Calcyon upregulation in adolescence impairs response inhibition and working memory in adulthood
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Calcyon regulates activity-dependent internalization of α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) glutamate receptors and long-term depression of excitatory synapses. Elevated levels of calcyon are consistently observed in brains from schizophrenic patients, and the calcyon gene is associated with attention-deficit hyperactivity disorder. Executive function deficits are common to both disorders, and at least for schizophrenia, the etiology appears to involve both heritable and neurodevelopmental factors. Here, we show with calcyon-overexpressing Cal(OE) transgenic mice that lifelong calcyon upregulation impairs executive functions including response inhibition and working memory, without producing learning and memory deficits in general. As response inhibition and working memory, as well as the underlying neural circuitry, continue to mature into early adulthood, we functionally silenced the transgene during postnatal days 28-49, a period corresponding to adolescence. Remarkably, the response inhibition and working memory deficits including perseverative behavior were absent in adult Cal(OE) mice with the transgene silenced in adolescence. Suppressing the calcyon transgene in adulthood only partially rescued the deficits, suggesting calcyon upregulation in adolescence irreversibly alters development of neural circuits supporting mature response inhibition and working memory. Brain regional immunoblots revealed a prominent downregulation of AMPA GluR1 subunits in hippocampus and GluR2/3 subunits in hippocampus and prefrontal cortex of the Cal(OE) mice. Silencing the transgene in adolescence prevented the decrease in hippocampal GluR1, further implicating altered fronto-hippocampal connectivity in the executive function deficits observed in the Cal(OE) mice. Treatments that mitigate the effects of high levels of calcyon during adolescence could preempt adult deficits in executive functions in individuals at risk for serious mental illness.
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Calcyon over-expression over the lifetime of the mouse resulted in marked impairment of contextual fear extinction (CFE) and working memory capacity, both dependent on normal PFC function.
“Vazdarjanova et al.133 utilized a transgenic mouse that over-expresses calcyon, a protein which mediates activity-dependent AMPAR internalization, and found that calcyon over-expression over the lifetime of the mouse resulted in marked impairment of contextual fear extinction (CFE) and working memory capacity, both dependent on normal PFC function.”
From A role for synaptic plasticity in the adolescent development of executive function (2013) · cites this paper as [133]
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Network‐Assisted Investigation of Antipsychotic Drugs and Their Targets
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- Authors
- Vazdarjanova, A., Bunting, K., Muthusamy, N., & Bergson, C.
- Corresponding author
- Vazdarjanova, A
- Bergson, C
- Venue
- Molecular Psychiatry
- Published
- 2011-03-15
- Volume
- 16
- Issue
- 6
- Pages
- 672-684
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC4076415
- OpenAlex
- W1976782226
- Cited by
- 20
- References
- 88
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 1 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 1 · 2014: 2 · 2013: 2 · 2012: 4
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense
- Medical College of Wisconsin
- National Institutes of Health
- National Institute of Mental Health (R01MH063271, P50MH068789, R21MH083188)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- AMPA receptor internalization, long-term depression, response inhibition, working memory, executive function, adolescence, transgene silencing, hippocampus, prefrontal cortex, perseveration, schizophrenia, attention deficit hyperactivity disorder, brain development, transgenic mice
- MeSH terms
- Animals, Animals, Newborn, Conditioning, Psychological, Disease Models, Animal, Doxycycline, Extinction, Psychological, Fear, Humans, Inhibition, Psychological, Membrane Proteins, Memory Disorders, Memory, Short-Term, Mice, Transgenic, Space Perception, Up-Regulation, Receptors, AMPA, Maze Learning, Mice, Calcium-Calmodulin-Dependent Protein Kinase Kinase
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