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Furthermore, in CRS rats, propranolol significantly decreased the spatial learning and memory abilities, and attenuated the fEPSP response during MWM test, and the BDNF expression and CREB activation in the dentate gyrus. Our results suggest that norepinephrine activation of β-adrenoceptors in the hippocampal dentate gyrus is involved in spatial learning and memory enhancement induced by CRS in aged rats, in part via modulations of synaptic efficiency and CREB-BDNF signaling pathway.Melatonin is a hormone synthesized and secreted by the pineal gland with the effect of regulating sleep rhythm. Circadian and sleep disturbances may be central for understanding the pathophysiology and treatment of depression. Recently, the melatonergic system has been implicated in the pathophysiology and treatment of depression. In this study, we observed the effects of melatonin on depression-like behavior induced by chronic unpredictable mild stress (CUMS) in rats, and its molecular mechanism was explored. Adult male Sprague-Dawley rats were exposed to CUMS for 4 weeks. Melatonin or saline was injected intraperitoneally. Behavioral changes of Sprague-Dawley rats were detected by the open field test, sugar preference test, elevated O maze test and forced swimming test. In addition, the plasma corticosterone level and the expression of endoplasmic reticulum stress-related protein in the hippocampus of rats were measured. Compared with the control group, the CUMS-exposed Sprague-Dawley rats showed depression-like behavior, which was significantly improved by melatonin treatment. Moreover, CUMS induced endoplasmic reticulum stress and JNK phosphorylation in the hippocampus. Melatonin treatment could significantly reverse the endoplasmic reticulum stress and JNK phosphorylation induced by CUMS. These results suggest that melatonin improves depression-like behavior by inhibiting endoplasmic reticulum stress induced by CUMS. This study demonstrates that melatonin can improve depression-like behavior induced by CUMS, which may be related to the inhibition of endoplasmic reticulum stress and JNK phosphorylation in rat hippocampus.Ar-turmerone, which is a major bioactive component found in the essential oil derived from Curcuma longa, has been reported to inhibit proliferation and induce apoptosis in cancer cell lines. Recently, ar-turmerone has been reported to increase the proliferation of neuronal stem cells, in contrast to its actions in cancer cells. These observations raise the possibility that ar-turmerone serves specific functions in neuronal cell lineages. However, the effects of ar-turmerone on postmitotic neurons remain elusive. In the present study, we investigated the neuroprotective functions of ar-turmerone in primary cerebellar granule neuronal cultures. We found that ar-turmerone increased the survival of neurons following activity deprivation. Consistently, the induction of cleaved caspase-3, a hallmark of apoptosis, was prevented by ar-turmerone, although neither the level of reactive oxygen species nor the mitochondrial membrane potential was affected. This study reports a neuroprotective function for ar-turmerone, providing new insights into the potential therapeutic applications of ar-turmerone for neurological disorders.
The aim of this study was to evaluate whether the effects of transcranial direct current stimulation (tDCS) on cognitive performance are influenced by the state-dependency of targeted cortical regions.

In a mixed within- and between-participants design, we targeted either the right parietal or left dorsolateral prefrontal cortex and measured effects on visual search versus inhibitory control (respectively). Critically, during active and sham stimulation, participants were exposed to an unrelated or task-congruent prime.

Analyses examined whether priming induced state-dependent changes in behavior on a subsequent visual search or inhibitory control task. Results demonstrated consistent support for the null hypothesis, with neither tDCS nor priming influencing behavioral outcomes.

This outcome does not provide direct support for state-dependency or activity-selectivity models of tDCS effects on cognitive outcomes. We discuss the possibility that behavioral patterns supporting these mechanistic models may only be found when the priming and outcome tasks share critical neurocognitive features. Overall, we found no evidence that offline (pretask) tDCS targeting the right parietal or left dorsolateral prefrontal induces reliable changes in visual search or inhibitory control behavior, and this pattern is not modulated by state-dependency induced by priming task-related activity.
This outcome does not provide direct support for state-dependency or activity-selectivity models of tDCS effects on cognitive outcomes. We discuss the possibility that behavioral patterns supporting these mechanistic models may only be found when the priming and outcome tasks share critical neurocognitive features. Overall, we found no evidence that offline (pretask) tDCS targeting the right parietal or left dorsolateral prefrontal induces reliable changes in visual search or inhibitory control behavior, and this pattern is not modulated by state-dependency induced by priming task-related activity.Neuroimaging studies have found altered functional connectivity of default mode network (DMN) and salience network (SN) in patients with focal epilepsy (FE). However, the structural basis underlying the functional connectivity disturbance in the patients is still unclear. Sixteen MRI-normal FE and 22 healthy controls were included in the current study. The T1 structural image of each participant was obtained. Seed-based structural covariance connectivity was employed to investigate changes of structural covariance connectivity of DMN and SN in FE patients. buy XCT790 We further evaluated gray matter volume changes of brain areas showing altered structural connectivity in the patients. We found that patients with FE showed reduced connectivity of posterior cingulate cortex and left medial prefrontal cortex, hippocampus and orbitofrontal cortex, and reduced connectivity of right fronto-insula cortex with left insula, orbitofrontal cortex, opercum part of inferior frontal cortex and right medial prefrontal cortex compared with healthy controls.
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