Neuroscience
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Organophosphorus (OP) compounds are deadly chemicals that exert their intoxicating effects through the irreversible inhibition of acetylcholinesterase (AChE). In addition to an excess of peripheral ailments, OP intoxication induces status epilepticus (SE) which if left untreated may lead to permanent brain damage or death. Benzodiazepines are typically the primary therapies for OP-induced SE, but these drugs lose efficacy as treatment time is delayed. ⋯ FJB staining demonstrated that none of the tested drugs had widespread neuroprotective abilities. Overall these data suggest that neurosteroids may represent the most promising anticonvulsant option for OP-induced SE out of the seven unique mechanisms tested here. Additionally, these results suggest that drugs that provide significant neuroprotection from OP-induced SE without some degree of anticonvulsant activity are elusive, which further highlights the necessity to continue screening novel adjunct treatments through the CNS program.
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Psychopath and neuropath often exhibit similar symptoms in clinical functional performances. However, few studies ever demonstrate the existence of overlapped brain functional mechanism between neurological and psychiatric disorders. ⋯ In these overlapped functions, we also find that the brain regions of neuropsychopathic disorders exhibit different cooperative patterns at different levels of brain activities. For example, strong-strong cooperative patterns were observed at high levels of brain activities in epilepsy, ADHD and schizophrenia.
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The ventral hippocampus is a component of the neural circuitry involved with context-associated memory for reward and generation of appropriate behavioral responses to context. Glycogen synthase kinase 3 beta (GSK3β) has been linked to the maintenance of synaptic plasticity, contextual memory retrieval, and is involved in the reconsolidation of cocaine-associated contextual memory. In this study, the effects of targeted downregulation of GSK3β in the ventral hippocampus were examined on a series of behavioral tests for assessing drug reward-context association and non-reward related memory. ⋯ Impaired object location memory was observed in mice with GSK3β downregulation in the ventral hippocampus, but novel object recognition remained intact. These results indicate that GSK3β signaling in the ventral hippocampus is differentially involved in the formation of place-drug reward association dependent upon drug class. Additionally, ventral hippocampal GSK3β signaling is important in detection of discrete spatial cues, but not recognition memory for objects.
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The neural mechanisms associated with the limited capacity of working memory (WM) has long been studied, but it is still unclear which neural regions are associated with the precision of visual WM. Here, an orientation recall task for estimating the trial-wise precision of visual WM was performed and then repeated two weeks later in an fMRI scanner. Results showed that activity in frontal and parietal regions during WM maintenance scaled with WM load, but not with the precision of WM (i.e., recall error in radians). ⋯ Interestingly, a region within the prefrontal cortex, the inferior frontal junction (IFJ), exhibited greater functional connectivity with LOC when the WM load increased. Together, our findings provide unique evidence that the LOC supports visual WM precision, while communication between the IFJ and LOC varies based on WM load demands. These results suggest an intriguing possibility that distinct neural mechanisms may be associated with general content (load) or detailed information (precision) of WM.
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Brachial plexus avulsion (BPA) represents the most devastating nerve injury in the upper extremity and is always considered as a sophisticated problem due to its resistance to most standard pain relief medications or neurosurgical interventions. There is also a lack of understanding on the underlying mechanisms. Our study aimed to investigate whether spinal CCL2-CCR2 signaling contributed to the development of neuropathic pain following BPA via modulating glutamate N-methyl-d-aspartate receptor (NMDAR). ⋯ However, these inhibitors didn't change the spinal NMDAR level in sham rats. CCR2 and NMDAR inhibition efficiently alleviated mechanical allodynia caused by BPA either at early or late phase of neuropathic pain. Collectively, CCL2-CCR2 axis is associated with mechanical pain after BPA by elevating NMDAR signaling.