BP 554 maleate |
| Catalog No.GC15311 |
Selective 5-HT1A agonist
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 82900-57-0
Sample solution is provided at 25 µL, 10mM.
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BP-554 maleate is a selective agonist of 5-HT1A receptor [1].
The 5-HT1A receptor is a G protein-coupled receptor for endogenous neurotransmitter serotonin (5-HT) and mediates inhibitory neurotransmission.
BP-554 maleate is a selective 5-HT1A receptor agonist. BP-554 showed higher affinity for 5-HT1A receptor than for 5-HT1-non-A, 5-HT2, α2-adrenergic, dopamine D2 and benzodiazepine receptors. In rat hippocampal membranes, BP-554 inhibited the activity of adenylate cyclase stimulated by forskolin [1].
In mice, BP-554 inhibited the accumulation of 5-hydroxytryptophan after decarboxylase inhibition and reduced the concentration of 5-hydroxy-indoleacetic acid in the brain. Also, BP-554 increased the levels of serum corticosterone and induced hypothermia [1]. The 5-HT1(A) receptor, 5-HT, brain-derived neurotrophic factor (BDNF) receptor trkB and BDNF formed an auto/paracrine loop to regulate the serotonergic phenotype. In rats, BP-554 dose-dependently increased amounts of neurons expressing serotonergic markers [2]. In monkeys, injection of BP554 into the primary visual cortex decreased multiunit activity (MUA) without influenced blood oxygen-level-dependent (BOLD) and local field potential (LFP) activity [3].
References:
[1]. Matsuda T, Seong YH, Aono H, et al. Agonist activity of a novel compound, 1-[3-(3,4-methylenedioxyphenoxy)propyl]-4-phenyl piperazine (BP-554), at central 5-HT1A receptors. Eur J Pharmacol, 1989, 170(1-2): 75-82.
[2]. Galter D, Unsicker K. Sequential activation of the 5-HT1(A) serotonin receptor and TrkB induces the serotonergic neuronal phenotype. Mol Cell Neurosci, 2000, 15(5): 446-455.
[3]. Rauch A, Rainer G, Logothetis NK. The effect of a serotonin-induced dissociation between spiking and perisynaptic activity on BOLD functional MRI. Proc Natl Acad Sci U S A, 2008, 105(18): 6759-6764.
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