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Biomolecules Jun 2020It was a pleasure to receive a proposal to organize and be a guest editor of a Special Issue ofBiomolecules. This is the field in which I am working and personally know...
It was a pleasure to receive a proposal to organize and be a guest editor of a Special Issue ofBiomolecules. This is the field in which I am working and personally know some of the leadingscientists. My narrow field is the research on the peptide and protein neurotoxins from animalvenoms and their application as sophisticated tools for analysis of nicotinic acetylcholine receptors(nAChRs) [...].
Topics: Acetylcholine; Animals; Humans; Receptors, Cholinergic
PubMed: 32503306
DOI: 10.3390/biom10060852 -
Topics in Current Chemistry (Cham) May 2023Acetylcholine (ACh) is one of the most crucial neurotransmitters of the cholinergic system found in vertebrates and invertebrates and is responsible for many processes... (Review)
Review
Acetylcholine (ACh) is one of the most crucial neurotransmitters of the cholinergic system found in vertebrates and invertebrates and is responsible for many processes in living organisms. Disturbances in ACh transmission are closely related to dementia in Alzheimer's and Parkinson's disease. ACh in biological samples is most often determined using chromatographic techniques, radioenzymatic assays, enzyme-linked immunosorbent assay (ELISA), or potentiometric methods. An alternative way to detect and determine acetylcholine is applying spectroscopic techniques, due to low limits of detection and quantification, which is not possible with the methods mentioned above. In this review article, we described a detailed overview of different spectroscopic methods used to determine ACh with a collection of validation parameters as a perspective tool for routine analysis, especially in basic research on animal models on central nervous system. In addition, there is a discussion of examples of other biological materials from clinical and preclinical studies to give the whole spectrum of spectroscopic methods application. Descriptions of the developed chemical sensors, as well as the use of flow technology, were also presented. It is worth emphasizing the inclusion in the article of multi-component analysis referring to other neurotransmitters, as well as the description of the tested biological samples and extraction procedures. The motivation to use spectroscopic techniques to conduct this type of analysis and future perspectives in this field are briefly discussed.
Topics: Animals; Acetylcholine; Spectrum Analysis
PubMed: 37169979
DOI: 10.1007/s41061-023-00426-9 -
Nihon Rinsho. Japanese Journal of... Jun 2002
Review
Topics: Acetylcholine; Animals; Humans; Male; Penile Erection; Penis; Receptors, Muscarinic
PubMed: 12166167
DOI: No ID Found -
Nature Methods Sep 2018
Topics: Acetylcholine; Animals; Receptors, G-Protein-Coupled
PubMed: 30171237
DOI: 10.1038/s41592-018-0131-y -
Scientific Reports Dec 2022Inhibitory control is a key executive function that limits unnecessary thoughts and actions, enabling an organism to appropriately execute goal-driven behaviors. The...
Inhibitory control is a key executive function that limits unnecessary thoughts and actions, enabling an organism to appropriately execute goal-driven behaviors. The efficiency of this inhibitory capacity declines with normal aging or in neurodegenerative dementias similar to memory or other cognitive functions. Acetylcholine signaling is crucial for executive function and also diminishes with aging. Acetylcholine's contribution to the aging- or dementia-related decline in inhibitory control, however, remains elusive. We addressed this in Drosophila using a Go/No-Go task that measures inhibition capacity. Here, we report that inhibition capacity declines with aging in wild-type flies, which is mitigated by lessening acetylcholine breakdown and augmented by reducing acetylcholine biosynthesis. We identified the mushroom body (MB) γ neurons as a chief neural site for acetylcholine's contribution to the aging-associated inhibitory control deficit. In addition, we found that the MB output neurons MBON-γ2α'1 having dendrites at the MB γ2 and α'1 lobes and axons projecting to the superior medial protocerebrum and the crepine is critical for sustained movement suppression per se. This study reveals, for the first time, the central role of acetylcholine in the aging-associated loss of inhibitory control and provides a framework for further mechanistic studies.
