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Using curcumin to prevent structural and behavioral changes of medial prefrontal cortex induced by sleep deprivation in rats.

ABSTRACT: Sleep Deprivation (SD) is known to result in a range of neurological consequences in chronically-afflicted subjects. Curcumin, a natural substance, has neuroprotective properties. This study aimed to evaluate the effects of curcumin on the medial Prefrontal Cortex (mPFC) of SD rats. Male rats were arbitrarily assigned to nine groups, including control, curcumin (100 mg/kg/day), olive oil, SD, SD+curcumin, SD+olive oil, grid, grid+curcumin, and grid+olive oil groups. SD was induced by a multiplatform box containing water. After a period of 21 days, the learning and memory of the rats were tested in an eight-arm radial maze. Afterwards, their brains were evaluated using stereological methods. Concomitant treatment of curcumin during SD caused fewer errors during evaluation of the working and reference memory errors in the acquisition and retention phases. The overall volume of the mPFC, Infralimbic Cortex (ILC), Prelimbic Cortex (PLC), Anterior Cingulate Cortex (ACC) and the total number of neurons and glial cells reduced by 20 %-40 % on average in the SD animals in comparison to the control group. This indicated atrophic changes and cell loss in these areas (p < 0.01). The dendrites' length and the number of spines per dendrite also reduced by 35 %-55 % in the SD rats compared to the ones in the control group (p < 0.01). Yet, treatment of the SD animals with curcumin prevented the atrophic changes of the mPFC, cell loss, and dendritic changes (p < 0.05). SD induced structural changes in the mPFC and memory impairment in the rats. However, curcumin could protect their PFC.

SUBMITTER: Noorafshan A

PROVIDER: S-EPMC5491911 | biostudies-other | 2017

REPOSITORIES: biostudies-other

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Project description:Clinical and experimental data suggest that fronto-cortical GABAergic deficits contribute to the pathophysiology of major depressive disorder (MDD). To further test this hypothesis, we used a well characterized rat model for depression and examined the effect of stress on GABAergic neuron numbers and GABA-mediated synaptic transmission in the medial prefrontal cortex (mPFC) of rats. Adult male Wistar rats were subjected to 9-weeks of chronic mild stress (CMS) and based on their hedonic-anhedonic behavior they were behaviorally phenotyped as being stress-susceptible (anhedonic) or stress-resilient. Post mortem quantitative histopathology was used to examine the effect of stress on parvalbumin (PV)-, calretinin- (CR), calbindin- (CB), cholecystokinin- (CCK), somatostatin-(SST) and neuropeptide Y-positive (NPY+) GABAergic neuron numbers in all cortical subareas of the mPFC (anterior cingulate (Cg1), prelimbic (PrL) and infralimbic (IL) cortexes). In vitro, whole-cell patch-clamp recordings from layer II-III pyramidal neurons of the ventral mPFC was used to examine GABAergic neurotransmission. The cognitive performance of the animals was assessed in a hippocampal-prefrontal-cortical circuit dependent learning task. Stress exposure reduced the number of CCK-, CR- and PV-positive GABAergic neurons in the mPFC, most prominently in the IL cortex. Interestingly, in the stress-resilient animals, we found higher number of neuropeptide Y-positive neurons in the entire mPFC. The electrophysiological analysis revealed reduced frequencies of spontaneous and miniature IPSCs in the anhedonic rats and decreased release probability of perisomatic-targeting GABAergic synapses and alterations in GABAB receptor mediated signaling. In turn, pyramidal neurons showed higher excitability. Anhedonic rats were also significantly impaired in the object-place paired-associate learning task. These data demonstrate that long-term stress results in functional and structural deficits of prefrontal GABAergic networks. Our findings support the concept that fronto-limbic GABAergic dysfunctions may contribute to emotional and cognitive symptoms of MDD.

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Using curcumin to prevent structural and behavioral changes of medial prefrontal cortex induced by sleep deprivation in rats.

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