A Systematic Review of the Role of Gummosin in Improving Memory in the Scopolamine Impaired Memory Model.

In this study, the role of gummosin in improving memory in the scopolamine memory impairment model was systematically examined. Memory and learning are the most developed and complex functions of the nervous system. Learning is the acquisition of new information that occurs as a change in behavior, and memory is the ability to store and retrieve learned information. In other words, memory is a combination of various processes of information acquisition, consolidation, storage and retrieval. The processes of memory consolidation and storage are the result of a series of time-dependent neurobiological events that occur after the initial formation of memory. In addition, this fluctuation of processes related to memory storage can fully occur shortly after the initial learning experience. Memory is a direct result of learning ,as it stores and retrieves learned experiences and information. The results of our study show that scopolamine leads to impaired memory, learning and synaptic plasticity, which is associated with a change in the expression of various genes and a reduction in the number of hippocampal neurons. The disorders that occurred in the rats of the scopolamine group confirm the model used in this study to induce memory and learning deficits, which is consistent with previous studies confirming the model used to induce Alzheimer's disease. The results of the behavioral tests in this study showed that, consistent with previous work, scopolamine caused a significant increase in anxiety behavior that was associated with a decrease in time spent in the central area compared to the control group, while donepezil injection resulted in a decrease in anxiety behavior. The time spent in the central area was increased compared to the scopolamine group.

Lithium attenuated the depressant and anxiogenic effect of juvenile social stress through mitigating the negative impact of interlukin-1ß and nitric oxide on hypothalamic-pituitary-adrenal axis function.

The neuroimmune-endocrine dysfunction has been accepted as one of fundamental mechanisms contributing to the pathophysiology of psychiatric disorders including depression and anxiety. In this study, we aimed to evaluate the involvement of hypothalamic-pituitary-adrenal (HPA) axis, interleukin-1ß, and nitrergic system in mediating the negative behavioral impacts of juvenile social isolation stress (SIS) in male mice. We also investigated the possible protective effects of lithium on behavioral and neurochemical changes in socially isolated animals. Results showed that experiencing 4-weeks of juvenile SIS provoked depressive and anxiety-like behaviors that were associated with hyper responsiveness of HPA axis, upregulation of interleukin-1ß, and nitric oxide (NO) overproduction in the pre-frontal cortex and hippocampus. Administration of lithium (10 mg/kg) significantly attenuated the depressant and anxiogenic effects of SIS in behavioral tests. Lithium also restored the negative effects of SIS on cortical and hippocampal interleukin-1ß and NO as well as HPA axis deregulation. Unlike the neutralizing effects of l-arginine (NO precursor), administration of l-NAME (3 mg/kg) and aminoguanidine (20 mg/kg) potentiated the positive effects of lithium on the behavioral and neurochemical profile of isolated mice. In conclusion, our results revealed that juvenile SIS-induced behavioral deficits are associated with abnormalities in HPA-immune function. Also, we suggest that alleviating effects of lithium on behavioral profile of isolated mice may be partly mediated by mitigating the negative impact of NO on HPA-immune function.