Glial Glutamate Transporter (GLT-1) Role in Dependence in Male Morphine-Treated Rats
Journal Title: The 1st Annual Meeting of Georgian Center for Neuroscience Research - Year 2020, Vol 2, Issue 20
Abstract
Addiction as a neuropsychiatric disorder affects a large number of people and imposes a high economic burden on the community. Similar to other diseases, a proper understanding of the biological basis of addiction will lead to more effective therapies. Opiates are the oldest and most well-known group of drugs that are used clinically as analgesics. But they are also abused. The incidence of dependence limits the therapeutic use of these drugs. Glutamatergic system appears to have an important role in opioid dependency but the mechanism remains poorly understood. Here, we evaluated the role of hippocampal glial glutamate transporter (GLT-1) in morphine dependence in male treated rats. Morphine (10 mg/kg) was injected subcutaneously at an interval of 12 h for 9 days to make rats dependent. Withdrawal signs were evaluated after intraperitoneally administration of naloxone (1.5 mg/kg) for 20 minutes. Morphine withdrawal signs were also assessed in rats which were treated by ceftriaxone (0.5 µl, 0.5 mmol) microinjection in CA1 region of hippocampus before morphine injection. Our results showed that pretreatment with ceftriaxone in male morphine treated rats in comparison with those which didn’t receive ceftriaxone reduced some signs of morphine withdrawal syndrome such as activity, ptosis, freezing and head tremor (unpaired t-test, P<0.001, P<0.01). Based on the obtained results, the present study revealed that susceptibility of CA1 neurons to dependence was changed due to chronic use of morphine and this alteration in neuronal function is mediated partly by glial cells in hippocampal CA1 area.
Authors and Affiliations
Negin Saeedi, Narges Hosseinmardi, Mahyar Janahmadi
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