ArticleNeuropharmacology2018
The neurokinin-1 receptor mediates escalated alcohol intake induced by multiple drinking models.
Article in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Yohimbine as a pharmacological probe for alcohol research: a systematic review of rodent and human studies.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Pooled it
- Neurokinin-1 receptors in the nucleus accumbens shell influence sensitivity to social defeat stress and stress-induced alcohol consumption in male mice.Addiction neuroscience · 2024Article
- Osteoporosis treatments for intervertebral disc degeneration and back pain: a perspective.JBMR plus · 2024Article
- Vicarious defeat stress induces increased alcohol consumption in female mice: Role of neurokinin-1 receptor and interleukin-6.Addiction biology · 2024Article
- The effects of lipopolysaccharide exposure on social interaction, cytokine expression, and alcohol consumption in male and female mice.Physiology & behavior · 2023Article
- The effect of concurrent access to alcohol and oxycodone on self-administration and reinstatement in rats.Psychopharmacology · 2022Article
- Neurokinin receptors in drug and alcohol addiction.Brain research · 2020Review
- Alcohol dependence potentiates substance P/neurokinin-1 receptor signaling in the rat central nucleus of amygdala.Science advances · 2020Article
- Article
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Authors and funding
10 authors at 3 institutions in 1 country.
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Abstract
We have previously demonstrated that the neurokinin-1 receptor (NK1R) is upregulated in the central nucleus of the amygdala of alcohol preferring (P) rats and that this receptor mediates escalated alcohol consumption in this strain. However, it is unclear if non-genetic models of escalated consumption are also mediated by NK1R signaling, and if so, what brain regions govern this effect. In the experiments presented here, we use two methods of inducing escalated alcohol intake in outbred Wistar rats: yohimbine pretreatment and intermittent alcohol access (Monday, Wednesday, and Friday availability; 20% alcohol). We found that escalated alcohol consumption induced by both yohimbine injection and intermittent access is attenuated by systemic administration of the NK1R antagonist L822429. Also, when compared to continuous alcohol access or access to water alone, NK1R expression was increased in the nucleus accumbens (NAC) and dorsal striatum, but not the amygdala. Escalated consumption induced by intermittent access was attenuated when the NK1R antagonist L822429 was infused directly into the dorsal striatum, but not when infused into the NAC. Taken together, these results suggest that NK1R upregulation contributes to escalated alcohol consumption that is induced by genetic selection, yohimbine injection, and intermittent access. However there is a dissociation between the regions involved in these behaviors with amygdalar upregulation contributing to genetic predisposition to escalated consumption and striatal upregulation driving escalation that is induced by environmental exposures.
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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.