There are different controversial results about the effect of morphine dependency on electrophysiological properties of hippocampal field potentials and induction and maintenance of long term potentiation (LTP). In this study the effect of chronic morphine treatment on hippocampal dentate gyrus baseline synaptic activity and long-term potentiation (LTP) was examined in vivo. The field excitatory postsynaptic potential (fEPSP) and population spikes (PS) was recorded from dentate gyrus following stimulation of perforant path in control and morphine-dependent anesthetized rats. Addiction protocol was 20 days subcutaneous injection of morphine (10 mg/kg) twice daily at 12 hours interval. To induce LTP, a 100-Hz high frequency stimulation (HFS) protocol was used.  Input-Output (I/O) curve plotting showed: 1) Morphine dependency potentiates baseline fEPSP slope in lower stimulation intensities which is reversed by Naloxone administration in anesthetized rats. 2) In contrast Morphine dependency has no effect on the baseline PS amplitude. LTP induction protocol showed: 1) with tetanic stimulation fEPSP-LTP induction impairs and approaching to normal level by Naloxone administration 5 min before or after HFS. 2) Morphine dependency has no significant effect on PS-LTP induction. These findings suggest that hippocampal dentate gyrus fEPSP-LTP is impaired in morphine dependent rats and can still be achieved in morphine withdrawal period by naloxone through mechanisms that may be inhibited by opiate exposure. The basal synaptic efficacy was potentiated in morphine dependency suggests that morphine dependency might cause an endogenous LTP, which influence the subsequent induction of LTP in dentate gyrus.

INTRODUCTION: THE CURRENT STUDY WAS DESIGNED TO EXAMINE LEARNING-INDUCED TRANSFORMATION OF EARLY-LTPINTO LATE-LTP…

INTRODUCTION: MORPHINE DEPENDENCE MODIFIES HIPPOCAMPAL SYNAPTIC PLASTICITY. CONSIDERING THE INCREASED ACTIVITY OF HIPPOCAMPAL MICRGLIA AND ASTROCYTES DUE TO MORPHINE ADMINISTRATION, IT IS PROBABLE THAT MORPHINE EFFECTS ON CA1 NEURONAL FUNCTION AND THEREFORE ON BEHAVIORAL CHANGES SUCH AS DEPENDENCE IS MEDIATED BY GLIAL CELLS.METHODS: AFTER MAKING RATS DEPENDENT TO MORPHINE BY SUBCUTANEOUS INJECTION OF MORPHINE SULFATE (10 MG/KG) AT AN INTERVAL OF 12 H FOR 9 DAYS, LONG TERM POTENTIATION (LTP) WERE ASSESSED BY IN VIVO FIELD POTENTIAL RECORDING, IN MORPHINE DEPENDENT RATS, IN DEPENDENT RATS RECEIVED FLUOROCITRATE, GLIAL CELLS INHIBITORS, (1NMOL/1 ML) BILATERALLY INTO THE HIPPOCAMPUS 120 MIN BEFORE MORPHINE INJECTION. FIELD EXCITATORY POST SYNAPTIC POTENTIALS (FEPSP) WERE RECORDED FROM STRATUM RADIATUM OF AREA CA1 FOLLOWING SCHAFFER COLLATERAL STIMULATION. TO INDUCE LONG TERM POTENTIATION (LTP), A 200 HZ TETANIC STIMULATION WAS USED.RESULTS: MORPHINE DEPENDENCE CAUSED AUGMENTED LTP IN CA1 AREA. FEPSP SLOPE POTENTIATION IN THIS GROUP (51.23±17.07%) WAS STATISTICALLY (UNPAIRED T-TEST, P<0.01) MORE THAN CONTROL ANIMALS (17.49±4.14%). ANIMALS RECEIVING INTRAHIPPOCAMPAL MICROINJECTION OF FLUOROCITRATE BEFORE MORPHINE, DEMONSTRATED A SIGNIFICANT REDUCTION (UNPAIRED T-TEST, P<0.001) IN POTENTIATION (12.44±10.34%) COMPARED TO THOSE WHICH RECEIVED VEHICLE (72.80±12.16%).CONCLUSION: THESES DATA SUGGEST THAT HIPPOCAMPAL GLIAL CELLS MEDIATE SOME EFFECTS OF MORPHINE ON CA1 SYNAPTIC PLASTICITY.