Acetylcholine cycle

Acetylchohne is a vasodilator that acts by causing relaxation of the smooth muscle of blood vessels. However, it does not act directly on smooth muscle. A key observation was that if endothefial cells were stripped away from underlying smooth muscle cells, acetylcholine no longer exerted its vasodilator effect. This finding indicated that vasodilators such as acetylcholine initially interact with the endothelial cells of small blood vessels via receptors. The receptors are coupled to the phos-phoinositide cycle, leading to the intracellular release of... 

Steriade, M. (2004). Acetylcholine systems and rhythmic activities during the waking - sleep cycle. Prog. Brain Res. 145, 179-6. 

Jouvet, M. (1972). The role of monoamines and acetylcholine-containing neurons in the regulation of the sleep-waking cycle. Ergeb. Physiol. 64, 166-307. 

Marrosu, F., Portas, C., Mascia, M. S. et al. (1995). Microdialysis measurement of cortical and hippocampal acetylcholine release during the sleep-wake cycle in freely moving cats. Brain Res. 671, 329-32. 

One of the most consistent findings is the sleep disturbance that often precedes and may even trigger a manic phase ( 46). Studies on circadian rhythms have demonstrated that many aspects of the sleep cycle are phase-advanced in mania (i.e., occur earlier than normal), and often these patterns resemble the free-running rhythms seen in normal individuals who are removed from all time cues. In addition, there is a blunting of amplitude and a doubling of the sleep-wake cycle up to 48 hours. Lithium is known to delay the sleep-wake cycle and often slow such free-running rhythms, which in turn are partly modulated by neurotransmitters such as NE, 5-HT, and acetylcholine. Further, manipulation of the sleep-wake cycle may prevent a manic episode or be used to treat the depressive phase (e.g., sleep deprivation therapy see also the section Experiments in Chapter 8). 

Phase plot of acetylcholine concentrations in (I) versus (II), after limit cycle has been reached (for t >= 0.4 Tend)... 

Next we display 13 single, double, or multiple plots drawn by our MATLAB program neurocycle.m of (a) the acetylcholine concentration profile in compartment (II) above the phase plot of the acetylcholine concentration in compartment (I) versus that in compartment (II), or (b) the limit cycle plot, or (c) the plot of all 8 profiles. We include interpretative comments on the solution s behavior in each case. 

When hf = 0.0045539, the initial chaotic behavior has stopped and the system s limit cycle is reached on the second pass through a large-amplitude drop in the acetylcholine concentration in compartment (II), as shown in Figure 4.60. 

Development of sexual behavior can be affected by neonatal pharmacological treatment with the monoamine oxidase inhibitor pargyline, the monoamine depletor reserpine as well as with the acetylcholine esterase inhibitor pyridostigmine. These results suggest that biogenic amines are involved in sexual differentiation of the brain (refs. 162, 163). Pargyline treatment from day 1 to 14 or day 15 to 28 resulted in earlier development of puberty in female rats and delayed appearance of puberty in male rats. Male sexual behavior was decreased in both sexes. Treatment with reserpine on days 1, 4, 7 and 10 delayed the manifestation of puberty in both sexes, and caused disturbed female ovarian cycles and decreased male mounting behavior. 

The mechanism for the hydrolysis that is catalyzed by the enzyme involves the hydroxy group of a serine amino acid residue in the protein acting as a nucleophile and attacking the carbonyl carbon of the acetylcholine ester. The ester is cleaved, and the acetyl group becomes bonded to the enzyme. Then the acetyl group is hydrolyzed off the enzyme. enabling it to perform another catalytic cycle. This hydrolysis is very facile, so a single enzyme molecule can catalyze the hydrolysis of many acetylcholine molecules ... 

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