Asset Details
Do you wish to reserve the book?
Neuronal deletion of CaV1.2 is associated with sex-specific behavioral phenotypes in mice
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Neuronal deletion of CaV1.2 is associated with sex-specific behavioral phenotypes in mice
Do you wish to request the book?
Neuronal deletion of CaV1.2 is associated with sex-specific behavioral phenotypes in mice
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Neuronal deletion of CaV1.2 is associated with sex-specific behavioral phenotypes in mice
2022
Overview
The gene
CACNA1C
, which encodes the pore forming subunit of the L-type calcium channel Ca
V
1.2, is associated with increased risk for neuropsychiatric disorders including schizophrenia, autism spectrum disorder, major depression, and bipolar disorder. Previous rodent work identified that loss or reduction of Ca
V
1.2 results in cognitive, affective, and motor deficits. Most previous work has either included non-neuronal cell populations (haploinsufficient and Nestin-Cre) or investigated a discrete neuronal cell population (e.g. CaMKII-Cre, Drd1-Cre), but few studies have examined the effects of more broad neuron-specific deletion of Ca
V
1.2. Additionally, most of these studies did not evaluate for sex-specific effects or used only male animals. Here, we sought to clarify whether there are sex-specific behavioral consequences of neuron-specific deletion of Ca
V
1.2 (neuronal Ca
V
1.2 cKO) using Syn1-Cre-mediated conditional deletion. We found that neuronal Ca
V
1.2 cKO mice have normal baseline locomotor function but female cKO mice display impaired motor performance learning. Male neuronal Ca
V
1.2 cKO display impaired startle response with intact pre-pulse inhibition. Male neuronal Ca
V
1.2 cKO mice did not display normal social preference, whereas female neuronal Ca
V
1.2 cKO mice did. Neuronal Ca
V
1.2 cKO mice displayed impaired associative learning in both sexes, as well as normal anxiety-like behavior and hedonic capacity. We conclude that deletion of neuronal Ca
V
1.2 alters motor performance, acoustic startle reflex, and social behaviors in a sex-specific manner, while associative learning deficits generalize across sexes. Our data provide evidence for both sex-specific and sex-independent phenotypes related to neuronal expression of Ca
V
1.2.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
