Age-related changes in the subtypes of voltage-dependent calcium channels in rat brain cortical synapses

Authors
Citation
Y. Tanaka et S. Ando, Age-related changes in the subtypes of voltage-dependent calcium channels in rat brain cortical synapses, NEUROSCI RE, 39(2), 2001, pp. 213-220
Citations number
46
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE RESEARCH
ISSN journal
0168-0102 → ACNP
Volume
39
Issue
2
Year of publication
2001
Pages
213 - 220
Database
ISI
SICI code
0168-0102(200102)39:2<213:ACITSO>2.0.ZU;2-Z
Abstract
Age-related changes in the relative contribution of voltage-dependent calci um channel (VDCC) subtypes to depolarization-induced Ca2+ influx and in the density of VDCC subtypes in cortical synapses were investigated using syna ptosomes and their membrane preparations from brain cortices of Wistar rats . The relative contribution of VDCC subtypes to Ca2+ influx was determined by measuring the inhibition of depolarization-induced Ca2+ influx with foul VDCC subtype-specific peptide blockers. In adult rat synaptosomes. L-, N-, P- and Q-type channels accounted for 24, 32, 27 and 12% of the total Ca2influx, respectively. Brain aging significantly reduced the relative contri butions of N- and P-type channels and increased the contribution of the cha nnels resistant to the four blockers used. The densities of VDCC subtypes. determined by binding experiments using radiolabeled PN200 -110, omega -con otoxin GVIA and omega -conotoxin IL MVIIC. were found to be significantly d ecreased in aged synaptic plasma membranes. On the contrary. the dissociati on constants of the blockers were not changed except for PN200-110-sensitiv e L-type channels. These results suggest that aging alters the relative con tributions of each VDCC subtype to depolarization-induced C2+ influx and de creases the number of VDCCs in rat brain cortical synapses. These changes i n VDCCs may lead to age-related hypofunction of synaptic neurotransmission in brain cortices. (C) 2001 Elsevier Science Ireland Ltd and the Japan Neur oscience Society. All rights reserved.