ArticleThe Journal of physiology2010
Substance P inhibits GABAB receptor signalling in the ventral tegmental area.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- A switch in kappa opioid receptor signaling from inhibitory to excitatory induced by stress in a subset of cortically-projecting dopamine neurons.bioRxiv : the preprint server for biology · 2025Article
- An atlas of transcriptionally defined cell populations in the rat ventral tegmental area.Cell reports · 2022Article
- Ethanol antagonizes P2X4 receptors in ventral tegmental area neurons.Neuroreport · 2020Article
- Evidence and explanation for the involvement of the nucleus accumbens in pain processing.Neural regeneration research · 2020Review
- Alcohol dependence potentiates substance P/neurokinin-1 receptor signaling in the rat central nucleus of amygdala.Science advances · 2020Article
- Article
- Calcium Release from Stores Inhibits GIRK.Cell reports · 2016Article
- Substance P excites GABAergic neurons in the mouse central amygdala through neurokinin 1 receptor activation.Journal of neurophysiology · 2015Article
- Nicotine enhances excitability of medial habenular neurons via facilitation of neurokinin signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Reversal of inhibition of putative dopaminergic neurons of the ventral tegmental area: interaction of GABA(B) and D2 receptors.Neuroscience · 2012Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substance P (SP) and its receptors are involved in anxiety-related behaviours and regulate the intake of drugs of abuse and alcohol. Within the midbrain ventral tegmental area (VTA), a region that is clearly involved in the control of these behaviours, SP is released by stress and has been shown to trigger relapse. SP activates neurokinin (NK) receptors, which excites midbrain dopamine (DA) neurons and leads to increased DA in target regions. In this study, we have investigated the mechanisms underlying SP actions in the VTA, specifically investigating interactions between SP and GABA(B) receptors. We show that in VTA neurons, NK receptor activation closes an inwardly rectifying potassium channel, and moreover inhibits GABA(B) receptor-mediated transmission through an interaction that depends upon phospholipase C (PLC), intracellular calcium and protein kinase C (PKC).
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What OpenQuestion holds
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.