Pacinian corpuscles (PCs) are tactile receptors composed of a nerve ending (neurite) that is encapsulated by layers of lamellar cells. PCs are classified as primary mechanoreceptors because there is no synapse between the transductive membrane and the site of actionpotential generation. These touch receptors respond in a rapidly adapting manner to sustained pressure (indentation or displacement), which until now was believed to be attributable solely to the mechanical properties of the capsule. However, evidence of positive immunoreactivity for GABA receptors on the neurite, as well as evidence for gene expression of synaptobrevin in the lamellar cells led to the hypothesis that GABAergic inhibition originating from the lamellar cells is involved in the rapid adaptation process of PCs. Electrophysiological data from isolated PCs demonstrates that, in the presence of either gabazine or picrotoxin (GABA receptor antagonists), many action potentials appear during the static portion of a sustained indentation stimulus (similar to slowly adapting receptors) and that these "static" spikes completely disappear in the presence of GABA. It was consequently hypothesized that glutamate, released by either the neurite itself or the lamellar cells, caused these action potentials. Indeed, the glutamate receptor blocker kynurenate either decreased or totally eliminated the static spikes. Together, these results suggest that GABA, emanating from the modified Schwann cells of the capsule, inhibits glutamatergic excitation during the static portion of sustained pressure, thus forming a "mechanochemical," rather than purely mechanical, rapid adaptation response. This glial-neuronal interaction is a completely novel finding for the PC.
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The role of the capsule encasing the Pacinian corpuscle's (PC's) neurite, where mechanotransduction occurs, may be more than mechanical. The inner core of the PC's capsule consists of lamellar cells that are of Schwann-cell origin. Previously, we found both voltage-gated Na+ and K+ channels in these inner-core lamellae. Research on astrocytes and Schwann cells shows bidirectional signaling between glia and neurons, a major component of which is glutamate. Furthermore, Merkel cells show positive immunoreactivity for glutamate receptor mGluR5, and the glutamate-receptor antagonist kynurenate greatly decreases the static activity of the slowly adapting neurons of Merkel cell-neurite complexes. To investigate the possibility of glutaminergic interaction in PCs, we applied antibodies to glutamate, glutamate receptors, glutamate transporters, and SNARE proteins to cat mesenteric PC sections. Positive labeling was seen in the inner-core lamellae, at inter-lamellar connections, where the lamellae contact the membrane of the neurite and at the lamellar tips. The presence of these proteins on the lamellae and neurite membranes, demonstrated both with immunofluorescent light microscopy as well as immunogold electron microscopy, suggests a chemical, possibly bidirectional, interaction between the lamellar cells and the neurite. Thus, the capsule of the PC, apart from having a mechanical filtering function, may also provide an environment for lamellar-neurite interaction, perhaps acting as a neuro-modulator of the initiation, and/or continuation, of the mechanical-electrical transduction process. At the very least, the presence of the aforementioned proteins suggest some sort of "synaptic-like" activity in these mechanoreceptors, which up until now has not been considered possible.
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