurons during nicotine SA. Adult male Sprague Dawley rats were given 23 h/d unlimited access to self-administer nicotine (0.03 mg/kg per injection, i.v.) for 19 d. Brains were double labeled with fluorescence in situ hybridization of CRF and AVP mRNAs and triple labeled after mFSS exposure for CRF and AVP mRNAs and c-Fos protein. Chronic nicotine SA significantly increased AVP mRNA signal and the number of pcPVN AVP-positive (AVP(+)) neurons (twofold to threefold), reduced the number of CRF-positive (CRF(+)) neurons by approximately 60%, but increased pcPVN CRF(+)/AVP(+) neuronal number fivefold. Significantly, although chronic nicotine SA did not affect total c-Fos expression induced by mFSS in pcPVN CRF(+) neurons, the majority of the new CRF(+)/AVP(+) population was activated by this heterotypic stressor. These phenotypic neuronal alterations may provide the pivotal mechanism underlying the capacity of chronically self-administered nicotine to cross-sensitize the HPA response to specific stressors, suggesting that nicotine may augment HPA responsiveness to specific stressors in human smokers.
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Registered trials
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.