Disease relevance of Cacna1b

• BIII 890 CL (3-30 mg/kg s.c.) reduced lesion size in mice and rats when administered 5 min after permanent focal cerebral ischemia at doses that did not impair motor coordination [1].
• Potent blockade of sodium channels and protection of brain tissue from ischemia by BIII 890 CL [1].
• MAT BIII cells therefore provide a model of LM from breast cancer with a reproducible clinical course and histologic features [2].

High impact information on Cacna1b

• BIII 890 CL inhibited veratridine-induced glutamate release in brain slices, as well as glutamate release and neurotoxicity in cultured cortical neurons [1].
• Point mutations F1764A and Y1771A in transmembrane segment S6 in domain IV of the alpha subunit reduced the voltage- and frequency-dependent block, findings which suggest that BIII 890 CL binds to the local anesthetic receptor site in the pore [1].
• Electrophoretic mobility-shift assays performed with rat brain nuclear extracts showed that three major DNA-protein complexes, named BI, BII and BIII, are formed by the FE65 minimal promoter [3].
• The clinically effective sodium channel blocker, mexiletine, was compared with crobenetine (BIII 890 CL), a new, highly use-dependent sodium channel blocker [4].
• Whole-cell voltage-clamp and single-channel recording were used to study the interaction of BIII 277 CL and its enantiomer BIII 281 CL with native NMDA receptors in cultured hippocampal neurons [5].

Biological context of Cacna1b

• In situ tissue distribution studies indicate a higher level of BII mRNA expression in the hippocamus compared to other brain regions, revealing important difference in the relative abundance of BI, BII, and BIII channels in brain tissues [6].

Anatomical context of Cacna1b

• We have examined functional properties of the calcium channel BII expressed from the cloned cDNA, in Xenopus oocytes, and compared the results with the other members of the non-L-type subfamily, the BI and BIII channels [6].
• Finally, BIII 277 CL (0.3 mg/kg s.c. 5 times over 24 h) reduced the cortical infarct area in mice that had been subjected previously to focal cerebral ischemia by unilateral occlusion of the middle cerebral artery [7].
• Cell suspensions of 13762 MAT BIII rat mammary carcinoma cells are injected into the cisterna magna of adult, female Fischer 344 rats under general anesthesia [2].

Associations of Cacna1b with chemical compounds

• We determined the ability of a new benzomorphan derivative [2R-[2 alpha, 3(R*),6 alpha]]-1,2,3,4,5,6-hexahydro-3-(2-methoxypropyl)- 6,11,11-trimethyl-2,6-methano-3-benzazocin-9-ol hydrochloride (BIII 277 CL) to inhibit the N-methyl-D-aspartic acid (NMDA) receptor-channel complex in vitro and in vivo [7].
• Both voltage-activated and deltamethrin-activated human Nav1.8 were inhibited by the sodium channel blockers BIII 890 CL, NW-1029, and mexiletine [8].

References