Page last updated: 2024-10-24

modification of synaptic structure

Definition

Target type: biologicalprocess

Any process that modifies the structure/morphology of a synapse. [GOC:dos]

Synaptic structure modification is a complex and dynamic process that underlies learning and memory. It involves changes in the morphology, composition, and function of synapses, the specialized junctions between neurons where communication occurs. These changes can be either strengthening (long-term potentiation, LTP) or weakening (long-term depression, LTD) of synaptic transmission.

**Key Processes Involved in Synaptic Structure Modification:**

**1. Presynaptic Changes:**

* **Neurotransmitter Release:** The amount of neurotransmitter released from the presynaptic terminal can be altered. This can involve changes in the number or size of synaptic vesicles, the machinery responsible for neurotransmitter packaging and release.
* **Synaptic Vesicle Recycling:** The efficiency of recycling synaptic vesicles after neurotransmitter release can be modulated. This process involves endocytosis, the uptake of vesicles from the synapse, and exocytosis, the release of vesicles into the synapse.
* **Presynaptic Protein Expression:** The expression of proteins involved in neurotransmitter synthesis, packaging, and release can be regulated, leading to changes in neurotransmitter availability and release.

**2. Postsynaptic Changes:**

* **Receptor Density and Sensitivity:** The number and sensitivity of postsynaptic receptors can be altered. This can involve changes in receptor trafficking, the movement of receptors to and from the synapse, or changes in receptor phosphorylation, a process that can modulate receptor activity.
* **Spine Morphology:** The shape and size of dendritic spines, the small protrusions on dendrites that receive synaptic input, can be modified. This can affect the efficiency of synaptic transmission and the stability of the synapse.
* **Postsynaptic Protein Expression:** The expression of proteins involved in signal transduction pathways, such as kinases and phosphatases, can be regulated. These proteins play a role in the activation and modulation of downstream signaling pathways that ultimately lead to changes in synaptic strength.

**3. Synaptic Connectivity:**

* **Synapse Formation:** New synapses can be formed, leading to an increase in the number of connections between neurons. This process is known as synaptogenesis.
* **Synapse Elimination:** Existing synapses can be eliminated, leading to a decrease in the number of connections between neurons. This process is known as synaptic pruning.

**4. Glial Cell Involvement:**

* **Astrocytes:** These glial cells play a role in regulating synaptic transmission, maintaining synaptic homeostasis, and providing support for synaptic plasticity.
* **Microglia:** These immune cells of the brain can remove damaged synapses and debris.

**Mechanisms Underlying Synaptic Structure Modification:**

* **Signal Transduction Pathways:** Various signaling pathways, including the calcium-calmodulin kinase II (CaMKII) pathway and the mitogen-activated protein kinase (MAPK) pathway, are activated by neuronal activity and contribute to changes in synaptic strength.
* **Gene Expression:** The expression of genes involved in synaptic structure and function can be regulated by neuronal activity. This can lead to changes in the synthesis of proteins involved in synaptic processes.
* **Epigenetic Mechanisms:** Epigenetic modifications, such as DNA methylation and histone acetylation, can alter gene expression and contribute to long-lasting changes in synaptic structure and function.

Synaptic structure modification is a fundamental process that allows the brain to adapt to changes in the environment and learn new information. It is a dynamic process that is constantly being regulated by neuronal activity, signaling pathways, and gene expression.'
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Proteins (1)

ProteinDefinitionTaxonomy
Cell division control protein 42 homologA cell division control protein 42 that is encoded in the genome of human. [PRO:DNx, UniProtKB:P60953]Homo sapiens (human)

Compounds (7)

CompoundDefinitionClassesRoles
fasudilfasudil : An isoquinoline substituted by a (1,4-diazepan-1-yl)sulfonyl group at position 5. It is a Rho-kinase inhibitor and its hydrochloride hydrate form is approved for the treatment of cerebral vasospasm and cerebral ischemia.

fasudil: intracellular calcium antagonist; structure in first source
isoquinolines;
N-sulfonyldiazepane
antihypertensive agent;
calcium channel blocker;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
geroprotector;
neuroprotective agent;
nootropic agent;
vasodilator agent
ketorolac5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid : A member of the class of pyrrolizines that is 2,3-dihydro-1H-pyrrolizine which is substituted at positions 1 and 5 by carboxy and benzoyl groups, respectively.

ketorolac : A racemate comprising equimolar amounts of (R)-(+)- and (S)-(-)-5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid. While only the (S)-(-) enantiomer is a COX1 and COX2 inhibitor, the (R)-(+) enantiomer exhibits potent analgesic activity. A non-steroidal anti-inflammatory drug, ketorolac is mainly used (generally as the tromethamine salt) for its potent analgesic properties in the short-term management of post-operative pain, and in eye drops to relieve the ocular itching associated with seasonal allergic conjunctivitis. It was withdrawn from the market in many countries in 1993 following association with haemorrhage and renal failure.

Ketorolac: A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed)
amino acid;
aromatic ketone;
monocarboxylic acid;
pyrrolizines;
racemate
analgesic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
sanguinarine chloride
chelerythrine chloride
2-[[benzamido(sulfanylidene)methyl]amino]-5,5-dimethyl-4,7-dihydrothieno[2,3-c]pyran-3-carboxylic acidCID1067700: a pan-GTPase inhibitor; structure in first sourcethienopyran
y 27632, dihydrochloride, (4(r)-trans)-isomer
secramine asecramine A: inhibits VSVG transport from the Golgi to the plasma membrane; also inhibits Cdc42-dependent cell functions; structure in first source