Acetylcholine reticular formation

Vazquez, J. Baghdoyan, H. A. (2004). GABAA receptors inhibit acetylcholine release in cat pontine reticular formation implications for REM sleep regulation. J. Neurophysiol. 92, 2198-206. 

Baghdoyan, H. A., Lydic, R. Fleegal, M. A. (1998). M2 muscarinic autoreceptors modulate acetylcholine release in the medial pontine reticular formation. 

Coleman, C. G., Baghdoyan, H. A. 8r Lydic, R. (2006). Dialysis delivery of an adenosine A2A agonist into the pontine reticular formation of C57BL/6J mouse increases pontine acetylcholine release and sleep. J. Neurochem. 96, 1750-9. 

Lydic, R., Keifer, J. C., Baghdoyan, H. A. Becker, L. (1993). Microdialysis of the pontine reticular formation reveals inhibition of acetylcholine release by morphine. Anesthesiology 79, 1003-12. 

The neural structures involved in the promotion of the waking (W) state are located in the (1) brainstem [dorsal raphe nucleus (DRN), median raphe nucleus (MRN), locus coeruleus (LC), laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT), and medial-pontine reticular formation (mPRF)] (2) hypothalamus [tuberomammillary nucleus (TMN) and lateral hypothalamus (LH)[ (3) basal forebrain (BFB) (medial septal area, nucleus basalis of Meynert) and (4) midbrain ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) (Pace-Schott Hobson, 2002 Jones, 2003). The following neurotransmitters function to promote W (1) acetylcholine (ACh LDT/PPT, BFB) (2) noradrenaline (NA LC) (3) serotonin (5-HT DRN, MRN) (4) histamine (HA TMN) (5) glutamate (GLU mPRF, BFB, thalamus) (6) orexin (OX LH) and (7) dopamine (DA VTA, SNc) (Zoltoski et al, 1999 Monti, 2004). 

A number of pathways contain acetylcholine, including neurons in the neostriatum, the medial septal nucleus, and the reticular formation. Cholinergic pathways appear to play an important role in cognitive functions, especially memory. Presenile dementia of the Alzheimer type is reportedly associated with a profound loss of cholinergic neurons. However, the specificity of this loss has been questioned because the levels of other putative transmitters, eg, somatostatin, are also decreased. 

The normally harmonious music of the aminergic neuronal spheres is contrapuntal to the brain stem cholinergic system, whose modulatory output is generally reciprocal to the aminergic groups and distinctly phasic and burstlike in character (rather than tonic and regular). In fact, the phasic bursts of acetylcholine (ACh) neuronal discharge appear to be strictly and precisely related to eye movement control by the paramedian reticular formation and the oculomotor system. 

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. 

Vasoactive Intestinal Peptide. The peptide is found in the same neurons of the reticular formation where acetylcholine is also present. On injection, it enhances REM sleep. 

Major site of action muscarinic-type acetylchohne receptors in the chemoreceptor trigger zone. In terms of nausea and vomiting prophylaxis, scopolamine is a competitive inhibitor of muscarinic acetylcholine receptors in the chemoreceptor trigger zone which communicates with the emetic center within the reticular formation of the brainstem. Outside the... 

Both inhibitory and excitatory actions of the amines have been revealed by microiontophoresis [59-61, 133, 134]. Noradrenaline appears to be excitatory in many parts of the brain stem but it does have inhibitory properties in the reticular formation [135]. Serotonin produces many more excitatory than inhibitory responses in the brain stem and excitation is much stronger and more prolonged than inhibition [133]. The role of noradrenaline and serotonin in basal ganglia function is therefore not as well defined as that of acetylcholine and dopamine, but nevertheless they do seem to be involved, albeit in a less direct way. 

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