ReviewSubstance abuse : research and treatment2013
Elevated Norepinephrine may be a Unifying Etiological Factor in the Abuse of a Broad Range of Substances: Alcohol, Nicotine, Marijuana, Heroin, Cocaine, and Caffeine.
Review in Substance abuse : research and treatment, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
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- Article
- Hunger Recruits a Parallel Circuit Encoding Alcohol Reward.bioRxiv : the preprint server for biology · 2025Article
- Cognitive Dysfunction in the Addictions (CDiA): protocol for a neuron-to-neighbourhood collaborative research program.Frontiers in psychiatry · 2025Article
- Optimal Dosing Recommendations of Clonidine in Pediatrics Using Physiologically Based Pharmacokinetic Modeling.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2024Article
- Benefits of exercise on cognitive impairment in alcohol use disorder following alcohol withdrawal.FEBS open bio · 2024Article
- Nutritional ketosis as treatment for alcohol withdrawal symptoms in female C57BL/6J mice.Scientific reports · 2024Article
- The mechanisms underlying alcohol-induced decreased splenic size: A network meta-analysis study.Alcohol, clinical & experimental research · 2024Article
- A historical perspective on clonidine as an alpha-2A receptor agonist in the treatment of addictive behaviors: Focus on opioid dependence.INNOSC theranostics & pharmacological sciences · 2024Article
- Catecholamine Variations in Pediatric Gastrointestinal Disorders and Their Neuropsychiatric Expression.Biomedicines · 2023Article
- Chronic administration of a norepinephrine antagonist prevents and partially reverses escalation of cocaine self-administration.Addiction biology · 2023Article
- Cross-talk between the HPA axis and addiction-related regions in stressful situations.Heliyon · 2023Review
- Repeated ethanol exposure and withdrawal alters angiotensin-converting enzyme 2 expression in discrete brain regions: Implications for SARS-CoV-2 neuroinvasion.Alcohol, clinical & experimental research · 2023Article
- Behavioral and biochemical effects of alcohol withdrawal in female C3H/HeNRj and C57BL/6JRj mice.Frontiers in behavioral neuroscience · 2023Article
- Sex differences in α-adrenergic receptor function contribute to impaired hypothalamic metaplasticity following chronic intermittent ethanol exposure.Alcoholism, clinical and experimental research · 2022Article
- Sex differences in stress-induced alcohol intake: a review of preclinical studies focused on amygdala and inflammatory pathways.Psychopharmacology · 2022Review
- Early Manifestation of Clozapine-Induced Cardiotoxicity: Detection, Pathophysiology, and Management.Cureus · 2022Article
- Noradrenergic circuits and signaling in substance use disorders.Neuropharmacology · 2022Review
- Is There a Novel Biosynthetic Pathway in Mice That Converts Alcohol to Dopamine, Norepinephrine and Epinephrine?Molecules (Basel, Switzerland) · 2022Article
- Repeated ethanol exposure and withdrawal alters ACE2 expression in discrete brain regions: Implications for SARS-CoV-2 infection.bioRxiv : the preprint server for biology · 2022Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A wide range of commonly abused drugs have effects on the noradrenergic neurotransmitter system, including alterations during acute intoxication and chronic use of these drugs. It is not established, however, that individual differences in noradrenergic signaling, which may be present prior to use of drugs, predispose certain persons to substance abuse. This paper puts forth the novel hypothesis that elevated noradrenergic signaling, which may be raised largely due to genetics but also due to environmental factors, is an etiological factor in the abuse of a wide range of substances, including alcohol, nicotine, marijuana, heroin, cocaine, and caffeine. Data are reviewed for each of these drugs comprising their interaction with norepinephrine during acute intoxication, long-term use, subsequent withdrawal, and stress-induced relapse. In general, the data suggest that these drugs acutely boost noradrenergic signaling, whereas long-term use also affects this neurotransmitter system, possibly suppressing it. During acute withdrawal after chronic drug use, noradrenergic signaling tends to be elevated, consistent with the observation that norepinephrine lowering drugs such as clonidine reduce withdrawal symptoms. Since psychological stress can promote relapse of drug seeking in susceptible individuals and stress produces elevated norepinephrine release, this suggests that these drugs may be suppressing noradrenergic signaling during chronic use or instead elevating it only in reward circuits of the brain. If elevated noradrenergic signaling is an etiological factor in the abuse of a broad range of substances, then chronic use of pharmacological agents that reduce noradrenergic signaling, such as clonidine, guanfacine, lofexidine, propranolol, or prazosin, may help prevent or treat drug abuse in general.
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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.