Abstract
Processes underlying mechanotransduction and its regulation are poorly understood. Inhibitors of Ca2+-activated K+ channels cause a dramatic increase in afferent output from stretched muscle spindles. We used immunocytochemistry to test for the presence and location of small conductance Ca2+-activated K+ channels (SK1-3) in primary endings of muscle spindles and lanceolate endings of hair follicles in the rat. Tissue sections were double immunolabelled with antibodies to one of the SK channel isoforms and to either synaptophysin (SYN, as a marker of synaptic like vesicles (SLV), present in many mechanosensitive endings) or S100 (a Ca2+-binding protein present in glial cells). SK channel immunoreactivity was also compared to immunolabelling for the Na+ ion channel ASIC2, previously reported in both spindle primary and lanceolate endings. SK1 was not detected in sensory terminals of either muscle spindles or lanceolate endings. SK2 was found in the terminals of both muscle spindles and lanceolate endings, where it colocalised with the SLV marker SYN (spindles and lanceolates) and the satellite glial cell (SGC) marker S100 (lanceolates). SK3 was not detected in muscle spindles; by contrast it was present in hair follicle endings, expressed predominantly in SGCs but perhaps also in the SGC: terminal interface, as judged by colocalisation statistical analysis of SYN and S100 immunoreactivity. The possibility that all three isoforms might be expressed in pre-terminal axons, especially at heminodes, cannot be ruled out. Differential distribution of SK channels is likely to be important in their function of responding to changes in intracellular [Ca2+] thereby modulating mechanosensory transduction by regulating the excitability of the sensory terminals. In particular, the presence of SK2 throughout the sensory terminals of both kinds of mechanoreceptor indicates an important role for an outward Ca2+-activated K+ current in the formation of the receptor potential in both types of ending.
Highlights
Ca2+-activated K+ channels (SK and BK channels, collectively KCa) are known to play various roles that involve repolarisation of cell membranes, including the regulation of firing rates in central neurons, of smooth muscle tone, and of synaptic transmission [1]
Using sensory endings of rat muscle spindles as a model of the role of SLVs we have presented evidence that they are involved in autogenic modulation of sensory-ending excitability, mediated by glutamate released from SLVs during their recycling [6]
SK2 We begin with SK2 as we found anti-SK2 immunoreactivity in the terminals both of sensory endings of muscle spindles and lanceolate endings of hair follicles
Summary
Ca2+-activated K+ channels (SK and BK channels, collectively KCa) are known to play various roles that involve repolarisation of cell membranes, including the regulation of firing rates in central neurons, of smooth muscle tone, and of synaptic transmission [1] They have been described in a variety of other cell types, including dorsal-root ganglion cells [2,3], though there are conflicting reports about the possible occurrence of KCa channels in sensory terminals of low-threshold mechanoreceptors, in particular those of the mammalian muscle spindle [4,5]. Using sensory endings of rat muscle spindles as a model of the role of SLVs we have presented evidence that they are involved in autogenic modulation of sensory-ending excitability, mediated by glutamate released from SLVs during their recycling [6] This presynaptic similarity of mechanosensory endings prompted us to investigate Ca-dependent mechanisms that might regulate SLV recycling, and/or afferent firing
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