Evidence map›Paper›PMID 22956827›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Impact of prefrontal cortex in nicotine-induced excitation of ventral tegmental area dopamine neurons in anesthetized rats.

Die Zhang, Ming Gao, Dan Xu, Wei-Xing Shi, Boris S Gutkin, Scott C Steffensen, Ronald J Lukas, Jie Wu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 29 citations in OpenAlex.

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  12. HIV-1 Proteins Influence Novelty-Seeking Behavior and Alter Region-Specific Transcriptional Responses to Chronic Nicotine Treatment in HIV-1Tg Rats.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2017
    Article
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  15. Cannabinoid CB2 receptors modulate midbrain dopamine neuronal activity and dopamine-related behavior in mice.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 3 countries.

Die ZhangDivision of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona 85013-4496, USA.
Ming Gao
Dan Xu
Wei-Xing Shi
Boris S Gutkin
Scott C Steffensen
Ronald J Lukas
Jie Wu
Loma Linda University · USShantou University · CNBarrow Neurological Institute · USBrigham Young University · USInserm · FR

Funding

Nicotine and Alcohol Co-DependenceR01DA035958 · NIDA · BRIGHAM YOUNG UNIVERSITY · PI STEFFENSEN, SCOTT C · 2014 to 2018
$2.0M
Molecular Bases for Effects of NicotineR01DA015389 · NIDA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI LUKAS, RONALD J · 2003 to 2007
$1.6M
Neuroplasticity with alcohol dependenceR01AA020919 · NIAAA · BRIGHAM YOUNG UNIVERSITY · PI STEFFENSEN, SCOTT C · 2012 to 2016
$1.5M
HOMOMERIC NICOTINIC ACETYLCHOLINE RECEPTORSR01NS040417 · NINDS · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI LUKAS, RONALD J · 2000 to 2002
$1.2M
NIAAA NIH HHS R01 AA020919NIDA NIH HHS R01 DA015389NIDA NIH HHS R01 DA035958NINDS NIH HHS R01 NS040417
6 · The paper itself

Abstract

Systemic administration of nicotine increases dopaminergic (DA) neuron firing in the ventral tegmental area (VTA), which is thought to underlie nicotine reward. Here, we report that the medial prefrontal cortex (mPFC) plays a critical role in nicotine-induced excitation of VTA DA neurons. In chloral hydrate-anesthetized rats, extracellular single-unit recordings showed that VTA DA neurons exhibited two types of firing responses to systemic nicotine. After nicotine injection, the neurons with type-I response showed a biphasic early inhibition and later excitation, whereas the neurons with type-II response showed a monophasic excitation. The neurons with type-I, but not type-II, response exhibited pronounced slow oscillations (SOs) in firing. Pharmacological or structural mPFC inactivation abolished SOs and prevented systemic nicotine-induced excitation in the neurons with type-I, but not type-II, response, suggesting that these VTA DA neurons are functionally coupled to the mPFC and nicotine increases firing rate in these neurons in part through the mPFC. Systemic nicotine also increased the firing rate and SOs in mPFC pyramidal neurons. mPFC infusion of a non-α7 nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine blocked the excitatory effect of systemic nicotine on the VTA DA neurons with type-I response, but mPFC infusion of nicotine failed to excite these neurons. These results suggest that nAChR activation in the mPFC is necessary, but not sufficient, for systemic nicotine-induced excitation of VTA neurons. Finally, systemic injection of bicuculline prevented nicotine-induced firing alterations in the neurons with type-I response. We propose that the mPFC plays a critical role in systemic nicotine-induced excitation of VTA DA neurons.

Indexed as

AnesthesiaAction PotentialsAnimalsDopaminergic NeuronsMaleNicotinePrefrontal CortexRatsRats, WistarVentral Tegmental AreaNicotine

Identifiers

PMID22956827
PMCPMC3516404
OpenAlexW2157472798

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.