TWO FORMS OF LONG-TERM POTENTIATION IN AREA CA1 ACTIVATE DIFFERENT SIGNAL
Cavu, Idil & Tim Teyler.
Neurobiology Department, Northeastern Ohio Universities College of
Medicine, 4209 State Rt. 44, P.O. Box 95, Rootstown, OH 44274-0095,
APStracts 3:0146N, 1996.
SUMMARY AND CONCLUSIONS
1. The effects of protein kinase inhibitors on N-methyl- D -aspartate (NMDA)
receptor-mediated, voltage-dependent calcium channel (VDCC)-mediated and 100
Hz long-term potentiation (LTP) were studied in area CA1 of rat hippocampal
slices. 2. Twenty five Hz tetanus induced a quickly developing potentiation
that was blocked by the NMDA antagonist D,L-2-amino-5-phosphonovaleric acid
(APV) and was not affected by the L-type VDCC inhibitor nifedipine, suggesting
that it was mediated by NMDA receptors (NMDA-LTP). 3. Application of 200 Hz
tetanus in APV induced a slowly developing NMDA receptor-independent
potentiation which was blocked by nifedipine, and hence named VDCC-LTP. NMDA-
and VDCC-LTP reached comparable magnitudes despite their different induction
parameters and developmental kinetics. 4. Bath perfusion of broad spectrum
serine/threonine kinase inhibitor H-7 blocked NMDA-LTP but not VDCC-LTP,
whereas the tyrosine kinase inhibitors genistein and lavendustin A blocked
VDCC-LTP, but not NMDA-LTP. These results suggest a differential involvement
of H-7-sensitive serine/threonine kinases and tyrosine kinases in the two
forms of LTP. 5. Tetanization with 200 Hz in control media resulted in a
compound potentiation twice as large as NMDA- or VDCC-LTP, implying that the
two forms of LTP did not facilitate or reduce each other's expression. The
often used 100 Hz tetanus (1 sec twice) induced a potentiation which was
comparable in size to the 200 Hz compound LTP. Nifedipine, genistein and
lavendustin A reduced the 100 Hz LTP by approximately 50 %, suggesting that
this LTP is also a compound potentiation consisting of NMDA- and VDCC-mediated
components and their corresponding signal transduction pathways.
Received 9 May 1996; accepted in final form 27 June 1996.
APS Manuscript Number J382-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996