Morphine Consumption During Lactation Impairs Short-Term Neuronal Plasticity in Rat Offspring CA1 Neurons

Background: Facing environmental factors during early postnatal life, directly or indirectly via mother-infant relationships, profoundly affects the structure and function of the mammals’ Central Nervous System (CNS). Objectives: This study aimed to evaluate the effect of morphine consumption during the lactation period on short-term synaptic plasticity of the hippocampal Cornu Ammonis 1 (CA1) neurons in rat offspring. Materials Methods: In addition to a group of control mother rats (CO), three groups subcutaneously received 5 (M5), 10 (M10), or 20 (M20) mg/kg morphine every 12 hours during the lactation period. At 45 days old, following the stimulation of the Schaffers’ collaterals, basic field Excitatory Post-Synaptic Potentials (fEPSPs) were recorded in their offspring’s hippocampal CA1 neuronal circuits. After the construction input/output curve, paired-pulse stimulations with the inter-stimulus intervals of 20, 80, and 200 ms were applied to determine the short-term synaptic plasticity, and the paired-pulse ratio was evaluated. Results: The baseline synaptic responses of the rats CA1 neurons whose mothers received 10 and 20 mg/kg morphine twice daily during the lactation period decreased compared to the CO animals (P 0.01 P 0.001, respectively). Furthermore, compared to the controls, the Paired-Pulse Ratio (PPR) of the CA1 neural circuits of M10 and M20 rats at 20 and 80 ms Inter-Stimulus Intervals (ISI) decreased (P 0.01). Conclusion: Morphine exposure during the lactation period has a detrimental impact on the primary synaptic activity and short-term synaptic plasticity of the hippocampal CA1 neuronal circuits of rats’ offspring.