Synaptic plasticity in stress-induced amnesia

Background and Aim : Extensive studies of the effects of stress on brain structures and synapses have been conducted for many years. Extensive issues with the onset of glucocorticoid release from the adrenal during HPA axis activity after stressor exposure have been studied. According to research, due to the lipophilic nature of these hormones, they are able to cross the blood-brain barrier and are therefore able to expose neurons. The receptors of these hormones in the brain are on two types of mineralocorticoids (MRs) and glucocorticoids(GRs). The distribution of these receptors at different brain sites is different. However, in general, the three major sites of PFC, hippocampus, and amygdala have a broad distribution of these receptors. Because of the functional nature of these three brain regions in terms of learning and memory and in general cognitive functions, as well as the importance of learning and memory-related studies as well as understanding the physiological pathways of memory impairment (such as Alzheimer s disease with an increased incidence rate in recent decades), these topics have been much studied. As research has shown, glucocorticoids can induce long-term potentiation or long-term depression (neuronal plasticity), which is dependent on the type of stressor involved by causing structural and physiological changes in their target neurons at these sites.Methods : The presentation is a review.Results : The presentation is a review.Conclusion : Stressed neurons from chronic stressor can experience long-term weakening/depression at some brain sites, which is evidence of memory loss and impaired memory function(amnesia). This article discusses these topics in detail. It is worth noting that research is being done every day, and that is adding to our knowledge of the various processes associated with synaptic plasticity in stress-induced amnesia.

کلیدواژه ها:

Learning and memory ، HPA axis ، synapse ، hippocampus