ArticleACS chemical neuroscience2015
Loss of dopamine D2 receptors increases parvalbumin-positive interneurons in the anterior cingulate cortex.
Article in ACS chemical neuroscience, 2015. 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
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.
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.
Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Prenatal fentanyl exposure affects social dominance and myelination patterns in the adult mouse brain.Neuropharmacology · 2025Article
- Article
- Network pharmacology combined with experimental verification for exploring the potential mechanism of phellodendrine against depression.Scientific reports · 2025Article
- Activation of dopamine 2 receptors modulates glutamate decarboxylases 65 and 67 during stroke recovery in mice.Neuroprotection (Chichester, England) · 2023Article
- Crosstalk between the endocannabinoid and mid-brain dopaminergic systems: Implication in dopamine dysregulation.Frontiers in behavioral neuroscience · 2023Review
- Dysregulated neuromodulation in the anterior cingulate cortex in chronic pain.Frontiers in pharmacology · 2023Review
- Dysregulation of brain dopamine systems in major depressive disorder.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Behavioral and Neuroanatomical Consequences of Cell-Type Specific Loss of Dopamine D2 Receptors in the Mouse Cerebral Cortex.Frontiers in behavioral neuroscience · 2021Article
- A novel mouse model of glucagon-like peptide-1 receptor expression: A look at the brain.The Journal of comparative neurology · 2020Article
- Deletion of Gαq in the telencephalon alters specific neurobehavioral outcomes.Synapse (New York, N.Y.) · 2015Article
- Long-term functional alterations following prenatal GLP-1R activation.Neurotoxicology and teratologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Disruption to dopamine homeostasis during brain development has been implicated in a variety of neuropsychiatric disorders, including depression and schizophrenia. Inappropriate expression or activity of GABAergic interneurons are common features of many of these disorders. We discovered a persistent upregulation of GAD67+ and parvalbumin+ neurons within the anterior cingulate cortex of dopamine D2 receptor knockout mice, while other GABAergic interneuron markers were unaffected. Interneuron distribution and number were not altered in the striatum or in the dopamine-poor somatosensory cortex. The changes were already present by postnatal day 14, indicating a developmental etiology. D2eGFP BAC transgenic mice demonstrated the presence of D2 receptor expression within a subset of parvalbumin-expressing cortical interneurons, suggesting the possibility of a direct cellular mechanism through which D2 receptor stimulation regulates interneuron differentiation or survival. D2 receptor knockout mice also exhibited decreased depressive-like behavior compared with wild-type controls in the tail suspension test. These data indicate that dopamine signaling modulates interneuron number and emotional behavior and that developmental D2 receptor loss or blockade could reveal a potential mechanism for the prodromal basis of neuropsychiatric disorders.
Indexed as
Identifiers
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.