Target type: biologicalprocess
The process by which synaptic transmission, induced by the arrival of a spike (action potential) at a synapse, acts to increase the amount of neurotransmitter released in response to the arrival of subsequent spikes. This effect is seen when a train of closely space spikes arrives at a synapse with a low initial release probability. It occurs in a timeframe of tens to hundreds of milliseconds. [GOC:dos, GOC:sp, ISBN:9780071120005, PMID:11826273, PMID:26738595]
Short-term synaptic potentiation (STP) is a transient enhancement of synaptic transmission that lasts for a few seconds to a few minutes. It is a form of synaptic plasticity that is thought to contribute to learning and memory. STP is typically induced by a brief train of high-frequency stimulation (HFS). HFS causes an increase in the amount of neurotransmitter released from the presynaptic terminal, leading to a larger postsynaptic response. This increase in neurotransmitter release is thought to be due to a number of mechanisms, including an increase in the probability of vesicle fusion, an increase in the number of vesicles released, and an increase in the size of the readily releasable pool of vesicles. STP is thought to be mediated by a number of molecular mechanisms, including the accumulation of calcium in the presynaptic terminal, the activation of protein kinases, and the phosphorylation of proteins involved in synaptic transmission. STP can be divided into two main types: facilitation and augmentation. Facilitation is a form of STP that is thought to be mediated by the accumulation of calcium in the presynaptic terminal. Augmentation is a form of STP that is thought to be mediated by the activation of protein kinases. STP is a dynamic process that can be modulated by a variety of factors, including the frequency of stimulation, the duration of the stimulation, and the presence of neuromodulators. It is a complex phenomenon that is not fully understood, but it is thought to play an important role in learning, memory, and other brain functions.'
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| Protein | Definition | Taxonomy |
|---|---|---|
| Nicastrin | A nicastrin that is encoded in the genome of human. [PRO:DNx, UniProtKB:Q92542] | Homo sapiens (human) |
| Compound | Definition | Classes | Roles |
|---|---|---|---|
| 7-amino-4-chloro-3-methoxy-2-benzopyran-1-one | isocoumarins | ||
| tarenflurbil | tarenflurbil: R-enantiomer of flurbiprofen but not a COX inhibitor; modulates NF-kB, gamma-secretase, amyloid beta-protein; | flurbiprofen | |
| cholanic acid | 5beta-cholanic acids; cholanic acid | ||
| t0901317 | T0901317: an LXRalpha and LXRbeta agonist | ||
| n-(n-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester | DAPT : A dipeptide consisting of alanylphenylglycine derivatised as a 3,5-difluorophenylacetamide at the amino terminal and a tert-butyl ester at the carboxy terminal. A gamma-secretase inhibitor. | carboxylic ester; difluorobenzene; dipeptide; tert-butyl ester | EC 3.4.23.46 (memapsin 2) inhibitor |
| sulindac sulfide | sulindac sulfide : An aryl sulfide that is a metabolite of sulindac. A non-steroidal anti-inflammatory drug, which also has anticancer activity. sulindac sulfide: sulfated analog of indomethacin & inhibitor of prostaglandin synthesis in vitro; RN given refers to cpd without isomeric designation; structure given in first source | aryl sulfide; monocarboxylic acid; organofluorine compound | antineoplastic agent; apoptosis inducer; non-steroidal anti-inflammatory drug |
| l 685458 | L 685458: a gamma-secretase inhibitor; structure in first source L-685,458 : A peptide and carboxamide that is L-leucyl-L-phenylalaninamide, L-Leu-L-Phe-NH2, which has been acylated on the N-terminus by a Phe-Phe hydroxyethylene dipeptide isotere, 2R-benzyl-5S-tert-butoxycarbonylamino-4R-hydroxy-6-phenylhexanoic acid. Compounds based on the structure of L-685,458 are potent inhibitors of gamma-secretase, which mediates the final catalytic step that generates the amyloid beta-peptide (Abeta), which assembles into the neurotoxic aggregates in the brains of sufferers of Alzheimer's disease. | carbamate ester; monocarboxylic acid amide; peptide; secondary alcohol | EC 3.4.23.46 (memapsin 2) inhibitor; peptidomimetic |
| mk 0752 | |||
| ly 450139 | peptide | ||
| chf 5074 | 1-(3',4'-dichloro-2-fluoro(1,1'-biphenyl)-4-yl)cyclopropanecarboxylic acid: a beta-amyloid(1-42) lowering agent; structure in first source | ||
| ly 411575 | dibenzoazepine; difluorobenzene; lactam; secondary alcohol | EC 3.4.23.46 (memapsin 2) inhibitor | |
| 4-(2-((1r)-1-(((4-chlorophenyl)sulfonyl)-2,5-difluoroanilino)ethyl)-5-fluorophenyl)butanoic acid | sulfonamide | ||
| begacestat | |||
| e 2012 | |||
| mrk 560 | MRK 560: a gamma-secretase inhibitor; MRK-560 is the (cis)-isomer; structure in first source | ||
| 1, 3-di-(n-carboxybenzoyl-leucyl-leucyl)amino acetone | 1, 3-di-(N-carboxybenzoyl-leucyl-leucyl)amino acetone: structure in first source | ||
| pf 3084014 | nirogacestat : A member of the class of imidazoles that is 1H-imidazole substituted by a 1-[(2,2-dimethylpropyl)amino]-2-methylpropan-2-yl group at position 1 and a {N-[(2S)-6,8-difluoro-1,2,3,4-tetrahydronaphthalen-2-yl]-L-norvalyl}amino group at position 4. It is a gamma-secretase inhibitor whose hydrobromide salt is indicated for adult patients with progressing desmoid tumours who require systemic treatment. nirogacestat: an antineoplastic agent | ||
| bms 708163 | BMS 708163: structure in first source | oxadiazole; ring assembly | |
| ro 4929097 | dibenzoazepine; dicarboxylic acid diamide; lactam; organofluorine compound | EC 3.4.23.46 (memapsin 2) inhibitor | |
| jnj 40418677 | |||
| (r)-4-cyclopropyl-7,8-difluoro-5-(4-(trifluoromethyl)phenylsulfonyl)-4,5-dihydro-1h-pyrazolo(4,3-c)quinoline | (R)-4-cyclopropyl-7,8-difluoro-5-(4-(trifluoromethyl)phenylsulfonyl)-4,5-dihydro-1H-pyrazolo(4,3-c)quinoline: gamma secretase inhibitor; structure in first source |