The article by Citri and Malenka provides a comprehensive review of synaptic plasticity, focusing on its mechanisms, functions, and roles in various brain processes. Synaptic plasticity refers to the activity-dependent modification of synaptic transmission strength, which is crucial for learning, memory, and behavioral adaptation. The review highlights two major forms of synaptic plasticity: short-term plasticity (STP) and long-term plasticity (LTP/LTD). **Short-Term Plasticity (STP):** - STP involves rapid changes in synaptic transmission lasting from milliseconds to several minutes. - These changes are triggered by short bursts of activity and can be facilitation or depression. - Paired-pulse facilitation and depression, augmentation, and post-tetanic potentiation (PTP) are key examples of STP. - Glial cells, particularly astrocytes, play a role in STP by regulating neurotransmitter clearance and modulating presynaptic receptors. - STP influences the information processing function of synapses, enabling them to act as filters with varying characteristics. **Long-Term Plasticity (LTP/LTD):** - LTP and LTD are long-lasting modifications of synaptic strength that can last from hours to days. - They are triggered by different patterns of activity, such as high-frequency stimulation or low-frequency stimulation. - NMDA receptors (NMDARs) are essential for the induction of LTP and LTD. - The induction of LTP involves the activation of NMDARs, leading to an increase in postsynaptic calcium concentration, which activates signaling cascades like CaMKII. - LTP is maintained through de novo protein synthesis and local dendritic protein synthesis. - LTD is characterized by the removal or endocytosis of AMPARs, leading to a decrease in synaptic strength. - The mechanisms of LTD involve calcium-dependent protein phosphatases like calcineurin and protein phosphatase 1 (PP1). The review also discusses the involvement of various signaling molecules, such as protein kinases and phosphatases, in the mechanisms of LTP and LTD. Additionally, it explores the structural changes that occur during these forms of plasticity, such as the enlargement of dendritic spines and the increase in the size of the presynaptic active zone. Overall, the article emphasizes the importance of understanding the detailed molecular mechanisms of synaptic plasticity for comprehending normal and pathological brain function, including the development of neuropsychiatric disorders.The article by Citri and Malenka provides a comprehensive review of synaptic plasticity, focusing on its mechanisms, functions, and roles in various brain processes. Synaptic plasticity refers to the activity-dependent modification of synaptic transmission strength, which is crucial for learning, memory, and behavioral adaptation. The review highlights two major forms of synaptic plasticity: short-term plasticity (STP) and long-term plasticity (LTP/LTD). **Short-Term Plasticity (STP):** - STP involves rapid changes in synaptic transmission lasting from milliseconds to several minutes. - These changes are triggered by short bursts of activity and can be facilitation or depression. - Paired-pulse facilitation and depression, augmentation, and post-tetanic potentiation (PTP) are key examples of STP. - Glial cells, particularly astrocytes, play a role in STP by regulating neurotransmitter clearance and modulating presynaptic receptors. - STP influences the information processing function of synapses, enabling them to act as filters with varying characteristics. **Long-Term Plasticity (LTP/LTD):** - LTP and LTD are long-lasting modifications of synaptic strength that can last from hours to days. - They are triggered by different patterns of activity, such as high-frequency stimulation or low-frequency stimulation. - NMDA receptors (NMDARs) are essential for the induction of LTP and LTD. - The induction of LTP involves the activation of NMDARs, leading to an increase in postsynaptic calcium concentration, which activates signaling cascades like CaMKII. - LTP is maintained through de novo protein synthesis and local dendritic protein synthesis. - LTD is characterized by the removal or endocytosis of AMPARs, leading to a decrease in synaptic strength. - The mechanisms of LTD involve calcium-dependent protein phosphatases like calcineurin and protein phosphatase 1 (PP1). The review also discusses the involvement of various signaling molecules, such as protein kinases and phosphatases, in the mechanisms of LTP and LTD. Additionally, it explores the structural changes that occur during these forms of plasticity, such as the enlargement of dendritic spines and the increase in the size of the presynaptic active zone. Overall, the article emphasizes the importance of understanding the detailed molecular mechanisms of synaptic plasticity for comprehending normal and pathological brain function, including the development of neuropsychiatric disorders.