Lamellar (Pacinian) corpuscles

Inner core

The inner core is populated by non-myelinating modified Schwann cells and consists of thin lamellae (30- 40 nm), becoming progressively thinner closer to the neurite. The lamellae are tightly packed so that there is a relatively small amount of fluid in the interlamellar spaces and the collagen-like fibers between the lamellae run longitudinally. Key characteristics of this stratum include elongated nuclei, the presence of mitochondria, polyribosomes, microtubules, concentric arrays of rough endoplasmic reticulum, and other membranous structures. The inner core is rich in gap junctions, thus facilitating intercellular communication and overall regulation of the environment proximal to the neurite. The successive lamellae are connected by “attachment plaques”, which, along with tight junctions, may play a role in intercellular attachment and the overall mechanical stability of the inner core.

Intermediate layer (growth zone)

This layer separates the inner from the outer core of the Pacinian corpuscle. The most prominent cellular population is modified endoneurial CD34+ fibroblasts; however, macrophages have also been detected. At later developmental stages, the cellular elements of the intermediate layer become incorporated into either the inner or outer core.

Outer core and external capsule

The outer core encapsulates the inner core and is surrounded by the external capsule. It consists of approximately 30 lamellae, identical to each other but significantly different from those comprising the inner core in terms of size, cellular composition and origin. Specifically, these concentrically arranged, flattened lamellae are wider than those found in the inner core, and are populated by perineurial cells. Collagen fibrils are present particularly on the outer surface of the lamellae and are circularly oriented.

Mechanotransduction

Mechanical stimuli deform the surface of non-specific cation channels found in the membrane of tactile receptors, causing an influx of sodium ions (Na⁺), which mediates the production of a receptor potential. The receptor potential is directly proportional to the intensity of the stimulus. When the cumulative effect of multiple receptor potentials reaches a threshold, an action potential is generated.

Both voltage-gated and voltage-independent channels have been proposed to mediate mechanotransduction. Voltage-dependent potassium channels (subtype: Kv7.4, also known as KCNQ) regulate the stimulus velocity and frequency sensitivity, whereas voltage-dependent sodium channels have a putative role in stimulus transduction (through the lamellae to the axon) and the generation of the axon potential. On the other hand, voltage-independent channels are divided into those that respond to membrane tension and those responding to membrane stretch. When the cell membrane is deformed, mechanosensitive channels transduce mechanical energy into electrical signals. The mechanical stimuli act solely on the lamellae and never directly reach the axon. The mechanical forces, along with the extracellular matrix and cytoskeletal elements, cause deformations in the axon membrane, thereby opening ion channels. Some of the most characteristic mechano-gated, voltage-independent channels include the PIEZO and TRP (Transient Receptor Potential) families.

Firing pattern

Axon potentials are generated at the onset and offset of the mechanical stimulus (off response). Specifically, spikes occur mainly during the dynamic and not the static phase of a stimulus. This is a characteristic of phasic receptors, which provide information regarding changes in the intensity of the stimulus. The absence of spikes during the static phase of the stimulus is the result of a process called adaptation.

Adaptation and the mechanochemical theory of mechanotransduction

Adaptation often results from mechanical characteristics of the capsule; however, a potential synaptic regulatory mechanism has also been proposed. The deformational properties of the capsule enable it to function as a band-pass filter, allowing only specific frequency ranges and blocking all others. Regarding the underlying synaptic mechanism of the phenomenon, glutamatergic neurotransmission has been suggested to promote the generation of action potentials during the static phase of the adapting response. Nevertheless, this excitatory effect is attenuated by the inhibitory neurotransmitter GABA (γ-aminobutyric acid), which is released from the modified Schwann cells of the inner core.