Galphimine B is a cyclodesiccated triterpenoid from Galphimia Glauca, which can regulate the synaptic transmission of dopaminergic ventral tegmental neurons and has a sedative effect.
Promotes proteasomal degradation of Miro1 (mitochondrial Rho GTPase 1). Reduces Miro1 levels in fibroblasts from Parkinson's disease (PD) patients (IC50 = 7.8 μM). Exhibits no significant effect on related outer mitochondrial membrane protein Mitofusin. Reduces stress-induced degeneration of dopaminergic neurons derived from PD patient iPSCs. Rescues age-dependent neuronal loss and prolongs lifespan in fly PD models.
D-DOPA is an enantiomer of the dopamine precursor L-DOPA . It can be converted to L-DOPAviasequential oxidation and transamination, which are mediated by D-amino acid oxidase (DAAO) and DOPA transaminase, respectively, in rat kidney homogenates.1It reduces the number of dopaminergic neurons in primary rat embryonic mesencephalic cultures in a concentration-dependent manner.2Intraventricular administration of D-DOPA (200 μg/animal) increases striatal dopamine levels in rats.3D-DOPA (20 mg/kg, i.p.) induces contralateral turns in a rat model of Parkinson's disease induced by 6-OHDA .4
1.Wu, M., Zhou, X.-J., Konno, R., et al.D-dopa is unidirectionally converted to L-dopa by D-amino acid oxidase, followed by dopa transaminaseClin. Exp. Pharmacol. Physiol.33(11)1042-1046(2006) 2.Ling, Z.-D., Pieri, S.C., and Carvey, P.M.Comparison of the neurotoxicity of dihydroxyphenylalanine stereoisomers in cultured dopamine neuronsClin. Neuropharmacol.19(4)360-365(1996) 3.Karoum, F., Freed, W.J., Chuang, L.-W., et al.D-dopa and L-dopa similarly elevate brain dopamine and produce turning behavior in ratsBrain Res.440(1)190-194(1988) 4.Moses, J., Siddiqui, A., and Silverman, P.B.Sodium benzoate differentially blocks circling induced by D-and L-dopa in the hemi-parkinsonian ratNeurosci. Lett.218(3)145-148(1996)
PAQ is a neuroprotective agent. It protects dopaminergic neurons from cell death without inhibiting glial cell proliferation in a rat midbrain culture model of Parkinson's disease when used at a concentration of 10 μM. PAQ (25 or 50 mg/kg, twice per day) prevents loss of dopaminergic neurons in the substantia nigra in a mouse model of Parkinson's disease induced by MPTP.
Certain chronic neurologic disorders, such as Parkinson's disease, are caused by an insufficiency of the neurotransmitter dopamine secondary to the degeneration of substantia nigra dopaminergic neurons. N-(α-Linolenoyl) tyrosine (NALT) is a simple α-amide conjugate between the ω-3 essential fatty acid α-linolenate and the amino acid tyrosine. α-Linolenate is an important precursor to docosahexaenoic acid (DHA), a prominent brain polyunsaturated fatty acid, while tyrosine is the metabolic precursor for neuronal dopamine synthesis. NALT was prepared as a method for enhancing central nervous system (CNS) dopamine content by facilitated transport of the tyrosine precursor across the blood-brain barrier. In experimental rat models of dopamine insufficiency, NALT increased CNS dopamine levels and exhibited an activity profile consistent with an anti-Parkinson's therapeutic agent.
T0467 is a chemical compound that activates the translocation of parkin to the mitochondria in a PINK1-dependent manner in vitro. However, T0467 does not induce the accumulation of PINK1 in the mitochondria of dopaminergic neurons. As a result, T0467 shows promise as a potential compound for activating the PINK1-Parkin signaling pathway and can be utilized in research related to Parkinson's disease and related disorders.
GBR-12935 is a potent and selective dopamine reuptake inhibitor. It was originally developed in its 3H radiolabelled form for the purpose of mapping the distribution of dopaminergic neurons in the brain by selective labelling of dopamine transporter proteins. This has led to potential clinical uses in the diagnosis of Parkinson's disease, although selective radioligands such as Ioflupane (¹²³I) are now available for this application. GBR-12935 is now widely used in animal research into Parkinson's disease and the dopamine pathways in the brain. (Source: http://en.wikipedia.org/wiki/GBR-12935).
RO-5328673 is a dual NK2/NK3 antagonist. O5328673. [(3)H]RO5328673 bound to a single saturable site on hNK2, hNK3 and gpNK3 with high-affinity. RO5328673 acted as an insurmountable antagonist at both human and guinea-pig NK3 receptors in the [(3)H]IP accumulation assay. In binding kinetic analyses, [(3)H]RO5328673 had fast association and dissociation rates at hNK2 while it had a fast association rate and a remarkably slow dissociation rate at gp and hNK3. In electrophysiological recordings of gp SNpc, RO5328673 inhibited the senktide-induced potentiation of spontaneous activity of dopaminergic neurons with an insurmountable mechanism of action. RO5328673 exhibited in-vivo activity in gerbils, robustly reversing the senktide-induced locomotor activity.