Author: Gianpiero Pescarmona
Date: 02/11/2008


Acetylcholine (often abbreviated ACh) is a neurotransmitter in both the peripheral nervous system (PNS), including Parasympathetic System, and central nervous system (CNS) in many organisms including humans.

Acetylcholine has muscarinic and nicotinic effects by stimulation of the corresponding receptors.

Acetylcholine synthesis

Acetylcholine (Metabocard HMDB00895) synthesis requires


Recycling pathway of acetylcholine (ACh) synthesis, release, action and breakdown at a cholinergic nerve terminal. AChE acetylcholinesterase, BChE butyrylcholinesterase, ChAT choline acetyltransferase, CHT1 high-affinity choline transporter-1, M muscarinic receptor, G-protein coupled, N nicotinic receptor, ligand-gated ion channel, VAChT vesicular ACh transporter


Vasodilating effect

Bronchial tree

The epithelial cholinergic system of the airways, 2008

Scenario of a local auto-/paracrine role of epithelial ACh in regulating various aspects on the innate mucosal defence mechanisms. Pro-proliferative effects both on the epithelium and on subepithelial fibroblasts may occur in parallel

Brain Cholinergic Pathways

Acetylcholine in mind: a neurotransmitter correlate of consciousness?, 1999

from Nancy J. Woolf, Ph.D site

Acetylcholine Imbalance in Early Memory Loss

Endothelium. 2000;7(2):83-92.
Endothelial cell calcium mobilization to acetylcholine is attenuated in copper-deficient rats.
Schuschke DA, Falcone JC, Saari JT, Fleming JT, Percival SS, Young SA, Pass JM, Miller FN.

Center for Applied Microcirculatory Research, University of Louisville School of Medicine, KY 40292, USA. DASCHU01@GWISE.LOUISVILLE.EDU
Dietary copper deficiency significantly attenuates nitric oxide (NO)-mediated vascular smooth muscle relaxation and vasodilation. There is evidence for both increased inactivation of the NO radical by superoxide anion, and oxidative damage to the endothelium where NO is produced. The current study was designed to examine the NO synthetic pathway in the endothelium during copper deficiency. Male weanling rats were fed a copper-adequate (CuA, 6.4 mg Cu/kg diet) or copper-deficient (CuD, 0.4 mg Cu/kg diet) diet for four weeks. Cremasteric arterioles (approximately 100 microm diameter) were isolated and used for the experiments. Western blot analysis of the arteriole endothelial nitric oxide synthase (eNOS) concentration did not show a difference between dietary groups. Acetylcholine (Ach)-induced vasodilation was significantly reduced in the CuD group both before and after pretreatment with the eNOS substrate L-arginine. Endothelial intracellular calcium ([Ca2+]i) stimulated by 10(-6) M Ach was significantly inhibited in the arterioles from CuD rats. Coincident with the inhibition of [Ca2+]i and vasodilation was a depression of vascular Cu/Zn-SOD activity and an increase in plasma peroxynitrite activity. These data suggest that endothelial Ca2+ signaling and agonist-stimulated NO-mediated vascular dilation are likely reduced by increased oxidative damage in copper-deficient rats.

Behav Brain Res. 2010 Feb 16. [Epub ahead of print]
The cholinergic system, nerve growth factor and the cytoskeleton., 2010

Niewiadomska G, Mietelska-Porowska A, Mazurkiewicz M.

Laboratory of Preclinical Studies in Neurodegenerative Diseases, Department of Neurophysiology, Nencki Institute, Warsaw, Poland.

Cholinergic neurons of the basal forebrain provide the major cholinergic innervation to the cortex and hippocampus, and play a key role in memory and attentional processes. Dysfunction of basal forebrain cholinergic neurons (BFCN) is a cardinal feature of Alzheimer's disease (AD) and correlates with cognitive decline. Survival of BFCN neurons depends upon binding of nerve growth factor (NGF), which is synthesized and secreted by cells in the cortex and hippocampus, with high-affinity (TrkA) and low-affinity (p75(NTR)) neurotrophin receptors produced within BFCN neurons. NGF released from target cells activates TrkA on axon terminals and triggers activation of PI3K/Akt, MEK/ERK, and PLCgamma signaling pathways. The signal then travels retrogradely along axon to cell body to promote neuronal survival. However, the nature of the retrograde signal remains mysterious. p75(NTR) receptors could mediate fundamentally different signaling pathway leading to apoptic cell death. Dysfunction of NGF and its receptors has been suggested to underlie the selective degeneration of the BFCN in end stage Alzheimer disease. In this regard, NGF, the founding member of the neurotrophin family, has generated great interest as a potential target for the treatment of AD. This review focuses on NGF-cholinergic dependency, NGF/receptor binding, signal transduction, retrograde transport, regulation of specific cellular endpoints, and the potential involvement of cytoskeleton dysfunction in defected NGF signaling. Copyright © 2010 Elsevier B.V. All rights reserved.

2021-03-25T18:49:12 - Gianpiero Pescarmona

Acetylcholine and Histamine

Eosinophil-Mediated Cholinergic Nerve Remodeling, 2006

Eosinophils are observed to localize to cholinergic nerves in a variety of inflammatory conditions such as asthma, rhinitis, eosinophilic gastroenteritis, and inflammatory bowel disease, where they are also responsible for the induction of cell signaling.

eosinophil granules content

We hypothesized that a consequence of eosinophil localization to cholinergic nerves would involve a neural remodeling process. Eosinophil co-culture with cholinergic IMR32 cells led to increased expression of the M2 muscarinic receptor, with this induction being mediated via an adhesion-dependent release of eosinophil proteins, including major basic protein and nerve growth factor.

Studies on the promoter sequence of the M2 receptor indicated that this induction was initiated at a transcription start site 145 kb upstream of the gene-coding region. This promoter site contains binding sites for a variety of transcription factors including SP1, AP1, and AP2.
Eosinophils also induced the expression of several cholinergic genes involved in the synthesis, storage, and metabolism of acetylcholine, including the enzymes choline acetyltransferase, vesicular acetylcholine transferase, and acetylcholinesterase.
The observed eosinophil-induced changes in enzyme content were associated with a reduction in intracellular neural acetylcholine but an increase in choline content, suggesting increased acetylcholine turnover and a reduction in acetylcholinesterase activity, in turn suggesting reduced catabolism of acetylcholine.
Together these data suggest that eosinophil localization to cholinergic nerves induces neural remodeling, promoting a cholinergic phenotype.

cholinergic+nerves+and+eosinophils Quetzal

2008-11-10T12:14:56 - Francesco Della Ferrera

Acetylcholine effects

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