Presynaptic Acetylcholine Receptors Modulate the Time Course of Action Potential-Evoked Acetylcholine Quanta Secretion at Neuromuscular Junctions

Abstract

For effective transmission of excitation in neuromuscular junctions, the postsynaptic response amplitude must exceed a critical level of depolarization to trigger action potential spreading along the muscle-fiber membrane. At the presynaptic level, the end-plate potential amplitude depends not only on the acetylcholine quanta number released from the nerve terminals in response to the nerve impulse but also on a degree of synchronicity of quanta releases. The time course of stimulus-phasic synchronous quanta secretion is modulated by many extra- and intracellular factors. One of the pathways to regulate the neurosecretion kinetics of acetylcholine quanta is an activation of presynaptic autoreceptors. This review discusses the contribution of acetylcholine presynaptic receptors to the control of the kinetics of evoked acetylcholine release from nerve terminals at the neuromuscular junctions. The timing characteristics of neurotransmitter release is nowadays considered an essential factor determining the plasticity and efficacy of synaptic transmission.

Early Alterations in Structural and Functional Properties in the Neuromuscular Junctions of Mutant FUS Mice

“…Exocytotic events can be divided into synchronous and asynchronous release with short (0-8 ms) and longer (8-50 ms) synaptic delays, respectively. Furthermore, synchronous exocytosis mainly occurs within 0-3 ms (the early synchronous component) followed by a late synchronous component (3-8 ms) [43,46]. At the pre-onset stage, the timing of neurotransmitter release (the contribution of early and later synchronous and asynchronous components) was unchanged (Figure 4C).…”

Muscarinic Cholinoreceptors in Skeletal Muscle: Localization and Functional Role

“…In addition to the regulation of the amount of ACh secreted from the nerve endings, activation of mAChRs may also lead to changes in the timing of the release process. Along with the EPP quantal content, the timing of transmitter release is a factor ensuring synaptic plasticity [ 39 , 40 ]. The degree of synchrony of neurosecretion in the NMJ depends on a number of factors such as temperature, the pattern of motor nerve firing, and the presence of physiologically active agents [ 40 , 41 , 42 ].…”

“…Along with the EPP quantal content, the timing of transmitter release is a factor ensuring synaptic plasticity [ 39 , 40 ]. The degree of synchrony of neurosecretion in the NMJ depends on a number of factors such as temperature, the pattern of motor nerve firing, and the presence of physiologically active agents [ 40 , 41 , 42 ]. In frog motor synapses, inactivation of the M2 mAChRs not only modulates the EPP quantal content, but also desynchronizes the ACh release process [ 11 , 43 ].…”

“…Помимо регуляции количества высвобождаемого из нервных окончаний медиатора, активация мХР приводит и к изменению кинетики процесса секреции. Наряду с квантовым составом ПКП, синхронность выделения медиатора является фактором, обеспечивающим синаптическую пластичность в НМС [39,40]. Степень синхронности нейросекреции в НМС обусловлена целым рядом факторов, таких, как температура, частота стимуляции двигательного нерва, присутствие физиологически ак-тивных агентов [40][41][42].…”

“…Наряду с квантовым составом ПКП, синхронность выделения медиатора является фактором, обеспечивающим синаптическую пластичность в НМС [39,40]. Степень синхронности нейросекреции в НМС обусловлена целым рядом факторов, таких, как температура, частота стимуляции двигательного нерва, присутствие физиологически ак-тивных агентов [40][41][42]. Оказалось, что в моторных синапсах лягушки инактивация М2 мХР не только модулирует квантовый состав ПКП, но и десинхронизирует секреторный процесс [11,43].…”