Asset Details
Do you wish to reserve the book?
The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and pathological brain function
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?
The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and pathological brain function
Do you wish to request the book?
The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and pathological brain function
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
The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and pathological brain function
2014
Overview
The use of specific activators and inhibitors that penetrate the central nervous system has suggested an essential functional role of L-type calcium channels (LTCC) in several important physiological processes of the brain, including the modulation of the mesoaccumbal dopamine signalling pathway, synaptic transmission of auditory stimuli and synaptic plasticity of neutral and aversive learning and memory processes. However, the lack of selectivity of available pharmacological agents towards the most prominent LTCC isoforms in the brain, namely Ca
v
1.2 and Ca
v
1.3, has hampered the elucidation of the precise contribution made by each specific channel isoform within these specific physiological processes. Modern genetic approaches, both in rodents and in human, have recently enhanced our understanding of the selective functional roles of Ca
v
1.2 and Ca
v
1.3 channels. In rodents, the characterisation of global and conditional isoform-specific knockouts suggests a contribution of Ca
v
1.2 channels in spatial memory formation, whereas Ca
v
1.3 channels seem to be involved in the consolidation of fear memories and in neurodegenerative mechanisms associated with the development of Parkinson’s disease. With regard to the molecular mechanisms underlying drug addiction, Ca
v
1.3 channels are necessary for the development and Ca
v
1.2 channels for the expression of cocaine and amphetamine behavioural sensitisation. In humans, both the identification of naturally occurring LTCC variants (“channelopathies”) and unbiased genome-wide association studies have linked LTCCs to working memory performance in healthy individuals and schizophrenic patients. Individually,
CACNA1C
polymorphisms and
CACNA1D
variants have been linked to a variety of psychiatric diseases and to congenital deafness, respectively. However, the contribution of individual LTCCs and their polymorphisms to human brain function and diseases remains unclear, necessitating the use of isoform-specific pharmacological agents.
Publisher
Springer Berlin Heidelberg
Subject
