Enhanced long-term potentiation and impaired learning in mice lacking alternative exon 33 of CaV1.2 calcium channel

The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the Ca V 1.2 channel is a prominent risk gene for neuropsychiatric and neurodegenerative disorders with cognitive and social impairments like schizophrenia, bipolar disorders, depression and autistic spectrum disorders (...

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Published inTranslational psychiatry Vol. 12; no. 1; p. 1
Main Authors Navakkode, Sheeja, Zhai, Jing, Wong, Yuk Peng, Li, Guang, Soong, Tuck Wah
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 10.01.2022
Nature Publishing Group
Subjects
631/378/1595/2167
64/60
692/699
9/30
Behavioral Sciences
Biological Psychology
Bipolar disorder
Medicine
Medicine & Public Health
Neurosciences
Pharmacotherapy
Psychiatry
Schizophrenia
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Abstract The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the Ca V 1.2 channel is a prominent risk gene for neuropsychiatric and neurodegenerative disorders with cognitive and social impairments like schizophrenia, bipolar disorders, depression and autistic spectrum disorders (ASD). We have shown previously that mice with exon 33 deleted from Ca V 1.2 channel (Ca V 1.2-exon 33 −/− ) displayed increased Ca V 1.2 current density and single channel open probability in cardiomyocytes, and were prone to develop arrhythmia. As Ca 2+ entry through Ca V 1.2 channels activates gene transcription in response to synaptic activity, we were intrigued to explore the possible role of Cav1.2 Δ 33 channels in synaptic plasticity and behaviour. Homozygous deletion of alternative exon 33 resulted in enhanced long-term potentiation (LTP), and lack of long- term depression (LTD), which did not correlate with enhanced learning. Exon 33 deletion also led to a decrease in social dominance, sociability and social novelty. Our findings shed light on the effect of gain-of-function of Ca V 1.2 Δ 33 signalling on synaptic plasticity and behaviour and provides evidence for a link between Ca V 1.2 and distinct cognitive and social behaviours associated with phenotypic features of psychiatric disorders like schizophrenia, bipolar disorder and ASD.
AbstractList Abstract The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the CaV1.2 channel is a prominent risk gene for neuropsychiatric and neurodegenerative disorders with cognitive and social impairments like schizophrenia, bipolar disorders, depression and autistic spectrum disorders (ASD). We have shown previously that mice with exon 33 deleted from CaV1.2 channel (CaV1.2-exon 33−/−) displayed increased CaV1.2 current density and single channel open probability in cardiomyocytes, and were prone to develop arrhythmia. As Ca2+ entry through CaV1.2 channels activates gene transcription in response to synaptic activity, we were intrigued to explore the possible role of Cav1.2Δ 33 channels in synaptic plasticity and behaviour. Homozygous deletion of alternative exon 33 resulted in enhanced long-term potentiation (LTP), and lack of long- term depression (LTD), which did not correlate with enhanced learning. Exon 33 deletion also led to a decrease in social dominance, sociability and social novelty. Our findings shed light on the effect of gain-of-function of CaV1.2Δ 33 signalling on synaptic plasticity and behaviour and provides evidence for a link between CaV1.2 and distinct cognitive and social behaviours associated with phenotypic features of psychiatric disorders like schizophrenia, bipolar disorder and ASD.
The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the CaV1.2 channel is a prominent risk gene for neuropsychiatric and neurodegenerative disorders with cognitive and social impairments like schizophrenia, bipolar disorders, depression and autistic spectrum disorders (ASD). We have shown previously that mice with exon 33 deleted from CaV1.2 channel (CaV1.2-exon 33−/−) displayed increased CaV1.2 current density and single channel open probability in cardiomyocytes, and were prone to develop arrhythmia. As Ca2+ entry through CaV1.2 channels activates gene transcription in response to synaptic activity, we were intrigued to explore the possible role of Cav1.2Δ33 channels in synaptic plasticity and behaviour. Homozygous deletion of alternative exon 33 resulted in enhanced long-term potentiation (LTP), and lack of long- term depression (LTD), which did not correlate with enhanced learning. Exon 33 deletion also led to a decrease in social dominance, sociability and social novelty. Our findings shed light on the effect of gain-of-function of CaV1.2Δ33 signalling on synaptic plasticity and behaviour and provides evidence for a link between CaV1.2 and distinct cognitive and social behaviours associated with phenotypic features of psychiatric disorders like schizophrenia, bipolar disorder and ASD.
The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the Ca V 1.2 channel is a prominent risk gene for neuropsychiatric and neurodegenerative disorders with cognitive and social impairments like schizophrenia, bipolar disorders, depression and autistic spectrum disorders (ASD). We have shown previously that mice with exon 33 deleted from Ca V 1.2 channel (Ca V 1.2-exon 33 −/− ) displayed increased Ca V 1.2 current density and single channel open probability in cardiomyocytes, and were prone to develop arrhythmia. As Ca 2+ entry through Ca V 1.2 channels activates gene transcription in response to synaptic activity, we were intrigued to explore the possible role of Cav1.2 Δ 33 channels in synaptic plasticity and behaviour. Homozygous deletion of alternative exon 33 resulted in enhanced long-term potentiation (LTP), and lack of long- term depression (LTD), which did not correlate with enhanced learning. Exon 33 deletion also led to a decrease in social dominance, sociability and social novelty. Our findings shed light on the effect of gain-of-function of Ca V 1.2 Δ 33 signalling on synaptic plasticity and behaviour and provides evidence for a link between Ca V 1.2 and distinct cognitive and social behaviours associated with phenotypic features of psychiatric disorders like schizophrenia, bipolar disorder and ASD.
ArticleNumber 1
Author Zhai, Jing
Wong, Yuk Peng
Li, Guang
Navakkode, Sheeja
Soong, Tuck Wah
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  givenname: Tuck Wah
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  organization: Department of Physiology, National University of Singapore, Healthy Longevity Research Programme, Yong Loo Lin School of Medicine, National University of Singapore
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SSID ssj0000548171
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Snippet The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the Ca V 1.2 channel is a prominent risk gene for neuropsychiatric and...
The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the CaV1.2 channel is a prominent risk gene for neuropsychiatric and...
Abstract The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the CaV1.2 channel is a prominent risk gene for neuropsychiatric and...
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Behavioral Sciences
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Title Enhanced long-term potentiation and impaired learning in mice lacking alternative exon 33 of CaV1.2 calcium channel
URI https://link.springer.com/article/10.1038/s41398-021-01683-2
https://www.proquest.com/docview/2618381968
https://search.proquest.com/docview/2618915984
https://pubmed.ncbi.nlm.nih.gov/PMC8748671
https://doaj.org/article/dd73fb88640c468987fe77c0e7a05eb1
Volume 12
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