Acetylcholine Release
Acetylcholine Release - Related Videos
06:39
Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
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Cited by 36 •
2016
Intracoronary acetylcholine testing has been established for the assessment of epicardial coronary spasm more than 30 years ago. Recently, the focus has shifted towards the microcirculation and it has been shown that microvascular spasm can be detected using ACH-testing. This article describes the ACH-test and its implementation in daily routine.
10:04
Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
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Cited by 23 •
2012
In this paper, we describe a useful method to study ligand-gated ion channel function in neurons of acutely isolated brain slices. This method involves the use of a drug-filled micropipette for local application of drugs to neurons recorded using standard patch clamp techniques.
07:59
Acetylcholine Re-Challenge After Intracoronary Nitroglycerine Administration
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Cited by 3 •
2022
This protocol presents the acetylcholine rechallenge after nitroglycerine as an add-on procedure to spasm provocation testing. The purpose of this technique is to unmask co-existing microvascular spasm in patients with epicardial spasm and to assess the protective efficacy of nitroglycerine on a per-patient level to guide medical therapy.
09:06
Localization of Plasma Membrane and Intracellular Neuronal Nicotinic Acetylcholine Receptors Using Quantitative Imaging in Mammalian Cells
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2025
This protocol describes expression and quantification of neuronal nicotinic acetylcholine receptors subunits using the mammalian Neuro-2a cell line. pH-sensitive fluorescent tags and confocal microscopy enable precise evaluation of receptor localization at the plasma membrane versus those expressed in pH-neutral intracellular compartments, facilitating the study of nAChR trafficking and pharmacological modulation.
05:58
Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders
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Cited by 6 •
2021
Coronary vasomotion disorders represent frequent functional causes of angina in patients with unobstructed coronaries. The underlying mechanism of angina (endotype) in these patients can be determined by a comprehensive invasive diagnostic procedure based on acetylcholine provocation testing followed by Doppler-derived assessment of the coronary flow reserve and microvascular resistance.
FAQs
Calcium influx provides the immediate signal that links electrical activity at the presynaptic terminal to vesicle fusion. When voltage-gated calcium channels open, entering calcium activates the coordinated fusion machinery, allowing synaptic vesicles to merge with the plasma membrane. This coupling determines whether an arriving action potential produces transmitter secretion and therefore influences downstream cholinergic signaling.
Released acetylcholine can act through two receptor classes, nicotinic and muscarinic, on target cells. Their presence helps determine how cholinergic signaling is expressed in neuromuscular, autonomic, or central nervous system settings. Consequently, studying receptor activation allows pharmacological research to distinguish effects produced at different target-cell systems rather than treating all acetylcholine responses as identical.
Acetylcholinesterase rapidly breaks down acetylcholine after its release. This limits the duration of transmitter action and helps separate one signaling event from the next. In pharmacology, the enzyme is therefore a critical control point: changes affecting its activity can alter the persistence of cholinergic signaling and influence outcomes involving muscle contraction, autonomic function, or cognition.
Pharmacological studies examine how interventions or toxins alter different points in the pathway, including secretion, receptor activation, and transmitter breakdown. Linking these changes to functional outcomes helps researchers investigate neuromuscular transmission, autonomic signaling, cognition, and muscle contraction. This pathway-based approach also supports the development or evaluation of treatments that modify cholinergic activity.
Three major contexts are neuromuscular, autonomic, and central nervous system function. At the neuromuscular level, altered signaling can affect muscle contraction; in autonomic pathways, it can change physiological communication; and in the central nervous system, it can relate to cognition. Considering these settings helps researchers connect molecular events with distinct pharmacological outcomes.
Researchers can assess effects on muscle contraction, autonomic signaling, cognition, and neuromuscular transmission when cholinergic activity changes. These outcomes reflect different points at which the pathway can be disrupted or modified, from release through receptor activation and enzymatic breakdown. Comparing them helps clarify whether an intervention produces primarily muscular, autonomic, or central nervous system consequences.