seeds of Griffonia simplicifolia
5-HYDROXY-TRYPTOPHAN/Tryptophan, 5-hydroxy-, DL-/5-Hydroxytryptophan DL-form/DL-5-HTP/2-Chloro-3-methylamine-5-trifluoromethylpyridine hydrochloride/Tryptophan, 5-hydroxy-/(±)-5-hydroxytryptophan/5-Hydroxytryptophan/5-Hydroxy Tryptophan/Dl-5-Hydroxytryptophan
520.6±50.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:56-69-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
In the present study, we tested possible ways of modification of the context long-term memory using the reconsolidation as a tool. Recently, using a depletion of the serotonin content, it was shown that the reinforcing neurotransmitter serotonin is necessary for successful repeated reconsolidation of context memory in terrestrial snails Helix lucorum (Balaban et al. in Sci Rep 6:36933, 2016), and in the present study, we investigated effects of serotonin increase in memory maintenance by injection of the serotonin precursor 5-hydroxytryptophan (5-HTP). We studied reinstatement of the context memory after its impairment during reconsolidation with a protein synthesis blocker anisomycin (ANI) or with a specific inhibitor of protein-kinase Mζ (ZIP). It was observed that applications of 5-HTP alone, known to increase the release of serotonin, or reactivation of memory alone did not restore the ZIP- or ANI-impaired context memory, while combination of the 5-HTP + reactivation of memory effectively reinstated the context memory. The data obtained confirmed the assumption that serotonin/reinforcing transmitter is a part of successful reconsolidation necessary for memory maintenance, demonstrated possible ways of long-term memory regulation during the reconsolidation process.
Anisomycin; Helix; Memory reactivation; Protein-kinase Mζ; Reinforcement; Serotonin
Increase in serotonin precursor levels reinstates the context memory during reconsolidation.
Zuzina AB1, Vinarskaya AK1, Balaban PM2.
2019 Jul 30;
5-Hydroxytryptophan (5-HTP), a precursor of serotonin, is therapeutically used for several psychiatric disorders such as anxiety and depression in the clinic. However, severe side effects, including abnormal mental functions, behavioral disturbances and intolerance are associated with this treatment. 5-HTP-induced elevation of plasma and brain serotonin levels may affect blood-brain barrier (BBB) breakdown, edema formation and regional cerebral blood flow (CBF) disturbances. Breakdown of BBB to serum proteins leads to vasogenic brain edema formation and cellular injuries. However, 5-HTP-neurotoxicity is still not well known. In this investigations 5-HTP induced elevation of endogenous plasma and brain serotonin levels and its effect on BBB breakdown, edema formation neuronal injuries was examined in a rat model. Furthermore, potential role of oxidative stress and nitric oxide (NO) was evaluated. In addition, several neurochemical agents such as p-CPA (5-HT synthesis inhibitor) indomethacin (prostaglandin synthase inhibitor), diazepam (ant stress drug), cyproheptadine, ketanserin (5-HT2 receptor antagonists) and vinblastine (inhibitor of microtubule function) were examined on 5-HT neurotoxicity. Our observations suggest that 4h after 5-HTP administrations, the endogenous serotonin levels increased by fourfold (150mg/kg) in the plasma and brain associated with profound hyperthermia (+3.86±0.24°C, oxidative stress and NO upregulation. Breakdown of the BBB to Evans blue albumin (EBA) in 8 brain regions and to Iodine in 14 brain regions was observed. The CBF exhibited marked reduction in all the brain regions examined. Brain edema and cellular injuries are present in the areas associated with BBB disruption. Drug treatments reduced the BBB breakdown, edema formation NO production and brain pathology. These observations are the first to point out that 5-HTP-neurotoxicity caused by BBB breakdown, edema formation and NO production is instrumental in causing adverse mental and behavioral abnormalities, not reported earlier.
© 2019 Elsevier Inc. All rights reserved.
5-Hydroxytryptamine; Blood-brain barrier; Brain edema; Diazepam; Indomethacin; Serotonin; Serotonin-2 receptors; Signal transduction mechanisms; Vesicular transport; Vinblastine
5-Hydroxytryptophan: A precursor of serotonin influences regional blood-brain barrier breakdown, cerebral blood flow, brain edema formation, and neuropathology.
Sharma A1, Castellani RJ2, Smith MA3, Muresanu DF4, Dey PK5, Sharma HS6.
Tyrosinase is the key enzyme that controls melanin formation. We found that a hot water extract of the lyophilized fruiting body of the fungus Lyophyllum decastes inhibited tyrosinase from Agaricus bisporus. The extract was fractionated by ODS column chromatography, and an active compound was obtained by purification through successive preparative HPLC using an ODS and a HILIC column. Using spectroscopic data, the compound was identified to be an uncommon amino acid, 6-hydroxytryptophan. 6-Hydroxy-L-tryptophan and 6-hydroxy-D-tryptophan were prepared through a Fenton reaction from L-tryptophan and D-tryptophan, respectively. The active compound was determined to be 6-hydroxy-L-tryptophan by comparison of their circular dichroism spectra and retention time on HPLC analysis of the Nα-(5-fluoro-2,4-dinitrophenyl)-L-leuciamide derivative with those of 6-hydroxy-L-tryptophan and 6-hydroxy-D-tryptophan. A Lineweaver-Burk plot of the enzyme reaction in the presence of 6-hydroxy-L-tryptophan indicated that this compound was a competitive inhibitor. The IC50 values of 6-hydroxy-L-tryptophan was 0.23 mM.
6-hydroxy-L-tryptophan; Lyophyllum decastes; Mushroom; tyrosinase inhibitor
Isolation of 6-hydroxy-L-tryptophan from the fruiting body of Lyophyllum decastes for use as a tyrosinase inhibitor.
Ishihara A1, Sugai N1, Bito T1, Ube N2, Ueno K1, Okuda Y3, Fukushima-Sakuno E3.
5-Hydroxytryptophan, a tryptophan metabolite, is a direct 5-hydroxytryptamine (5-HT) precursor and an L-aromatic amino acid decarboxylase substrate. .