Cholinergic input

Sarter, M. Bruno, J. P. (2000). Cortical cholinergic inputs mediating arousal, attentional processing and dreaming differential afferent regulation of the basal forebrain by telencephahc and brainstem afferents. Neuroscience 95,... 

Cholinergic input reduces rapid eye movement sleep (REM) latency, and decreased REM latency is seen in depression ... 

The available data are consistent with the present thesis that cholinergic inputs to cerebral cortex mediate intradendritic events fundamental to conscious activity as a primary role, and that cholinergic modulation of electrophysiological activity may be secondary, even epiphenomenal. Transduction pathways exist whereby muscarinic receptors (and possibly nicotinic receptors acting presynaptically to inhibit acetylcholine release) may lead to actions on the cytoskeleton directly relevant to consciousness. The thesis presented here describes these pathways and also suggests a possible explanation for the diversity of neuromodulators and metabotropic receptors. Accordingly, qualitative aspects of our consciousness would be finely tuned by a number of neurochemicals, prominent among which is acetylcholine. 

Muscarinic antagonists can cause urinary retention by blocking the excitatory effect of ACh on the detrusor muscle of the bladder. During urination, cholinergic input to this smooth muscle is activated by a stretch reflex. 

Additional effects of nicotine include an increase in gastric acid secretion and an increase in the tone and motility of the gastrointestinal tract. These effects are produced because of the predominance of cholinergic input to these effector systems. 

The reinforcing actions of nicotine are very similar to those of cocaine and amphetamine, since dopaminergic cells in the mesolimbic dopamine pathway receive direct nicotinic cholinergic input, which is stimulated by cigarette smoking (Figs. 

Bolam JP, Francis CM, Henderson Z. 1991. Cholinergic input to dopaminergic neurons in the substantia nigra A double immunocytochemical study. Neuroscience 41 483-494. 

The vagus nerve acts to decelerate heart rate via a cholinergic input to the sinoatrial node, and atropine blocks this action, leading to an increase in heart rate. Effects are noted at doses as low as 0.6 mg per 70 kg of body weight, and the maximum increase of 35 to 50 beats per min is achieved at doses of 2 to 3 mg per 70 kg of body weight. Heart rate begins to increase within 15 min of an IM injection, peaks at 60 to 90 min, and can persist for 4 hr (Penetar, 1990 Penetar, Haegerstrom-Portnoy, Jones, 1988). 

Cholinergic Actions in MOB Only limited information is available about cholinergic actions in MOB. Electrical activation of NDB has been reported to depress (Nickell and Shipley, 1988a) or increase (Kunze et al., 1991, 1992) mitral cell activity indirectly via primary effects on GABAergic GCs. NDB stimulation also reduced the field potential in the MOB caused by stimulation of the anterior commissure (Nickell and Shipley, 1993), an effect mediated by presynaptic inhibition of anterior commissure terminals via muscarinic receptors. One interpretation of these results is that cholinergic input to MOB may function to modulate interhemispheric transmission of olfactory information. In this regard, it is noteworthy that anterior commissural fibers are required for access and recall of olfactory memories between the two hemispheres. Infusion of ACh into MOB was reported to reduce paired-pulse depression of lateral olfactory tract (LOT)-evoked field potentials recorded in the GCL. This effect was attributed to... 

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