The effect of morphine on hippocampal cart gene expression in the presence and absence of neuroaid

Nasrin Malboosi,1,* Mohammad nasehi,2

1. Islamic Azad University, Tehran Medical Branch



Currently, addiction is one of the biggest problems concerning not only physicians but also all people who care about their personal and social health and well-being. it has long been established that genetic factors along with environmental (e.g., psychosocial) factors are significant contributors to addiction vulnerability. addiction can be divided into physical and mental types, in other words, it distracts the neural circuits involved in the reward system, stimulation and memory in the brain, resulting in biologic, physiologic, social and mental subsequences. cerebral reward system consists of dopamine-creating neurons in ventral tegmental areas of the mid-brain which send signals to various parts of the frontal areas of the brain involving the accumbens nucleus (one of its nuclei, amygdala (mass below the cortex often known to affect the brains emotional reactions) and the hippocampus (is a major component of the brains and the main part of the brain in long-term memory). morphine mechanism involves altering the central nervous system that decreases pain, so it is a strong type of opioid which comes from opium and is considered opium’s most important effective combination, that it can be a highly addictive drug. most of the studies in transcription factors engaged in addiction involved the accumbens nucleus of the brain. former studies presented the importance of cocaine and amphetamine in the regulation of cart peptide in drug reward and support system, mental stimuli in particular. there is no available information regarding the different stages of addiction and their effect in cart expression and the relationship between cart and drug abuse. in the present study, the changes in cart mrna expression levels are studied and the reward system related to drug abuse is considered in different sections.


This study was performed on 20 wistar male wistar rats weighing 220-240 were bought from pharmacology college of tehran university (tehran, iran). animals were randomly divided into 4 groups (5 animals in each group): control group were the first group, the second group was neuroaid, the third group were morphine, the fourth group was morphine- neuroaid. animals in each cage of plexiglas (25 x 40 x 40 x 40 cm) with free food and freely ad libitum, under 12:12-h light/dark cycle (light on at 07:00 a.m.) and the temperature maintained at 22 ± 2 ºc. animals were allowed to adapt to the laboratory conditions for at least 1 week before the experiments and each animal was tested only once. rats in the morphine and morphine- neuroaid group were administered 2 mg/kg morphine daily for the first 7 days, followed by 14 days of an increasing-dose regimen (10,12,14,16,18,20,22,24 ,36 mg/kg/day) and neuroaid 2.5mg/kg injected every other day . rna extraction and cdna synthesis were performed and real-time pcr was measured by expression cart.


From the results of this study, morphine addiction significantly reduced cart peptide expression (p<0.001) in the hippocampus. regarding the use of supplementary medication, the neuroaid increased the expression of the cart. regarding the presence of morphine, neuroaid improved cart expression (p<0.001) induced by morphine.


The interest in the action of morphine in the central nervous system has remarkably developed during the last decade. this is due in part to the growing significance of morphine addiction and its subsequences in terms of life quality and costs for popular health systems in industrialized countries. the data showed that neuroaid can block morphine addiction effect on cart peptide thus neuroaid may decrease some effects of morphine in both behavioral and molecular field.


Morphine, neuroaid, hippocampal nucleus, cart.