Topics: Animals; Acetylcholine; Synaptic Transmission; Aging; Causality; Cognition; Drosophila
PubMed: 36463374
DOI: 10.1038/s41598-022-25402-z -
International Review of Neurobiology 1993ACh is released from cholinergic nerve terminals under both resting and stimulated conditions. Stimulated release is mediated by exocytosis of synaptic vesicle contents.... (Review)
Review
ACh is released from cholinergic nerve terminals under both resting and stimulated conditions. Stimulated release is mediated by exocytosis of synaptic vesicle contents. The structure and function of cholinergic vesicles are becoming known. The concentration of ACh in vesicles is about 100-fold greater than the concentration in the cytoplasm. The AChT exhibits the lowest binding specificity among known ACh-binding proteins. It is driven by efflux of protons pumped into the vesicle by the V-type ATPase. A potent pharmacology of the AChT based on the allosteric VR has been developed. It has promise for clinical applications that include in vivo evaluation of the density of cholinergic innervation in organs based on PET and SPECT. The microscopic kinetics model that has been developed and the very low transport specificity of the vesicular AChT-VR suggest that the transporter has a channel-like or multidrug resistance protein-like structure. The AChT-VR has been shown to be tightly associated with proteoglycan, which is an unexpected macromolecular relationship. Vesamicol and its analogs block evoked release of ACh from cholinergic nerve terminals after a lag period that depends on the rate of release. Recycling quanta of ACh that are sensitive to vesamicol have been identified electrophysiologically, and they constitute a functional correlate of the biochemically identified VP2 synaptic vesicles. The concept of transmitter mobilization, including the observation that the most recently synthesized ACh is the first to be released, has been greatly clarified because of the availability of vesamicol. Differences among different cholinergic nerve terminal types in the sensitivity to vesamicol, the relative amounts of readily and less releasable ACh, and other aspects of the intracellular metabolism of ACh probably are more apparent than real. They easily could arise from differences in the relative rates of competing or sequential steps in the complicated intraterminal metabolism of ACh rather than from fundamental differences among the terminals. Nonquantal release of ACh from motor nerve terminals arises at least in part from the movement of cytoplasmic ACh through the AChT located in the cytoplasmic membrane, and it is blocked by vesamicol. Possibly, the proteoglycan component of the AChT-VR produces long-term residence of the macromolecular complex in the cytoplasmic membrane through interaction with the synaptic matrix. The preponderance of evidence suggests that a significant fraction of what previously, heretofore, had been considered to be nonquantal release from the motor neuron actually is quantal release from the neuron at sites not detected electrophysiologically.(ABSTRACT TRUNCATED AT 400 WORDS)
Topics: Acetylcholine; Animals; Biological Transport; Humans
PubMed: 8463062
DOI: 10.1016/s0074-7742(08)60572-3 -
Pharmacology & Therapeutics Jan 1998Acetylcholine acts as a neurotransmitter in the central and peripheral nervous systems in humans. However, recent experiments demonstrate a widespread expression of the... (Review)
Review
Acetylcholine acts as a neurotransmitter in the central and peripheral nervous systems in humans. However, recent experiments demonstrate a widespread expression of the cholinergic system in non-neuronal cells in humans. The synthesizing enzyme choline acetyltransferase, the signalling molecule acetylcholine, and the respective receptors (nicotinic or muscarinic) are expressed in epithelial cells (human airways, alimentary tract, epidermis). Acetylcholine is also found in mesothelial, endothelial, glial, and circulating blood cells (platelets, mononuclear cells), as well as in alveolar macrophages. The existence of non-neuronal acetylcholine explains the widespread expression of muscarinic and nicotinic receptors in cells not innervated by cholinergic neurons. Non-neuronal acetylcholine appears to be involved in the regulation of important cell functions, such as mitosis, trophic functions, automaticity, locomotion, ciliary activity, cell-cell contact, cytoskeleton, as well as barrier and immune functions. The most important tasks for the future will be to clarify the multiple biological roles of non-neuronal acetylcholine in detail and to identify pathological conditions in which this system is up- or down-regulated. This could provide the basis for the development of new therapeutic strategies to target the non-neuronal cholinergic system.
Topics: Acetylcholine; Choline O-Acetyltransferase; Circadian Rhythm; Humans
PubMed: 9500159
DOI: 10.1016/s0163-7258(97)00085-5 -
The New England Journal of Medicine May 1972
Review
Topics: Acetylcholine; Acetylcholinesterase; Animals; Binding Sites; Cholinesterase Inhibitors; Humans; Parasympathomimetics; Receptors, Cholinergic; Synaptic Transmission
PubMed: 4336251
DOI: 10.1056/NEJM197205182862006 -
Vascular Pharmacology 2005Acetylcholine (ACh) and bradykinin (BK) are potent pharmacological agents which mimic ischemic preconditioning (IPC) enabling hearts to resist infarction during a... (Review)
Review
Acetylcholine (ACh) and bradykinin (BK) are potent pharmacological agents which mimic ischemic preconditioning (IPC) enabling hearts to resist infarction during a subsequent period of ischemia. The cardioprotective pathways activated by BK but not ACh may also protect when activated at reperfusion. ACh and BK stimulate Gi/o-linked receptors and ultimately mediate protection by opening mitochondrial ATP-sensitive potassium channels with the generation of reactive oxygen species that act as second messengers to activate protein kinase C (PKC). There appear to be key differences, however, in the pathways prior to potassium channel opening for these two receptors. This review aims to summarize what is currently known about pharmacological preconditioning by ACh and BK with an emphasis on differences that are seen in the signal transduction cascades. Understanding the cellular basis of protection by ACh and BK is a critical step towards developing pharmacological agents that will prevent infarction during ischemia resulting from coronary occlusion or heart attack.
Topics: Acetylcholine; Animals; Bradykinin; Humans; Ischemic Preconditioning, Myocardial
PubMed: 15922253
DOI: 10.1016/j.vph.2005.02.007 -
Neurobiology of Learning and Memory Nov 2003
Topics: Acetylcholine; Brain; Cognition; Humans
PubMed: 14521861
DOI: 10.1016/j.nlm.2003.07.002