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چکیده:  
Introduction: Antidepressants can modulate brain monoamines by pre- and post-synaptic receptors. The monoamine effect can decrease by autoreceptors on somatodendritic or pre-synaptic regions despite its counter effects post-synaptically. The direct effect of some antidepressants related to its temporal and spatial bioviability in vicinity of these receptors and are under controversies. This research evaluated the direct effect of acute bupropion on the ventral tegmental area (VTA) dopaminergic neuronal firing rate.
Methods: Male Wistar rats divided into intracerebroventricular and microiontophoretic groups with 14 subgroups (n=5 in each subgroup). Amounts  of 1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol of bupropion (5 μl/3 min) were microinfused in first and ejected amounts of bupropion at -500, -300, -150, -50 nA of electrical currents (1 mol, pH=4.5, 5 min) applied in second groups. Control and sham subgroups studied in each group. Units with stable firing extracted and the effect of bupropion has been evaluated statistically with least p<0.05 level of significance.
Results: The highest amount of bupropion in the intracerebroventricular application could excite 42% and inhibit 56%, but the highest amount of microiontophoretic application of bupropion could inhibit 97.5% of the neurons. The neuronal response to bupropion was amount dependent in all treated groups.
Conclusion: The dual effects of intracerebroventricular bupropion on the VTA dopaminergic neurons but solo inhibitory effect  of its microiontophoretic application reflect the intra- and extra- VTA heterogenic cellular and molecular control on the dopaminergic outflow that can mediated by different receptors. The dopamine autoreceptors on the VTA dopaminergic neurons have complex modulatory effects on the dopaminergic response.
نوع مطالعه: Original | موضوع مقاله: Behavioral Neuroscience
دریافت: ۱۳۹۶/۷/۱۸ | پذیرش: ۱۳۹۷/۲/۱

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