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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Addiction,GABA-A receptor antagonists GABA-B receptor antagonists Morphine Prefrontal cortex
- چکیده:
- چکیده انگلیسی: Objective(s): Many studies have focused on ventral tegmental area than of other mesocorticolimbic areas, and implicated a key role for the medial prefrontal cortex (mPFC) in the development of addictive behaviors. So far, the role of gamma-aminobutyric acid (GABA) receptors in the discriminative properties of morphine has received little attention and few studies evaluated the role of these receptors in drug dependence. Hence, we investigated the role of this receptor on morphine- induced GABA/ glutamate (GLU) changes in the mPFC following morphine administration using in vivo microdialysis.
Materials and Methods: In this study, 60 rats weighing 270-300 g were divided into six groups. First, microdialysis probe was inserted into the mPFC and was perfused with artificial cerebrospinal fluid and collected the baseline samples in all groups. In saline and morphine groups, the saline, in phaclophen and (phaclofen+morphine) groups, phaclofen (100 nmol), and in bicuculline and (bicuculline+morphine) groups, bicuculline (20 nmol) was injected intracerebroventricular. In saline, phaclofen and bicuculline groups 20 min later, animals received saline (0.2 ml, IP) and others groups received morphine (20 mg/kg, IP).
Results: Our results showed that morphine increased the average concentration of GABA and decreased the concentration of GLU within mPFC. Pretreatment with phaclofen and bicuculline 20 min before morphine administration had no effect on GABA and GLU release for 100 min.
Conclusion: The present study indicated that morphine influence the GABA and GLU transmission in mPFC. Therefore evaluation of neurochemistry changes of this neural circuitry may provide further insight into the mechanisms underlying drug dependence.- انتشار مقاله: 01-10-1396
- نویسندگان: Effat Ramshini,Hojjat Allah Alaei,Parham Reisi,Naser Naghdi,Hossein Afrozi,Samaneh Alaei,Maryam Alehashem,Shahrzad Eftekharvaghefi
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Addiction,GABA-A receptor antagonists GABA-B receptor antagonists Morphine Prefrontal cortex
- چکیده:
- چکیده انگلیسی: Objective(s): Many studies have focused on ventral tegmental area than of other mesocorticolimbic areas, and implicated a key role for the medial prefrontal cortex (mPFC) in the development of addictive behaviors. So far, the role of gamma-aminobutyric acid (GABA) receptors in the discriminative properties of morphine has received little attention and few studies evaluated the role of these receptors in drug dependence. Hence, we investigated the role of this receptor on morphine- induced GABA/ glutamate (GLU) changes in the mPFC following morphine administration using in vivo microdialysis.
Materials and Methods: In this study, 60 rats weighing 270-300 g were divided into six groups. First, microdialysis probe was inserted into the mPFC and was perfused with artificial cerebrospinal fluid and collected the baseline samples in all groups. In saline and morphine groups, the saline, in phaclophen and (phaclofen+morphine) groups, phaclofen (100 nmol), and in bicuculline and (bicuculline+morphine) groups, bicuculline (20 nmol) was injected intracerebroventricular. In saline, phaclofen and bicuculline groups 20 min later, animals received saline (0.2 ml, IP) and others groups received morphine (20 mg/kg, IP).
Results: Our results showed that morphine increased the average concentration of GABA and decreased the concentration of GLU within mPFC. Pretreatment with phaclofen and bicuculline 20 min before morphine administration had no effect on GABA and GLU release for 100 min.
Conclusion: The present study indicated that morphine influence the GABA and GLU transmission in mPFC. Therefore evaluation of neurochemistry changes of this neural circuitry may provide further insight into the mechanisms underlying drug dependence.- انتشار مقاله: 01-10-1396
- نویسندگان: Effat Ramshini,Hojjat Allah Alaei,Parham Reisi,Naser Naghdi,Hossein Afrozi,Samaneh Alaei,Maryam Alehashem,Shahrzad Eftekharvaghefi
- مشاهده
- جایگاه : پژوهشی
- مجله: Addiction and Health
- نوع مقاله: Journal Article
- کلمات کلیدی: Methamphetamine,Neurodegeneration,cerebellum,CB1 receptor
- چکیده:
- چکیده انگلیسی: Background: A number of neuroimaging studies on human addicts have revealed that abuse of Methamphetamine (METH) can induce neurodegenerative changes in various brain regions like the cerebral cortex and cerebellum. Although the underlying mechanisms of METH-induced neurotoxicity have been studied, the cellular and molecular mechanisms of METH-induced neurotoxicity remain to be clarified. Previous studies implicated that cannabinoid type 1 receptors (CB1Rs) exert neuroprotective effects on several models of cerebral toxicity, but their role in METH-induced neurotoxicity has been rarely investigated. Moreover, the cerebellum was considered as a potential target to evaluate the effects of cannabinoids on locomotion activity as the CB1Rs are most widely distributed in the molecular layer of cerebellum. Therefore, the present study was carried out to evaluate whether neurodegeneration induced in the cerebellum tissue implicated in locomotion deficit induced by METH.Methods: In the current study, open field test was used to examine locomotor activity. Using hematoxylin and eosin (H&E) staining, morphology of the cerebellar vermis was investigated after repeated exposure to METH. Then, the effects of CB1Rs antagonist [SR17141A, 10 mg/kg, intraperitoneally (IP)] and CB1Rs agonist [WIN55, 212-2 (WIN), 3 mg/kg] against METH-induced neurodegeneration and locomotor deficit were assessed.Findings: The results of the present study demonstrated that repeated exposure to METH increased cerebellar degeneration level as compared to the saline and dimethyl sulfoxide (DMSO) groups. In addition, METH-treated rats showed hyperactivity as compared to the saline and DMSO groups. Pretreatment with WIN significantly attenuated neurodegeneration and hyperactivity induced by METH.Conclusion: The findings of this study provided evidence that CB1Rs may serve as a therapeutic strategy for attenuation of METH-induced locomotor deficits.
- انتشار مقاله: 07-10-1396
- نویسندگان: Effat Ramshini,Shahriar Dabiri,Shokouh Arjmand,Gholamreza Sepehri,Mohammad Khaksari,Meysam Ahmadi,Mohammad Shabani
- مشاهده