Abstract
The neuromuscular junction (NMJ) is a chemical synapse formed between a presynaptic motor neuron and a postsynaptic muscle cell. NMJs in most vertebrate species share many essential features; however, some differences distinguish human NMJs from others. This review will describe the pre- and postsynaptic structures of human NMJs and compare them to NMJs of laboratory animals. We will focus on age-dependent declines in function and changes in the structure of human NMJs. Furthermore, we will describe insights into the aging process revealed from mouse models of accelerated aging. In addition, we will compare aging phenotypes to other human pathologies that cause impairments of pre- and postsynaptic structures at NMJs. Finally, we will discuss potential intervention approaches for attenuating age-related NMJ dysfunction and sarcopenia in humans.
Highlights
Synapses are required to maintain the proper function of the nervous system both in health and during disease
The macromolecules in the active zones interact with docked synaptic vesicles, which has been revealed in frog and mouse neuromuscular junction (NMJ) by electron microscopy tomography (Harlow et al, 2001; Nagwaney et al, 2009; Szule et al, 2012; Harlow et al, 2013; Jung et al, 2018)
The acetylcholine receptors (AChR) of human NMJs have only been investigated at confocal-level resolution and has not yet been analyzed using super-resolution microscopy (Jones et al, 2017)
Summary
The neuromuscular junction (NMJ) is a chemical synapse formed between a presynaptic motor neuron and a postsynaptic muscle cell. NMJs in most vertebrate species share many essential features; some differences distinguish human NMJs from others. This review will describe the pre- and postsynaptic structures of human NMJs and compare them to NMJs of laboratory animals. We will focus on age-dependent declines in function and changes in the structure of human NMJs. we will describe insights into the aging process revealed from mouse models of accelerated aging. We will compare aging phenotypes to other human pathologies that cause impairments of pre- and postsynaptic structures at NMJs. we will discuss potential intervention approaches for attenuating age-related NMJ dysfunction and sarcopenia in humans
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