ArticleHuman molecular genetics2021
Cognitive deficits in episodic ataxia type 2 mouse models.
Article in Human molecular genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Neural Correlates of Intellectual Dysfunction in Episodic Ataxia Type 2.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Episodic Ataxia Type 2 Presenting with Fluctuating Weakness in a Child with a De Novo CACNA1A Variant.Children (Basel, Switzerland) · 2026Article
- CACNA1A haploinsufficiency leads to reduced synaptic function and increased intrinsic excitability.Brain : a journal of neurology · 2025Article
- Chemogenetic Modulation of Astrocytic Activity Rescues Hippocampus Associated Neurodegeneration in Alzheimer's Disease Mice Model 5xFAD.Neural plasticity · 2025Article
- Intellectual Disability in Episodic Ataxia Type 2: Beyond Paroxysmal Vertigo and Ataxia.Journal of clinical neurology (Seoul, Korea) · 2024Article
- A combination of chlorzoxazone and folic acid improves recognition memory, anxiety and depression in SCA3-84Q mice.Human molecular genetics · 2024Article
- Impairments of cerebellar structure and function in a zebrafish KO of neuropsychiatric risk gene znf536.Translational psychiatry · 2024Article
- Memory decline, anxiety and depression in the mouse model of spinocerebellar ataxia type 3.Human molecular genetics · 2024Article
- Cognitive Decline and Mood Alterations in the Mouse Model of Spinocerebellar Ataxia Type 2.Cerebellum (London, England) · 2024Article
- A chlorzoxazone-folic acid combination improves cognitive affective decline in SCA2-58Q mice.Scientific reports · 2023Article
- Experimental Treatment with Edaravone in a Mouse Model of Spinocerebellar Ataxia 1.International journal of molecular sciences · 2023Article
- Cerebellar contribution to threat probability in a SCA6 mouse model.Human molecular genetics · 2022Article
- Deletion of the P/Q-Type Calcium Channel from Serotonergic Neurons Drives Male Aggression in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Episodic ataxia type 2 (EA2) is a rare autosomal dominant disorder characterized by motor incoordination, paroxysmal dystonia, vertigo, nystagmus and more recently cognitive deficits. To date over 100 mutations in the CACNA1A gene have been identified in EA2 patients leading to a loss of P/Q-type channel activity, dysfunction of cerebellar Purkinje cells and motor incoordination. To determine if the cerebellum is contributing to these cognitive deficits, we examined two different EA2 mouse models for cognition impairments where CACNA1A was removed specifically from cerebellar Purkinje or granule cells postnatally. Both mutant mouse models showed anxiolytic behavior to lighted, open areas in the open field and light/dark place preference tests but enhanced anxiousness in the novel suppressed feeding test. However, EA2 mice continued to show augmented latencies in the light/dark preference test and when the arena was divided into two dark zones in the dark/dark preference test. Moreover, increased latencies were also displayed in the novel object recognition test, indicating that EA2 mice are indecisive and anxious to explore new territories and objects and may have memory recognition deficits. Exposure to a foreign mouse led to deficiencies in attention and sniffing as well as in social and genital sniffing. These data suggest that postnatal removal of the P/Q type calcium channel from the cerebellum regulates neuronal activity involved in anxiety, memory, decision making and social interactions. Our EA2 mice will provide a model to identify the mechanisms and therapeutic agents underlying cognitive and psychiatric disorders seen in EA2 patients.
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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.