Abstract
Merkel cells (MCs) have been proposed to form a part of the MC-neurite complex with sensory neurons through synaptic contact. However, the detailed mechanisms for intercellular communication between MCs and neurons have yet to be clarified. The present study examined the increases in intracellular free Ca2+ concentration ([Ca2+]i) induced by direct mechanical stimulation of MCs. We also measured [Ca2+]i in the trigeminal ganglion neurons (TGs) following direct mechanical stimulation to the MCs in an MC-TGs coculture. The MCs were isolated from hamster buccal mucosa, while TGs were isolated from neonatal Wistar rats. Both cell populations showed depolarization-induced [Ca2+]i. Direct mechanical stimulation to MCs increased [Ca2+]i, showing stimulation strength dependence. In the MC-TGs coculture, the application of direct mechanical stimulation to MCs resulted in increased [Ca2+]i in the TGs. These changes were significantly suppressed by antagonists of glutamate-permeable anion channels (4,4′-diisothiocyanato-2,2′-stilbenedisulfonic acid; DIDS), and non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptors (MK801). Apyrase, an ATP-degrading enzyme, and suramin, a non-selective P2 purinergic receptor antagonist, did not exert inhibitory effects on these [Ca2+]i increases in the TGs following MC stimulation. These results indicated that MCs are capable of releasing glutamate, but not ATP, in response to cellular deformation by direct mechanical stimulation. The released glutamate activates the NMDA receptors on TGs. We suggest that MCs act as mechanoelectrical transducers and establish synaptic transmission with neurons, through the MC-neurite complex, to mediate mechanosensory transduction.
Highlights
Merkel cells (MCs) have been proposed to form a part of the MC-neurite complex by establishing synaptic contact with primary sensory afferents of myelinated Aβ neurons (Halata et al, 2003)
To elucidate the functional properties of neurotransmission in the MC-neurite complexes, and to determine the neurotransmitters that are released from mechanically stimulated MCs to the associated nerve endings, we investigated the changes in intracellular free Ca2+ concentration ([Ca2+]i) in the trigeminal ganglion neurons (TGs) following direct mechanical stimulation to MCs in an MC-TGs coculture system
To clarify the substrate of neurotransmitters released by MCs following mechanical stimulation, we examined the effects of apyrase and suramin on [Ca2+]i in stimulated MCs and neighboring TGs following mechanical stimulation of MCs
Summary
Merkel cells (MCs) have been proposed to form a part of the MC-neurite complex by establishing synaptic contact with primary sensory afferents of myelinated Aβ neurons (Halata et al, 2003). The MC-neurite complexes act as slowly adapting type I mechanoreceptors, which produce pressure sensation in both the skin and mucosa. Deformations of the skin initiate action potential firing in slowly adapting type I sensory afferents through the activation of mechanotransduction channels at the onset of stimuli. The Ca2+ entry is thought to release neurotransmitters to the sensory afferent that generates sustained action potential firing, the substrate of neurotransmitter(s) to drive neural communication between MCs and neurons has yet to be elucidated
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