Synaptic plasticity refers to the activity-dependent modification of synaptic transmission strength at preexisting synapses, playing a central role in memory formation and neural circuit development. This review discusses the mechanisms of major forms of synaptic plasticity, including short-term and long-term plasticity, and their roles in normal and pathological brain function. Short-term synaptic plasticity includes paired-pulse facilitation and depression, which are influenced by presynaptic calcium levels and receptor activation. These processes are crucial for short-term memory and behavioral adaptation. Long-term plasticity, such as long-term potentiation (LTP) and long-term depression (LTD), involves persistent changes in synaptic strength and is essential for memory storage. LTP is typically induced by high-frequency stimulation and requires NMDA receptor activation, leading to increased AMPA receptor insertion into the postsynaptic density. LTD, on the other hand, is induced by low-frequency stimulation and involves the endocytosis of AMPA receptors. The molecular mechanisms underlying LTP include the activation of CaMKII, which leads to the phosphorylation of AMPA receptors and their incorporation into the postsynaptic density. LTP also involves structural changes in dendritic spines and synapses, contributing to long-term synaptic strength. LTD is mediated by the dephosphorylation of AMPA receptors and their endocytosis, often involving protein phosphatases like PP1. Glia and presynaptic receptors also play roles in synaptic plasticity, modulating neurotransmitter release and synaptic efficacy. The interplay between LTP and LTD allows for bidirectional modulation of synaptic strength, essential for learning and memory. Understanding these mechanisms is crucial for elucidating the neural basis of both normal and pathological brain function.Synaptic plasticity refers to the activity-dependent modification of synaptic transmission strength at preexisting synapses, playing a central role in memory formation and neural circuit development. This review discusses the mechanisms of major forms of synaptic plasticity, including short-term and long-term plasticity, and their roles in normal and pathological brain function. Short-term synaptic plasticity includes paired-pulse facilitation and depression, which are influenced by presynaptic calcium levels and receptor activation. These processes are crucial for short-term memory and behavioral adaptation. Long-term plasticity, such as long-term potentiation (LTP) and long-term depression (LTD), involves persistent changes in synaptic strength and is essential for memory storage. LTP is typically induced by high-frequency stimulation and requires NMDA receptor activation, leading to increased AMPA receptor insertion into the postsynaptic density. LTD, on the other hand, is induced by low-frequency stimulation and involves the endocytosis of AMPA receptors. The molecular mechanisms underlying LTP include the activation of CaMKII, which leads to the phosphorylation of AMPA receptors and their incorporation into the postsynaptic density. LTP also involves structural changes in dendritic spines and synapses, contributing to long-term synaptic strength. LTD is mediated by the dephosphorylation of AMPA receptors and their endocytosis, often involving protein phosphatases like PP1. Glia and presynaptic receptors also play roles in synaptic plasticity, modulating neurotransmitter release and synaptic efficacy. The interplay between LTP and LTD allows for bidirectional modulation of synaptic strength, essential for learning and memory. Understanding these mechanisms is crucial for elucidating the neural basis of both normal and pathological brain function.