Abstract
The focus of this review is on the principal sensory ending of the mammalian muscle spindle, known as the primary ending. The process of mechanosensory transduction in the primary ending is examined under five headings: (i) action potential responses to defined mechanical stimuli—representing the ending's input–output properties; (ii) the receptor potential—including the currents giving rise to it; (iii) sensory-terminal deformation—measurable changes in the shape of the primary-ending terminals correlated with intrafusal sarcomere length, and what may cause them; (iv) putative stretch-sensitive channels—pharmacological and immunocytochemical clues to their identity; and (v) synaptic-like vesicles—the physiology and pharmacology of an intrinsic glutamatergic system in the primary and other mechanosensory endings, with some thoughts on the possible role of the system. Thus, the review highlights spindle stretch-evoked output is the product of multi-ionic receptor currents plus complex and sophisticated regulatory gain controls, both positive and negative in nature, as befits its status as the most complex sensory organ after the special senses.Electronic supplementary materialThe online version of this article (doi:10.1007/s00424-014-1536-9) contains supplementary material, which is available to authorized users.
Highlights
In 1926, Adrian and Zotterman [1] published one of the landmark papers in neuroscience
We shall examine the process of mechanosensory transduction in the primary ending under five headings: (i) action-potential responses to defined mechanical stimuli—representing the ending’s input–output properties; (ii) the receptor potential—including the currents giving rise to it; (iii) sensory-terminal deformation—measurable changes in the shape of the primaryending terminals correlated with intrafusal sarcomere length, and what may cause them; (iv) putative stretchsensitive channels—pharmacological and immunocytochemical clues to their identity; and (v) synaptic-like vesicles—the physiology and pharmacology of an intrinsic glutamatergic system in the primary and other mechanosensory endings, with some thoughts on the possible role of the system
Action-potential responses to defined mechanical stimuli. This is not the place to present a comprehensive account of the responses of muscle-spindle primary endings, which would require a detailed consideration of the actions of the intrafusal motor supply as well as a wide range of mechanical stimuli defined in the time [39] or frequency domain [61]
Summary
In 1926, Adrian and Zotterman [1] published one of the landmark papers in neuroscience. We shall examine the process of mechanosensory transduction in the primary ending under five headings: (i) action-potential responses to defined mechanical stimuli—representing the ending’s input–output properties; (ii) the receptor potential—including the currents giving rise to it; (iii) sensory-terminal deformation—measurable changes in the shape of the primaryending terminals correlated with intrafusal sarcomere length, and what may cause them; (iv) putative stretchsensitive channels—pharmacological and immunocytochemical clues to their identity; and (v) synaptic-like vesicles—the physiology and pharmacology of an intrinsic glutamatergic system in the primary and other mechanosensory endings, with some thoughts on the possible role of the system This is not the place to present a comprehensive account of the responses of muscle-spindle primary endings, which would require a detailed consideration of the actions of the intrafusal motor supply as well as a wide range of mechanical stimuli defined in the time [39] or frequency domain [61]. The implicit question: ‘How is the activity of the primary ending regulated so as to produce an appropriate output for a given input?’ is one to which we shall return in the sections on putative channels and synaptic-like vesicles
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