ArticleMolecular neurobiology2017
Loss of Adenylyl Cyclase Type-5 in the Dorsal Striatum Produces Autistic-Like Behaviors.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Pooled it
- Copper deficiency impairs oligodendrocyte maturation and social behavior via mitophagy and mTOR suppression in ASD.Science advances · 2026Article
- Artemisinin alleviates Parkinson's disease by targeting Adcy5-Gch1 axis to trigger a cascade generation of BH4 and dopamine in rats.Genome biology · 2025Article
- Lactobacillus paracasei-derived extracellular vesicles reverse molecular and behavioral deficits in mouse models of autism spectrum disorder.Experimental & molecular medicine · 2025Article
- Emotional stress increases GluA2 expression and potentiates fear memory via adenylyl cyclase 5.Cell reports · 2025Article
- A bipolar disorder-associated missense variant alters adenylyl cyclase 2 activity and promotes mania-like behavior.Molecular psychiatry · 2025Article
- Chinese acupuncture: A potential treatment for autism rat model via improving synaptic function.Heliyon · 2024Article
- Patterns of neuronal activation following ethanol-induced social facilitation and social inhibition in adolescent cFos-LacZ male and female rats.Behavioural brain research · 2024Article
- Paternal aging impacts expression and epigenetic markers as early as the first embryonic tissue lineage differentiation.Human genomics · 2024Article
- The effect of selective nigrostriatal dopamine excess on behaviors linked to the cognitive and negative symptoms of schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Exploring the common pathogenesis of Alzheimer's disease and type 2 diabetes mellitusFrontiers in aging neuroscience · 2023Article
- Continuous high-frequency deep brain stimulation of the anterior insula modulates autism-like behavior in a valproic acid-induced rat model.Journal of translational medicine · 2022Article
- The role of the dorsal striatum in a mouse model for fragile X syndrome: Behavioral and dendritic spine assessment.Brain research · 2022Article
- Transcriptomic analysis in the striatum reveals the involvement of Nurr1 in the social behavior of prenatally valproic acid-exposed male mice.Translational psychiatry · 2022Article
- Physiological roles of mammalian transmembrane adenylyl cyclase isoforms.Physiological reviews · 2022Review
- Cerebellar and Striatal Implications in Autism Spectrum Disorders: From Clinical Observations to Animal Models.International journal of molecular sciences · 2022Review
- Effects of Whole-Body Adenylyl Cyclase 5 (International journal of molecular sciences · 2021Article
- Carbamazepine Restores Neuronal Signaling, Protein Synthesis, and Cognitive Function in a Mouse Model of Fragile X Syndrome.International journal of molecular sciences · 2020Article
- Aging increases vulnerability to stress-induced depression via upregulation of NADPH oxidase in mice.Communications biology · 2020Article
- ADCY5-Related Dyskinesia: Improving Clinical Detection of an Evolving Disorder.Movement disorders clinical practice · 2019Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Autism spectrum disorders (ASDs) are a heterogeneous group of psychiatric illness characterized by common core symptoms including sociability deficits and stereotyped behaviors. ASD is caused by various genetic and non-genetic factors. The genetic effects of autism-related genes are usually global and are presented with multiple symptoms, which hamper understanding of the mechanism through which the diverse causes of ASD produce common symptoms. In the present study, we demonstrate that genetic or molecular disruption of an array of molecular networks centered on adenylyl cyclase type-5 (AC5 or ADCY5) in the dorsal striatum produces autistic-like behaviors. AC5 knockout (KO) mice exhibit increased repetitive behaviors and sociability deficits, the two core domains of ASD, and that siRNA-mediated suppression of AC5 within the dorsal striatum is sufficient to replicate these behavioral phenotypes. Notably, the autistic-like behaviors of AC5 KO mice are rescued by blocking mGluR5 glutamate receptors within the dorsal striatum. Furthermore, pharmacological or siRNA-mediated inhibition of mGluR3, GluA and GluN glutamate receptors in the dorsal striatum in wildtype mice also induces autistic-like behaviors. Optogenetic inhibition of the prelimbic cortical neurons projecting to the dorsal striatum in AC5 KO mice rescues the deficits in social and object novelty preferences. Our results suggest that AC5 mutation produces autistic-like symptoms through the upregulation of mGluR5 functions in the dorsal striatum and that the dorsal striatum regulated by AC5 is a neural correlate responsible for core ASD symptoms.
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Registered trials
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