Evidence map›Paper›PMID 40028168›Full record

ArticleFrontiers in pharmacology2025

The effect of cannabinoid type Ⅱ receptor on the excitability of substantia nigra dopaminergic neurons.

Sha Zhao, Shunfeng Liu, Yongxin Gong, Zegang Ma

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

4 authors.

Sha ZhaoDepartment of Physiology, School of Basic Medicine, Qingdao University, Qingdao, China.
Shunfeng LiuDepartment of Physiology, School of Basic Medicine, Qingdao University, Qingdao, China.
Yongxin GongDepartment of Physiology, School of Basic Medicine, Qingdao University, Qingdao, China.
Zegang MaDepartment of Physiology, School of Basic Medicine, Qingdao University, Qingdao, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biological effects of cannabinoids are mainly mediated by two members of the G-protein-coupled-receptor family: cannabinoid type 1 receptor (CB1R) and cannabinoid type 2 receptor (CB2R). Unlike CB1R, CB2R is considered a "peripheral" cannabinoid receptor. However, recent studies have found that CB2R is widely expressed in the central nervous system and is involved in dopamine related behavioral regulation, including dietary behavior, weight regulation, anxiety, and schizophrenia like behavior. Our previous laboratory research demonstrated that activating CB2R on dopaminergic neurons in the ventral tegmental area can regulate addictive behavior in animals by inhibiting neuronal excitability. However, it is currently unclear whether CB2R on dopaminergic neurons in the substantia nigra compacta (SNc) has similar therapeutic potential. Brain patch clamp results have shown that the CB2R agonist JWH133 significantly inhibits the discharge of SNc dopamine neurons in a concentration dependent manner. The pharmacological blocker AM630 of CB2R can reverse this inhibitory effect, indicating that the expression of CB2R in SNc dopaminergic neurons is functional. After treatment with JWH133, the number of induced action potentials decreased, and the peak potential interval time, action potential start time, and potential amplitude after hyperpolarization amplitude all increased. In addition, synaptic current results showed that JWH133 can significantly reduce the frequency of miniature excitatory postsynaptic currents, indicating that activating CB2R to some extent inhibits the release of presynaptic glutamate and indirectly excites postsynaptic neurons.

Indexed as

AM630cannabinoid type II receptordopamine neuronsfiring activityJWH133substantial nigra

Identifiers

PMID40028168
PMCPMC11867961

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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.