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Overview
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Background
Ki: 19 and 64 nM for VGlut andVMAT, respectivelyRose Bengal is a potent VGlut and vesicular monoamine transporter (VMAT) inhibitor. The common biochemical l-glutamate (Glu) is widely recognized as the major excitatory neurotransmitter in the vertebrate CNS. Proper Glu transmission plays a critical role in physiological brain functions, such as learning and memory formation as well as basic neural communication.In vitro: Rose Bengal was a quite potent membrane-permeant inhibitor of glutamate uptake into isolated synaptic vesicles. Such vesicular Glu uptake inhibition was achieved without affecting H1-pump ATPase. It was found that various degrees of reduction elicited by Rose Bengal in [3H]Glu in synaptic vesicles inside the synaptosome [1]. In vivo: The distribution of i.v. administered rose bengal was found to depend on its dose. At a low dose, rose bengal could be found almost solely in the liver and plasma. However, at higher doses, the amount of rose bengal found in extra-hepatic tissues gradually increased. The hepatic transfer maximum of rose bengal amounted to 146 micrograms/kg/min. By increasing the dose from 10 to 200 mg/kg, the hepatic concentration of rose bengal also approached a maximum. The storage capacity of the liver, however, did not limit the transfer maximum of rose bengal [1]. Clinical trial: N/A
[1] Ogita K,Hirata K,Bole DG,Yoshida S,Tamura Y,Leckenby AM,Ueda T. Inhibition of vesicular glutamate storage and exocytotic release by Rose Bengal. J Neurochem.2001 Apr;77(1):34-42.
[2] Fischer E,Varga F. Hepatic storage and biliary excretion of rose bengal in the rat. Acta Physiol Acad Sci Hung.1979;54(1):89-94.
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