The effect of chronic morphine treatment on hippocampal CA1-long-term potentiation (LTP) was examined in vitro. The field excitatory postsynaptic potential (fEPSP) was recorded from stratum radiatum of area CA1 following stimulation of Schaffer collaterals in slices taken from control and morphine-dependent rats. To induce LTP, a 100-Hz primed burst stimulation (PBs) was used. Slices from rats exposed to chronic morphine showed no effect on baseline synaptic responses. Slices from control rats or rats exposed to chronic morphine maintained in ACSF with either morphine or naloxone also had no effect on baseline synaptic responses. Control slices perfused with medium containing either morphine or naloxone as well as both drugs exhibited hippocampal CA1 LTP. Similarly, slices from morphine-dependent rats maintained in ACSF with either naloxone or just morphine free ACSF also exhibited hippocampal CA1 LTP. However, slices from morphine-dependent rats maintained in ACSF with morphine significantly attenuated hippocampal CA1 LTP. These findings suggest that hippocampal CA1-LTP can still be achieved in slices from morphine-dependent rats exhibiting morphine withdrawal through mechanisms that may be inhibited by opiate exposure. Such studies can be helpful in understanding the neurophysiological substrate of memory deficits seen in opiate addicts.
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