Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia

Abstract The voltage-gated calcium channel (VGCC) subunit complex is comprised of the α1 subunit, the ion-permeable channel, and three auxiliary subunits: β, α2δ, and γ. β is the most extensively studied auxiliary subunit and is necessary for forward trafficking of the α1 subunit to the plasma membr...

Full description

Saved in:
Bibliographic Details
Main Authors: Emily M. Parker, Nathan L. Kindja, Rebecca A. DeGiosio, Ryan B. Salisbury, Josh M. Krivinko, Claire E. J. Cheetham, Matthew L. MacDonald, Weijia Fan, Bin Cheng, Robert A. Sweet
Format: Article
Language:English
Published: Nature Publishing Group 2024-12-01
Series:Translational Psychiatry
Online Access:https://doi.org/10.1038/s41398-024-03181-7
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850136839405436928
author Emily M. Parker
Nathan L. Kindja
Rebecca A. DeGiosio
Ryan B. Salisbury
Josh M. Krivinko
Claire E. J. Cheetham
Matthew L. MacDonald
Weijia Fan
Bin Cheng
Robert A. Sweet
author_facet Emily M. Parker
Nathan L. Kindja
Rebecca A. DeGiosio
Ryan B. Salisbury
Josh M. Krivinko
Claire E. J. Cheetham
Matthew L. MacDonald
Weijia Fan
Bin Cheng
Robert A. Sweet
author_sort Emily M. Parker
collection DOAJ
description Abstract The voltage-gated calcium channel (VGCC) subunit complex is comprised of the α1 subunit, the ion-permeable channel, and three auxiliary subunits: β, α2δ, and γ. β is the most extensively studied auxiliary subunit and is necessary for forward trafficking of the α1 subunit to the plasma membrane. VGCCs mediate voltage-dependent movement of calcium ions into neuronal cytoplasm, including at dendrites, where intracellular calcium spikes initiate signaling cascades that shape the structural plasticity of dendritic spines. Genetic studies strongly implicate calcium signaling dysfunction in the etiology of neurodevelopmental disorders including schizophrenia. Dendritic spine density is significantly decreased in schizophrenia in the primary auditory cortex where it is driven by the loss of small spines, and small spine loss associated with increased peptide levels of ALFDFLK found in the VGCC β subunit β4. Overexpressing the gene that encodes the voltage-gated calcium channel subunit β4, CACNB4, selectively reduced small spine density in vitro. In the current study we extended this observation in an intact mammalian system within a relevant neurodevelopmental context. We overexpressed CACNB4 in early development, assessed spine density and morphology in adult male and female mouse cortex, and characterized β1-4 protein levels and β4 protein-protein interactions. Overexpression reduced small spine density in females. This effect was not dependent on the estrous stage. Instead, it corresponded to sex differences in the murine β4 interactome. The VGCC subunit β1b was significantly enriched in the β4 interactome of male relative to female mice, and thus may have served to mitigate VGCC overexpression-mediated spine loss in male mice.
format Article
id doaj-art-cd8e4bb070fd4d37975c26a69ca13f45
institution OA Journals
issn 2158-3188
language English
publishDate 2024-12-01
publisher Nature Publishing Group
record_format Article
series Translational Psychiatry
spelling doaj-art-cd8e4bb070fd4d37975c26a69ca13f452025-08-20T02:31:00ZengNature Publishing GroupTranslational Psychiatry2158-31882024-12-0114111110.1038/s41398-024-03181-7Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophreniaEmily M. Parker0Nathan L. Kindja1Rebecca A. DeGiosio2Ryan B. Salisbury3Josh M. Krivinko4Claire E. J. Cheetham5Matthew L. MacDonald6Weijia Fan7Bin Cheng8Robert A. Sweet9Center for Neuroscience, University of PittsburghTranslational Neuroscience Program, University of PittsburghCenter for Neuroscience, University of PittsburghTranslational Neuroscience Program, University of PittsburghTranslational Neuroscience Program, University of PittsburghCenter for Neuroscience, University of PittsburghCenter for Neuroscience, University of PittsburghDepartment of Biostatistics, Columbia UniversityDepartment of Biostatistics, Columbia UniversityCenter for Neuroscience, University of PittsburghAbstract The voltage-gated calcium channel (VGCC) subunit complex is comprised of the α1 subunit, the ion-permeable channel, and three auxiliary subunits: β, α2δ, and γ. β is the most extensively studied auxiliary subunit and is necessary for forward trafficking of the α1 subunit to the plasma membrane. VGCCs mediate voltage-dependent movement of calcium ions into neuronal cytoplasm, including at dendrites, where intracellular calcium spikes initiate signaling cascades that shape the structural plasticity of dendritic spines. Genetic studies strongly implicate calcium signaling dysfunction in the etiology of neurodevelopmental disorders including schizophrenia. Dendritic spine density is significantly decreased in schizophrenia in the primary auditory cortex where it is driven by the loss of small spines, and small spine loss associated with increased peptide levels of ALFDFLK found in the VGCC β subunit β4. Overexpressing the gene that encodes the voltage-gated calcium channel subunit β4, CACNB4, selectively reduced small spine density in vitro. In the current study we extended this observation in an intact mammalian system within a relevant neurodevelopmental context. We overexpressed CACNB4 in early development, assessed spine density and morphology in adult male and female mouse cortex, and characterized β1-4 protein levels and β4 protein-protein interactions. Overexpression reduced small spine density in females. This effect was not dependent on the estrous stage. Instead, it corresponded to sex differences in the murine β4 interactome. The VGCC subunit β1b was significantly enriched in the β4 interactome of male relative to female mice, and thus may have served to mitigate VGCC overexpression-mediated spine loss in male mice.https://doi.org/10.1038/s41398-024-03181-7
spellingShingle Emily M. Parker
Nathan L. Kindja
Rebecca A. DeGiosio
Ryan B. Salisbury
Josh M. Krivinko
Claire E. J. Cheetham
Matthew L. MacDonald
Weijia Fan
Bin Cheng
Robert A. Sweet
Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia
Translational Psychiatry
title Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia
title_full Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia
title_fullStr Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia
title_full_unstemmed Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia
title_short Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia
title_sort impacts of cacnb4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia
url https://doi.org/10.1038/s41398-024-03181-7
work_keys_str_mv AT emilymparker impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT nathanlkindja impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT rebeccaadegiosio impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT ryanbsalisbury impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT joshmkrivinko impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT claireejcheetham impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT matthewlmacdonald impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT weijiafan impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT bincheng impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia
AT robertasweet impactsofcacnb4overexpressionondendriticspinedensityinbothsexesandrelevancetoschizophrenia