ArticleFrontiers in behavioral neuroscience2011
Unraveling the differential functions and regulation of striatal neuron sub-populations in motor control, reward, and motivational processes.
Article in Frontiers in behavioral neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 35 citations in OpenAlex.
- Deletion of N-ethylmaleimide-sensitive factor in dopamine D2 receptor-expressing cells impairs striatal development and dopaminergic function and induces ADHD-like behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Personalized neural responses to self and filial reward: Functional and structural responses to motivational cues.AIMS neuroscience · 2025Article
- The respective activation and silencing of striatal direct and indirect pathway neurons support behavior encoding.Nature communications · 2023Article
- Evolutionarily conservative and non-conservative regulatory networks during primate interneuron development revealed by single-cell RNA and ATAC sequencing.Cell research · 2022Article
- Insights into the Promising Prospect of G Protein and GPCR-Mediated Signaling in Neuropathophysiology and Its Therapeutic Regulation.Oxidative medicine and cellular longevity · 2022Review
- Article
- Higher levels of (Internet) Gaming Disorder symptoms according to the WHO and APA frameworks associate with lower striatal volume.Journal of behavioral addictions · 2020Article
- Potential Utility of Biased GPCR Signaling for Treatment of Psychiatric Disorders.International journal of molecular sciences · 2019Review
- Adenosine Augmentation Evoked by an ENT1 Inhibitor Improves Memory Impairment and Neuronal Plasticity in the APP/PS1 Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2018Article
- Shaping vulnerability to addiction - the contribution of behavior, neural circuits and molecular mechanisms.Neuroscience and biobehavioral reviews · 2018Review
- Neuro-psychopharmacological perspective of Orphan receptors of Rhodopsin (class A) family of G protein-coupled receptors.Psychopharmacology · 2017Review
- Viral vector-based tools advance knowledge of basal ganglia anatomy and physiology.Journal of neurophysiology · 2016Review
- A human brain atlas derived via n-cut parcellation of resting-state and task-based fMRI data.Magnetic resonance imaging · 2016Article
- Cholinergic interneurons in the dorsal and ventral striatum: anatomical and functional considerations in normal and diseased conditions.Annals of the New York Academy of Sciences · 2015Review
- Novel Therapeutic GPCRs for Psychiatric Disorders.International journal of molecular sciences · 2015Review
- Article
- Motor Skill Learning Is Associated with Phase-Dependent Modifications in the Striatal cAMP/PKA/DARPP-32 Signaling Pathway in Rodents.PloS one · 2015Article
- Striatal enkephalinergic differences in rats selectively bred for intrinsic running capacity.Brain research · 2014Article
- Article
- Adenosine signaling in striatal circuits and alcohol use disorders.Molecules and cells · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The striatum, the major input structure of the basal ganglia, is critically involved in motor control and learning of habits and skills, and is also involved in motivational and reward processes. The dorsal striatum, caudate-putamen, is primarily implicated in motor functions whereas the ventral striatum, the nucleus accumbens, is essential for motivation and drug reinforcement. Severe basal ganglia dysfunction occurs in movement disorders as Parkinson's and Huntington's disease, and in psychiatric disorders such as schizophrenia and drug addiction. The striatum is essentially composed of GABAergic medium-sized spiny neurons (MSNs) that are output neurons giving rise to the so-called direct and indirect pathways and are targets of the cerebral cortex and mesencephalic dopaminergic neurons. Although the involvement of striatal sub-areas in motor control and motivation has been thoroughly characterized, major issues remained concerning the specific and respective functions of the two MSNs sub-populations, D(2)R-striatopallidal (dopamine D(2) receptor-positive) and D(1)R-striatonigral (dopamine D(1) receptor-positive) neurons, as well as their specific regulation. Here, we review recent advances that gave new insight in the understanding of the differential roles of striatopallidal and striatonigral neurons in the basal ganglia circuit. We discuss innovative techniques developed in the last decade which allowed a much precise evaluation of molecular pathways implicated in motivational processes and functional roles of striatopallidal and striatonigral neurons in motor control and in the establishment of reward-associated behavior.
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.