Long-term potentiation of Ca2+ signal in the rat auditory cortex

Citation
K. Seki et al., Long-term potentiation of Ca2+ signal in the rat auditory cortex, NEUROSCI RE, 34(3), 1999, pp. 187-197
Citations number
59
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE RESEARCH
ISSN journal
01680102 → ACNP
Volume
34
Issue
3
Year of publication
1999
Pages
187 - 197
Database
ISI
SICI code
0168-0102(199908)34:3<187:LPOCSI>2.0.ZU;2-P
Abstract
The Ca2+ signal in supragranular layers of the rat auditory cortex (AC) was studied in slice preparations using rhod-2, a Ca2+ indicator. White matter stimulation elicited an increase in the Ca2+ signal, which was maximal in the image taken 34 ms after stimulation. This peak time was the same as tha t of the Ca2+ signal in pyramidal neurons injected with rhod-2. The intensi ty of the Ca2+ signal was proportional to the amplitude of the field potent ials in supragranular layers. The Ca2+ signal was inhibited almost complete ly by 200 mu M Ni2+, but only slightly by 50 mu M D-2-amino-5-phosphonovale rate (APV), an NMDA-receptor antagonist. Tetanic stimulation of the white m atter or supragranular layers elicited long-term potentiation (LTP) of the Ca2+ signal in AC slices, but the potentiation was not clear in slices of t he visual cortex (VC). The induction of LTP of the field potentials in AC s lices was blocked by 50 mu M APV or 50 mu M Ni2+. These results indicate th at Ca2+ influx through Ni2+-sensitive Ca2+ channels in pyramidal neurons is potentiated by tetanic stimulation in parallel with LTP of neural activiti es and might be important for the induction of LTP in AC slices. (C) 1999 P ublished by Elsevier Science Ireland Ltd. All rights reserved.