ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996
Mouse model of hyperkinesis implicates SNAP-25 in behavioral regulation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.
- The Association of SNAP25 Gene Polymorphisms in Attention Deficit/Hyperactivity Disorder: a Systematic Review and Meta-Analysis.Molecular neurobiology · 2017Pooled it
- Efficacy and safety of lisdexamfetamine dimesylate in children with attention-deficit/hyperactivity disorder and recent methylphenidate use.Advances in therapy · 2013Trial
- Animal models for the study of ADHD: the need for next-generation models.Frontiers in psychiatry · 2026Review
- Unraveling Predominantly Inattentive ADHD (ADHD-PI): Insights from Proteomic Analysis of the Striatum of Thyroid Hormone-Responsive Protein (THRSP)-Overexpressing Mice.Molecular neurobiology · 2025Article
- Rodent research of attention-deficit/hyperactivity disorder: insights into widely used animal models.Laboratory animal research · 2025Review
- Review
- Transcriptomic Dysregulation in Animal Models of Attention-Deficit Hyperactivity Disorder and Nicotine Dependence Suggests Shared Neural Mechanisms.Brain and behavior · 2025Article
- An updated review on animal models to study attention-deficit hyperactivity disorder.Translational psychiatry · 2024Review
- The role of snare proteins in cortical development.Developmental neurobiology · 2022Review
- Modelling Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) Using Mice and Zebrafish.International journal of molecular sciences · 2022Review
- Review of rodent models of attention deficit hyperactivity disorder.Neuroscience and biobehavioral reviews · 2022Review
- Article
- Animal Models of ADHD?Current topics in behavioral neurosciences · 2022Article
- ADHD-like behaviors caused by inactivation of a transcription factor controlling the balance of inhibitory and excitatory neuron development in the mouse anterior brainstem.Translational psychiatry · 2020Article
- Neonatal 6-OHDA Lesion Model in Mouse Induces Cognitive Dysfunctions of Attention-Deficit/Hyperactivity Disorder (ADHD) During Young Age.Frontiers in behavioral neuroscience · 2020Article
- Localising movement disorders in childhood.The Lancet. Child & adolescent health · 2019Review
- Article
- Restoration of Cdk5, TrkB and Soluble N-ethylmaleimide-Sensitive Factor Attachment Protein Receptor Proteins after Chronic Methylphenidate Treatment in Spontaneous Hypertensive Rats, a Model for Attention-Deficit Hyperactivity Disorder.Psychiatry investigation · 2019Article
- Cell-Specific Loss of SNAP25 from Cortical Projection Neurons Allows Normal Development but Causes Subsequent Neurodegeneration.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Exploring the Validity of Proposed Transgenic Animal Models of Attention-Deficit Hyperactivity Disorder (ADHD).Molecular neurobiology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Although hyperkinesis is expressed in several neurological disorders, the biological basis of this phenotype is unknown. The mouse mutant coloboma (Cml+) exhibits profound spontaneous locomotor hyperactivity resulting from a deletion mutation. This deletion encompasses several genes including Snap, which encodes SNAP-25, a nerve terminal protein involved in neurotransmitter release. Administration of amphetamine, a drug that acts presynaptically, markedly reduced the locomotor activity in coloboma mice but increased the activity of control mice implicating presynaptic function in the behavioral abnormality. In contrast, the psychostimulant methylphenidate increased locomotor activity in both coloboma and control mice. When a transgene encoding SNAP-25 was bred into the coloboma strain to complement the Snap deletion, the hyperactivity expressed by these mice was rescued, returning these corrected mice to normal levels of locomotor activity. These results demonstrate that the hyperactivity exhibited by these mice is the result of abnormalities in presynaptic function specifically attributable to deficits in SNAP-25 expression.
Indexed as
Identifiers
8622140PMC6579059W1908021040What 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.