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Basic and Clinical Neuroscience، جلد ۱۳، شماره ۶، صفحات ۰-۰
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| عنوان فارسی |
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| چکیده فارسی مقاله |
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| کلیدواژه‌های فارسی مقاله |
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| عنوان انگلیسی |
The Anxiolytic Effects of N-Acetyl-L-Cysteine (NAC) Supplementation in FST Model for Screening Antidepressants |
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| چکیده انگلیسی مقاله |
Purpose of the study: This study was aimed at evaluating the antidepressant mechanism of N- Acetyl Cysteine (NAC), a glutamate precursor on Forced Swim Test (FST) animal model for screening antidepressant drugs using fluoxetine, a selective serotonin reuptake inhibitors (SSRIs) as standard antidepressant drug. Methods: Thirty (30) adult male Wistar rats used for this study were randomly divided into six groups each with five (n=5) rats. The control group (A) received 1 ml of normal saline daily, group B served as the FST model, group C received 200mg/kg/day of NAC, group D received 20mg/kg/day of fluoxetine, group E the FST model treated with 200mg/kg/day of NAC, and F is the FST model treated with 20mg/kg/day of fluoxetine. Drugs were given orally. The effects of NAC on brain weights, the FST paradigms, sucrose preference test (SPT) for anhedonia were assessed and data analyzed using ANOVA where Tukey post-hoc test for statistical significance was set at (p < 0.05). The brains fixed in 4% paraformaldehyde, were processed and the paraffin embedded tissue were serially sectioned at 5 µm thick to be stained using Haematoxylin and Eosin (H and E) stain, immuno-histochemistry for synaptophysin (p38) and astrocytes (GFAP) activities in the prefrontal cortex (PFC). Results: Findings showed that NAC prevented FST induced anxiety like behaviours demonstrated by an increased SPT (that alleviates anhedonia), mobility time and a reduced immobility time. NAC caused an increase in brain weights and prevented FST induced neurodegeneration, proliferation of reactive astrocytes and diminished synaptophysin immunoreactivity in the prefrontal cortex (PFC) similar to that seen in fluoxetine a standard anti-depressant drug. Conclusion: NAC treatment significantly exhibits its neuroprotective mechanism via inhibiting the proliferation of reactive astrocytes, that protects neurons and synapses from oxidative tissue damage induced by FST, hence an increase in synaptophysin activity that culminates in an increased neural activity, increased SPT and reduced immobility time. |
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| کلیدواژه‌های انگلیسی مقاله |
N-acetyl cysteine, Anxiety, Astrocytes, Synaptophysin, Anhedonia, Prefrontal cortex |
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| نویسندگان مقاله |
| Adejoke Elizabeth Memudu
Department of Anatomy, Faculty of Basic Medical Sciences, College of Medical Science, Uzairue, Nigeria.
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| نشانی اینترنتی |
http://bcn.iums.ac.ir/browse.php?a_code=A-10-2356-2&slc_lang=en&sid=1 |
| فایل مقاله |
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| کد مقاله (doi) |
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| زبان مقاله منتشر شده |
en |
| موضوعات مقاله منتشر شده |
Behavioral Neuroscience |
| نوع مقاله منتشر شده |
Original |
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