Investigating the Mechanisms Involved in Scopolamine-Induced Memory Degradation

摘要: In the present study, the mechanisms involved in scopolamine-induced memory impairment have been investigated. The molecular events that take place during memory mostly include mechanisms that are seen in the acquisition phase. Results show that one of the mechanisms of memory destruction caused by scopolamine, in addition to weakening the cholinergic system, is the indirect effect of scopolamine on other neurotransmitter systems, including the glutamatergic system. Scopolamine injection increases dopamine by inhibiting M2/4 muscarinic auto receptors. These auto receptors are located on dopaminergic presynaptic neurons, and their activation reduces the release of dopamine. Therefore, blocking these auto receptors by scopolamine can increase the release of dopamine. Both D1 and D2 receptors are involved in the process of learning and memory. In general, stimulation of dopamine D1 receptors follows an inverted U-shaped dose-response curve, meaning that both insufficient and excessive amounts of dopamine cause memory impairment. Therefore, one of the mechanisms of scopolamine-induced memory impairment can be an indirect effect on the dopaminergic system. Effect on cell membrane potential, effect on neuron plasticity and interaction with acetylcholine. Serotonin plays a complex role in memory and learning. Serotonin receptors (5-HT2A) also play a role in memory function through their effect on calcium transport. This action is similar to dopamine receptors and other G-protein-coupled receptors, which activate phospholipase C, enter calcium into the cell, and activate calcineurin. Activation of 5-HT2A receptors …