Publication date: June 2018
Source:Brain Research Bulletin, Volume 140
Author(s): Azadeh Elahi-Mahani, Soomaayeh Heysieattalab, Narges Hosseinmardi, Mahyar Janahmadi, Fatemehsadat Seyedaghamiri, Habibeh Khoshbouei
Drugs of abuse mediate adaptive mechanisms leading to alterations in the synaptic plasticity that has been shown to underlie addictive behaviors. Glial cells play a critical role in modulation of synaptic strength and are potentially involved in drug addiction. Chronic administration of morphine has been shown to increase glial cell activation; therefore, it is possible that altered neuroplasticity induced by drugs of abuse is in part mediated by the activity of glial cells. We investigated the effect of hippocampal glial inhibition on synaptic plasticity in morphine treated rats. The fluorocitrate (an inhibitor of glial cells) was microinjected into the CA1 area before morphine injection. The rats received subcutaneous (s.c.) injections of morphine sulfate (10 mg/kg) every 12 h for 9 days. Field excitatory postsynaptic potentials (fEPSP) were recorded from the stratum radiatum of the CA1 area following Schaffer collateral stimulation. Our results indicated that morphine treatment increases long-term potentiation (LTP) and inhibition of glial cells prevents morphine-induced LTP enhancement. Morphine exposed rats exhibited a resistance to LTD induction, whereas, pretreatment with fluorocitrate reduced this resistance. Glial inhibition did not affect LTP and LTD in the untreated animals. The paired pulse ratio (PPR) in inter stimulus intervals (ISI) of 80 ms in the morphine treated group was significantly higher than the control group, while glial inhibition significantly decreased the PPR in morphine treated rats. Our results suggest that morphine exposure modulates hippocampal short- and long-term synaptic plasticity and these alterations in neuronal activity are in part due to glial activity.
Graphical abstract
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