Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 34, Issue -, Pages 903-909Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST0340903
Keywords
brain function; Ca2+ channel; cardiovascular disease; central nervous system; dihydropyridine; voltage-gated L-type Ca2+ channel
Categories
Funding
- Austrian Science Fund FWF [P 17159, P 17109] Funding Source: Medline
Ask authors/readers for more resources
Voltage-gated LTCCs (L-type Ca2+ channels) are established drug targets for the treatment of cardiovascular diseases. LTCCs are also expressed outside the cardiovascular system. in the brain, LTCCs control synaptic plasticity in neurons, and DHP (dihydropyridine) LTCC blockers such as nifedipine modulate brain function (such as fear memory extinction and depression-like behaviour). Voltage-sensitive Ca2+ channels Ca(v)1.2 and Ca(v)1.3 are the predominant brain LTCCs. As DHPs and other classes of organic LTCC blockers inhibit both isoforms, their pharmacological distinction is impossible and their individual contributions to defined brain functions remain largely unknown. Here, we summarize our recent experiments with two genetically modified mouse strains, which we generated to explore the individual biophysical features of Cav1.2 and Cav1.3 LTCCs and to determine their relative contributions to various physiological peripheral and neuronal functions. The results described here also allow predictions about the pharmacotherapeutic potential of isoform-selective LTCC modulators.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available