Dendritic spines are the primary recipients of excitatory input in the central nervous system, providing biochemical compartments that regulate synaptic signaling. Hippocampal spines exhibit structural plasticity, which underlies learning and memory. Spine structure is regulated by molecular mechanisms influenced by developmental age, synaptic activity, brain region, and experimental conditions. Structural and functional changes in spines impact local and global signal integration within dendrites. Advances in imaging and computing technologies may enable reconstruction of entire neural circuits, requiring high resolution to identify extrinsic and intrinsic factors involved in synapse formation and maintenance.
Dendritic spines vary in size and shape, with mushroom-shaped spines having larger, more complex postsynaptic densities (PSDs) and containing more glutamate receptors. Smaller spines are more flexible and respond rapidly to synaptic activation. The PSD contains proteins such as NMDA, AMPA, and metabotropic glutamate receptors, scaffolding proteins like PSD-95, and signaling proteins like CamKII. PSD size and shape can reflect functional differences in dendritic function. Spine shape and PSD composition change during long-term potentiation (LTP) and long-term depression (LTD), with LTP increasing spine size and PSD complexity, while LTD decreases spine size and number.
Actin filaments regulate spine formation and morphology, with LTP causing actin depolymerization and LTD leading to actin depolymerization and spine elongation. Actin-binding proteins such as profilin and cofilin regulate actin polymerization and depolymerization, influencing spine size and shape. Recycling endosomes and exocytosis are essential for spine growth and maintenance, with LTP requiring exocytosis of AMPA receptors and LTD leading to their internalization. Polyribosomes and proteasomes regulate protein synthesis and degradation, with CamKII playing a key role in LTP and synaptic plasticity.
Mitochondria are abundant in dendritic shafts and provide energy for signal transduction, while mitochondria are rarely found in spines. SER regulates calcium and is involved in spine morphology, with laminae of SER forming a spine apparatus in some spines. Synaptopodin is an actin-associated protein involved in spine apparatus formation and synaptic plasticity. Mitochondria and SER dynamics may be influenced by synaptic plasticity.
Dendritic spines undergo development, with filopodia becoming spines during maturation. Synaptogenesis requires filopodia to find presynaptic partners, with proteins like telencephalin and SynGAP maintaining filopodia during synaptogenesis. MicroRNAs such as miR-134 regulate spine size by inhibiting protein translation. In the mature hippocampus, spine formation and stabilization are influenced by synaptic activity, with LTP and LTD affecting spine number and shape.
Adhesion molecules and trans-synaptic signaling play roles in spine stabilization and synaptic plasticity, with NDendritic spines are the primary recipients of excitatory input in the central nervous system, providing biochemical compartments that regulate synaptic signaling. Hippocampal spines exhibit structural plasticity, which underlies learning and memory. Spine structure is regulated by molecular mechanisms influenced by developmental age, synaptic activity, brain region, and experimental conditions. Structural and functional changes in spines impact local and global signal integration within dendrites. Advances in imaging and computing technologies may enable reconstruction of entire neural circuits, requiring high resolution to identify extrinsic and intrinsic factors involved in synapse formation and maintenance.
Dendritic spines vary in size and shape, with mushroom-shaped spines having larger, more complex postsynaptic densities (PSDs) and containing more glutamate receptors. Smaller spines are more flexible and respond rapidly to synaptic activation. The PSD contains proteins such as NMDA, AMPA, and metabotropic glutamate receptors, scaffolding proteins like PSD-95, and signaling proteins like CamKII. PSD size and shape can reflect functional differences in dendritic function. Spine shape and PSD composition change during long-term potentiation (LTP) and long-term depression (LTD), with LTP increasing spine size and PSD complexity, while LTD decreases spine size and number.
Actin filaments regulate spine formation and morphology, with LTP causing actin depolymerization and LTD leading to actin depolymerization and spine elongation. Actin-binding proteins such as profilin and cofilin regulate actin polymerization and depolymerization, influencing spine size and shape. Recycling endosomes and exocytosis are essential for spine growth and maintenance, with LTP requiring exocytosis of AMPA receptors and LTD leading to their internalization. Polyribosomes and proteasomes regulate protein synthesis and degradation, with CamKII playing a key role in LTP and synaptic plasticity.
Mitochondria are abundant in dendritic shafts and provide energy for signal transduction, while mitochondria are rarely found in spines. SER regulates calcium and is involved in spine morphology, with laminae of SER forming a spine apparatus in some spines. Synaptopodin is an actin-associated protein involved in spine apparatus formation and synaptic plasticity. Mitochondria and SER dynamics may be influenced by synaptic plasticity.
Dendritic spines undergo development, with filopodia becoming spines during maturation. Synaptogenesis requires filopodia to find presynaptic partners, with proteins like telencephalin and SynGAP maintaining filopodia during synaptogenesis. MicroRNAs such as miR-134 regulate spine size by inhibiting protein translation. In the mature hippocampus, spine formation and stabilization are influenced by synaptic activity, with LTP and LTD affecting spine number and shape.
Adhesion molecules and trans-synaptic signaling play roles in spine stabilization and synaptic plasticity, with N