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Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning
L‐type voltage‐gated calcium channels are important regulators of neuronal activity and are widely expressed throughout the brain. One of the major L‐type voltage‐gated calcium channel isoforms in the brain is Ca(V)1.3. Mice lacking Ca(V)1.3 are reported to have impairments in fear conditioning and...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9744532/ https://www.ncbi.nlm.nih.gov/pubmed/35044095 http://dx.doi.org/10.1111/gbb.12791 |
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author | Lauffer, Marisol Wen, Hsiang Myers, Bryn Plumb, Ashley Parker, Krystal Williams, Aislinn |
author_facet | Lauffer, Marisol Wen, Hsiang Myers, Bryn Plumb, Ashley Parker, Krystal Williams, Aislinn |
author_sort | Lauffer, Marisol |
collection | PubMed |
description | L‐type voltage‐gated calcium channels are important regulators of neuronal activity and are widely expressed throughout the brain. One of the major L‐type voltage‐gated calcium channel isoforms in the brain is Ca(V)1.3. Mice lacking Ca(V)1.3 are reported to have impairments in fear conditioning and depressive‐like behaviors, which have been linked to Ca(V)1.3 function in the hippocampus and amygdala. Genetic variation in Ca(V)1.3 has been linked to a variety of psychiatric disorders, including autism and schizophrenia, which are associated with altered motor learning, associative learning and social function. Here, we explored whether Ca(V)1.3 plays a role in these behaviors. We found that Ca(V)1.3 knockout mice have deficits in rotarod learning despite normal locomotor function. Deletion of Ca(V)1.3 is also associated with impaired gait adaptation and associative learning on the Erasmus Ladder. We did not observe any impairments in Ca(V)1.3 knockout mice on assays of anxiety‐like, depression‐like or social preference behaviors. Our results suggest an important role for Ca(V)1.3 in neural circuits involved in motor learning and concur with previous data showing its involvement in associative learning. |
format | Online Article Text |
id | pubmed-9744532 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-97445322023-02-08 Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning Lauffer, Marisol Wen, Hsiang Myers, Bryn Plumb, Ashley Parker, Krystal Williams, Aislinn Genes Brain Behav Original Articles L‐type voltage‐gated calcium channels are important regulators of neuronal activity and are widely expressed throughout the brain. One of the major L‐type voltage‐gated calcium channel isoforms in the brain is Ca(V)1.3. Mice lacking Ca(V)1.3 are reported to have impairments in fear conditioning and depressive‐like behaviors, which have been linked to Ca(V)1.3 function in the hippocampus and amygdala. Genetic variation in Ca(V)1.3 has been linked to a variety of psychiatric disorders, including autism and schizophrenia, which are associated with altered motor learning, associative learning and social function. Here, we explored whether Ca(V)1.3 plays a role in these behaviors. We found that Ca(V)1.3 knockout mice have deficits in rotarod learning despite normal locomotor function. Deletion of Ca(V)1.3 is also associated with impaired gait adaptation and associative learning on the Erasmus Ladder. We did not observe any impairments in Ca(V)1.3 knockout mice on assays of anxiety‐like, depression‐like or social preference behaviors. Our results suggest an important role for Ca(V)1.3 in neural circuits involved in motor learning and concur with previous data showing its involvement in associative learning. Blackwell Publishing Ltd 2022-01-19 /pmc/articles/PMC9744532/ /pubmed/35044095 http://dx.doi.org/10.1111/gbb.12791 Text en © 2021 The Authors. Genes, Brain and Behavior published by International Behavioural and Neural Genetics Society and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Lauffer, Marisol Wen, Hsiang Myers, Bryn Plumb, Ashley Parker, Krystal Williams, Aislinn Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning |
title | Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning |
title_full | Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning |
title_fullStr | Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning |
title_full_unstemmed | Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning |
title_short | Deletion of the voltage‐gated calcium channel, Ca(V)1.3, causes deficits in motor performance and associative learning |
title_sort | deletion of the voltage‐gated calcium channel, ca(v)1.3, causes deficits in motor performance and associative learning |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9744532/ https://www.ncbi.nlm.nih.gov/pubmed/35044095 http://dx.doi.org/10.1111/gbb.12791 |
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