Hippocampal long-term potentiation (LTP) and long-term depression (LTD) are Hebbian forms of synaptic plasticity that are widely believed to underlie associative learning. They involve persistent, input-specific changes in synaptic efficacy that can last for days or weeks in rodents. Persistent LTP and LTD exhibit distinct frequency dependencies and molecular profiles in hippocampal subfields. Causal and genetic studies in behaving rodents indicate that both LTP and LTD play specific and complementary roles in the acquisition and retention of spatial memory. LTP is likely responsible for generating a record of spatial experience, which may serve as an associative schema for subsequent learning. In contrast, LTD enables modification and dynamic updating of this representation, allowing detailed spatial information to be included and the schema to be unique. Together, LTP and LTD engage in a dynamic interplay that supports the generation of complex associative memories resistant to generalization. LTP is characterized by persistent synaptic strengthening, with different durations depending on the subfield and stimulation parameters. For example, in the CA1 region, LTP lasting over 4 hours is NMDAR-dependent, while longer-lasting LTP requires protein translation and transcription. In contrast, LTD in the CA1 region can be induced by low-frequency stimulation and is NMDAR-independent. The molecular basis of LTP and LTD varies across hippocampal subfields, with some forms requiring NMDAR activation, others requiring protein synthesis, and some being NMDAR-independent. LTD also exhibits frequency-dependent variations, with persistent LTD in the CA1 region induced by low-frequency stimulation. The molecular mechanisms of LTD differ across subfields, with some forms requiring NMDAR activation, others requiring protein synthesis, and some being NMDAR-independent. The interplay between LTP and LTD is crucial for the acquisition and retention of detailed spatial representations. LTP helps form a schema for spatial memory, while LTD refines and updates this schema to ensure it is unique and distinguishable from other similar memories. Synaptic plasticity is not the only change in synaptic efficacy in the hippocampus; metaplasticity and slow-onset potentiation (SOP) also play roles. Metaplasticity refers to the ability of a synapse to change its plasticity response based on prior experience, while SOP involves a gradual increase in synaptic efficacy over time. These processes, along with LTP and LTD, contribute to the encoding and retention of spatial and associative memories. Causal evidence suggests that LTP and LTD are essential for the acquisition and retention of long-term associative memories. LTP enables the formation of a schema for spatial memory, while LTD refines and updates this schema. The interplay between LTP and LTD is crucial for the dynamic modification of spatial representations, ensuring that memories are accurate and distinguishable. The hippocampus is influenced by various factors, including attention, arousal, and neuromodulators, which modulate the induction and maintenance of LTPHippocampal long-term potentiation (LTP) and long-term depression (LTD) are Hebbian forms of synaptic plasticity that are widely believed to underlie associative learning. They involve persistent, input-specific changes in synaptic efficacy that can last for days or weeks in rodents. Persistent LTP and LTD exhibit distinct frequency dependencies and molecular profiles in hippocampal subfields. Causal and genetic studies in behaving rodents indicate that both LTP and LTD play specific and complementary roles in the acquisition and retention of spatial memory. LTP is likely responsible for generating a record of spatial experience, which may serve as an associative schema for subsequent learning. In contrast, LTD enables modification and dynamic updating of this representation, allowing detailed spatial information to be included and the schema to be unique. Together, LTP and LTD engage in a dynamic interplay that supports the generation of complex associative memories resistant to generalization. LTP is characterized by persistent synaptic strengthening, with different durations depending on the subfield and stimulation parameters. For example, in the CA1 region, LTP lasting over 4 hours is NMDAR-dependent, while longer-lasting LTP requires protein translation and transcription. In contrast, LTD in the CA1 region can be induced by low-frequency stimulation and is NMDAR-independent. The molecular basis of LTP and LTD varies across hippocampal subfields, with some forms requiring NMDAR activation, others requiring protein synthesis, and some being NMDAR-independent. LTD also exhibits frequency-dependent variations, with persistent LTD in the CA1 region induced by low-frequency stimulation. The molecular mechanisms of LTD differ across subfields, with some forms requiring NMDAR activation, others requiring protein synthesis, and some being NMDAR-independent. The interplay between LTP and LTD is crucial for the acquisition and retention of detailed spatial representations. LTP helps form a schema for spatial memory, while LTD refines and updates this schema to ensure it is unique and distinguishable from other similar memories. Synaptic plasticity is not the only change in synaptic efficacy in the hippocampus; metaplasticity and slow-onset potentiation (SOP) also play roles. Metaplasticity refers to the ability of a synapse to change its plasticity response based on prior experience, while SOP involves a gradual increase in synaptic efficacy over time. These processes, along with LTP and LTD, contribute to the encoding and retention of spatial and associative memories. Causal evidence suggests that LTP and LTD are essential for the acquisition and retention of long-term associative memories. LTP enables the formation of a schema for spatial memory, while LTD refines and updates this schema. The interplay between LTP and LTD is crucial for the dynamic modification of spatial representations, ensuring that memories are accurate and distinguishable. The hippocampus is influenced by various factors, including attention, arousal, and neuromodulators, which modulate the induction and maintenance of LTP