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

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).

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.

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.

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).

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.