Cholinergic transmission/activity

Paton DM (1981) Structure-activity relations for presynaptic inhibition of noradrenergic and cholinergic transmission by adenosine evidence for action on Ai receptors. J Auton Pharmacol... 

Nerve agents phosphorylate or phosphonylate the serine hydroxyl group at the esteratic part of the active site of the enzyme acetylcholinesterase (AChE EC 3.1.1.7) (Figure 66.2). AChE plays a key role in cholinergic transmission in the peripheral and central nervous system and, consequently, its inhibition is hfe-endangering (Taylor, 1996 Marrs, 1993). 

L9 Neurotransmitters and REM Sleep In Humans. Neurotransmitters have both a direct and indirect action on REM sleep. The indirect action is manifested by a self-inhibitory feed back mechanism (Equation 5.5). Cholinergic transmission (acetylcholine)activate neurons in their pontine reticular formation (PRF) and produce REM sleep. REM sleep gradually activates REM-ofif monoamin-ergic neurons, which produce a self-inhibitory feedback and eventually terminates REM sleep. As the REM sleep period changes to NREM sleep, the REM-off neuronal activity gradually decreases during NREM sleep, and. is at minimum at the onset of REM sleep. 

The primary pathway of cholinergic transmission in autonomic ganglia is similar to that at the neuromuscular junction of skeletal muscle. The initial depolarization is the result of activation of nicotinic ACh receptors, which are ligand-gated cation channels with properties similar to those found at the neuromuscular junction. Several secondary transmitters or modulators either enhance or diminish the sensitivity of the postganglionic cell to ACh. Ganglionic transmission is discussed in more detail in Chapter 9. 

It appeared that cholinergic transmission performed other new functions. It can modulate various aspects of immune function, both innate and adaptive. Cholinergic transmission influences immune cell proliferation, cytokine production, differentiation of T-helper cells, and antigen presentation. These effects are mediated by cholinergic mAChR and nAQiR and other cholinergic components present in immune cells, for example, a7 nAQiR has the ability to induce anti-inflammatory activity [89]. This is probably one of the reasons why acetylcholinesterase inhibitors (AChEIs) act far broader than just to the inhibition of AChE. 

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