Dependence on morphine leads to a prominent sharing among the different mechanisms of long-term potentiation in the CA1 region of rat hippocampus.

摘要

Here, we examined chronic exposure to morphine to determine if this treatment shifted LTP mechanism in the CA1 field in vitro. Long-term potentiation (LTP) of population spikes induced by a 200 Hz theta pattern primed bursts (PBs) stimulation. Verapamil was used to isolate NMDA-dependent LTP. In control slices, a 200 Hz tetanus induced a compound potentiation, consisted of two pharmacologically separable components: nmdaLTP and vdccLTP. LTP in slices taken from morphine dependent rats was completely abolished by either APV or verapamil. These data suggest that morphine dependence in rats does not interfere with the induction and maintenance of hippocampal CA1 LTP. While in control rats both NMDA and voltage-dependent Ca(2+) channel (VDCC) antagonists must have been used concurrently to prevent the induction of LTP, in morphine-dependent rats, each of the antagonist could prevent the LTP induction suggesting a tighter coupling between these two calcium influx regulating processes.