• A Pourmotabbed, F Motamedi, Y Fathollahi, F A Mansouri, and S Semnanian.
• Department of physiology, School of Medicine, Shaheed Beheshti University of Medical Sciences, P.O. Box 19835-181, Evin, Tehran, Iran. motabbed@ibb.ut.ac.ir
• Brain Res. 1998 Aug 31; 804 (1): 125-34.

AbstractThe involvement of NMDA receptors and voltage-dependent calcium channels on augmentation of long-term potentiation (LTP) was investigated at the Schaffer collateral-CA1 pyramidal cell synapses in hippocampal slices of morphine dependent rats, using primed-bursts tetanic stimulation. The amplitude of population spike was measured as an index of increase in postsynaptic excitability. d, l-AP5 and nifedipine were used as NMDA receptor antagonist and voltage-dependent calcium channel blocker, respectively. The amount of LTP of orthodromic population spike amplitude was higher in slices from dependent rats. Perfusion of slices from control or dependent rats with ACSF containing either D,L-AP5 (25 microM) or nifedipine (10 microM) and delivering tetanic stimulation, showed that D,L-AP5 completely blocked LTP of OPS in slices from both control and dependent rats, while nifedipine attenuated the amount of LTP of OPS in dependent slices and had no effect on control ones. The results suggest that the enhanced LTP of OPS in the CA1 area of hippocampal slices from morphine dependent rats is primarily induced by the NMDA receptors activity and the voltage-dependent calcium channels may also be partially involved in the phenomenon.Copyright 1998 Elsevier Science B.V.

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