M140
Methylcarbamylcholine chloride
solid, ≥97% (NMR)
别名:
Methylcarbachol
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关于此项目
线性分子式:
(CH3)3N+CH2CH2OC(O)NHCH3 Cl-
化学文摘社编号:
分子量:
196.68
UNSPSC Code:
12352200
MDL number:
assay
≥97% (NMR)
form
solid
storage condition
desiccated
color
white
solubility
H2O: soluble, methanol: soluble
Gene Information
Biochem/physiol Actions
Studies of correlation between receptor changes and behavioral function as result of chronic administration of the nicotinic agonist, methylcarbamylcholine (MCC) or the competitive antagonist dihydro-beta-erythroidine (DHBE) in rats shown that the treatment reversibly increased the apparent Bmax and Kd of cortical nAChRs in a dose- and time-dependent manner. DHBE pretreatment inhibited the MCC-induced behavioral changes. The time course of the development of tolerance to MCC as well as the extent of inhibition of DHBE were well correlated with the time course for receptor up-regulation and inhibition of the increase in binding parameters, respectively. Like chronic MCC treatment, chronic DHBE increased the number of [3H]cytisine binding sites but without concomitant development of behavioral tolerance. DHBE pretreatment inhibited the MCC-induced behavioral changes.
Disclaimer
Hygroscopic
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
法规信息
新产品
此项目有
D M Araujo et al.
Journal of neurochemistry, 51(1), 292-299 (1988-07-01)
The present experiments show that N-[3H]-methylcarbamylcholine ([3H]MCC) binds specifically and with high affinity to rat hippocampus, frontal cortex, and striatum. The highest maximal density of binding sites was apparent in frontal cortex and the lowest in hippocampus. [3H]MCC binding was
S J Lansdell et al.
Neuropharmacology, 39(4), 671-679 (2000-03-23)
A series of cell lines stably expressing recombinant nicotinic acetylcholine receptors (nAChRs) has been established by transfection of mammalian (rat) and insect (Drosophila) nicotinic subunit cDNAs. By equilibrium radioligand binding, we have examined the influence of individual subunits upon the
X Yang et al.
The Journal of pharmacology and experimental therapeutics, 271(2), 651-659 (1994-11-01)
Chronic administration of nicotine results in increased numbers of specific nicotinic acetylcholine receptors (nAChRs) within the central nervous system. The purpose of this study was to determine: 1) whether chronic administration of the nicotinic agonist, methylcarbamylcholine (MCC) or the competitive
P A Lapchak et al.
Journal of neurochemistry, 52(2), 483-491 (1989-02-01)
It has been reported that N-methylcarbamylcholine (MCC), a nicotinic agonist, binds to central nicotinic receptors and causes an increase of acetylcholine (ACh) release from certain central cholinergic nerve terminals. The present experiments determine whether these two phenomena change in response
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