Title:Impact of Buprenorphine on Learning and Memory Ability, Oxidative Status and Inflammation in the Hippocampus of Rats
Volume: 14
Author(s): Mohammad Samini, Tahereh Farkhondeh, Mohsen Azimi-Nezhad and Saeed Samarghandian*
Affiliation:
- Noncommunicable Diseases Research Center, Neyshabur University of Medical Sciences, Neyshabur,Iran
Keywords:
Buprenorphine, learning, memory, oxidative stress, inflammation, hippocampus.
Abstract:
Background: Buprenorphine (BUP), a “synthetic derivative of the opioid alkaloid thebaine”,
may be associated with cellular damage in the central nervous system.
Aims: This study was designed to investigate the effects of low and high doses of BUP on oxidative
and inflammatory indices in the hippocampus and learning and memory behavior in an animal
model.
Objective: The association between BUP administration and oxidative and inflammatory damage
and also learning and memory impairment is not clear.
Methods: For this reason, twenty-four male Wistar rats were randomly allocated into one control
and two BUP-treated groups (0.3 and 1 mg/kg, SC), (n=8, for each group). After 4 weeks, learning
and memory abilities were assessed by using Y-maze test. Then, oxidative stress indices including
glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase
(GPx) and catalase (CAT) were assessed in the serum and hippocampus of each animal by using
spectrophotometer. Inflammatory parameters such as tumor necrotic factor-α (TNF-α), interleukin-
6 (IL-6), and interleukin-1β (IL-1β) were also measured in the serum and hippocampus of rats
by using ELISA.
Results: The present findings indicated that the memory and learning time was lengthened in BUP
(1mg/kg)-treated rats versus control animals (p<0.05). Additionally, it was observed that BUP (1
mg/kg) significantly increased the serum and hippocampal levels of MDA and TNF-α and also decreased
GSH levels versus the control group (p< 0.05).
Conclusion: The results of the present study revealed that BUP may cause learning and memory
dysfunction by inducing oxidative stress and inflammation in the hippocampus.
