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.