Memory genes

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Despite being often overlooked, the brain possesses an impressive ability to restrict the creation and manifestation of memories. In 1998, the phrase "memory suppressor gene" was introduced to account for findings indicating that certain genes had the potential to restrict memory. Initially, only a small number of memory suppressor genes were identified, and their mechanism of action was believed to involve the limitation of cAMP-dependent consolidation. However, over the years, nearly 100 memory suppressor genes with varying functions have been uncovered, impacting not just consolidation but also acquisition and forgetting.

Memory suppressor genes are responsible for limiting memory in a wild-type animal and are comparable to tumor suppressor genes. These genes work to suppress the process of memory formation, storage, or recall. Conversely, memory enhancer genes, such as the NMDA receptor subunit NR2B, increase memory formation when their activity is increased. When overexpressed in the mouse forebrain, NR2B enhances long-term memory in various tasks, including fear conditioning, novel object recognition, and Morris water maze performance, along with increased hippocampal long-term potentiation. Conversely, reducing the NR2B subunit impairs spatial memory and LTP.

Memory suppressor molecules, such as repressors of CREB like ApCREB2 in Aplysia, were identified as early as possible. When anti-ApCREB2 antiserum is injected into Aplysia's sensory neurons to inhibit ApCREB2 activity, long-term facilitation (LTF) can be formed after only one application of serotonin, whereas LTF is typically produced only with multiple applications of serotonin. Therefore, ApCREB2 represses CREB function and suppresses the formation of LTF. Studies on CREB repressors, such as ATF4 in mice, provide evidence across species that negative regulators of CREB function as memory suppressor molecules.

New findings suggest a connection between the mammalian dopaminergic system and memory loss. When a D1DA receptor antagonist is injected into the rat hippocampus after training, it improves the memory of food and cocaine-place conditioning after 7 days. This suggests that the D1 receptor may be responsible for memory loss in mammals. Recent research has also examined the impact of rat D1 receptors on retrieval-induced forgetting, which occurs when recalling a memory causes other related memories to be forgotten.

So far, studies on memory suppressors have shown that they affect all aspects of memory that have been tested, including acquisition, consolidation, and forgetting. This framework can guide future research in this area.

Follow the link of the selected polymorphism to read a brief description of how the selected polymorphism affects Memory and see a list of existing studies.

SNP polymorphisms related to the topic Memory: