Neostigmine

Neostigmine [(3-dimethylcarbamoylpbenyl)trimethyIammonium] bromide [114-80-7] M 303.2, m 176 (dec). Crystd from EtOH/diethyl ether. Highly TOXIC). 

Neostigmine methyl sulfate [51-60-5] M 334.4, m 142-145 . Crystd from EtOH. (Highly TOXIC.]... 

A further development of this subject is due to Aeschlimann and Reinert, who found that in the series represented by (XLI) thedimethyl-carbamic ester (XLI R = Me) and the methylphenylcarbamic ester (XLI R = Ph) were at least as active as physostigmine in stimulating peristalsis. The miotic activity of the dimethylcarbamic ester (prostig-mine, neostigmine) is similar to that of physostigmine, that of the methylphenylcarbamic ester being weak. 

The relative inaccessibility of physostigmine led to molecular dissection studies to define the parts of the molecule necessary for activity. A surprisingly simple derivative of m-hydroxy-aniline, neostigmine (40), proved to have the same activity as the complex heterocyclic molecule. In addition, this drug has found use as a cholinsterase inhibitor in pathologic conditions such as myasthenia gravis, marked by insufficient muscle tone. Reaction of m-dimethylaminophenol (37) witn pnosgene affords tne... 

The dosage of neostigmine is 0.022 mg/kg. Wliat dosage would the nurse expect the primary care provider to prescribe for a patient who weighs 150 pounds ... 

Robinul Neostigmine (Anpharm)-comb. Intrastigmina (Lusofarmaco)... 

NBP reagent la 90, 359 Neatan perservation la 134 Neoamygdalline lb 121 Neo-kestose lb 423 Neomycin la 287,423 Neostigmine lb 290 Nephopam la 45 Nerol la 76,327 -, glucoside la 327 Netilmicin la 105,286,287 Nettle leaf extract lb 217 Neuroleptics lb 352 Nickel-DMSO complex lb 259 Nickel cations la 144,145,311 lb 259-260... 

Released ACh is broken down by membrane-bound acetylcholinesterase, often called the true or specific cholinesterase to distinguish it from butyrylcholinesterase, a pseudo-or non-specific plasma cholinesterase. It is an extremely efficient enzyme with one molecule capable of dealing with something like 10000 molecules of ACh each second, which means a short life and rapid turnover (100 ps) for each molecule of ACh. It seems that about 50% of the choline freed by the hydrolysis of ACh is taken back into the nerve. There is a wide range of anticholinesterases which can be used to prolong and potentiate the action of ACh. Some of these, such as physostigmine, which can cross the blood-brain barrier to produce central effects and neostigmine, which does not readily... 

In fact, there is a good deal of evidence to support this suggestion. First, more than half the neurons in the PPT fire rhythmically only when PGO waves are evident and their firing starts immediately before the PGO waves appear. Second, in cats, REM sleep is augmented by direct injection of either carbachol, or more selective muscarinic agonists, or the anticholinesterase, neostigmine, into the pontine reticular formation (one of the projection sites for PPT). Third, REM sleep is abolished by lesion of the PPT nucleus but, interestingly, not by lesion of the LDT. 

Baghdoyan H. A., Monaco, A. P., Rodrigo-Angulo, M. L. et al. (1984a). Microinjection of neostigmine into the pontine reticular formation of cats enhances desynchronized sleep signs. J. Pharmacol. Exp. Then 231, 173-80. 

The most recent species to be studied with respect to cholinergic REM sleep enhancement is mouse (Lydic et al, 2002). Microinjection of neostigmine into the pontine reticular formation of C57BL/6J (B6) mouse has now been shown to cause a REM sleep-like state (Fig. 5.3). REM sleep also can be enhanced in B6.v-lepob... 

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