Lamellar cells in Pacinian and Meissner corpuscles are touch sensors

The skin covering the human palm and other specialized tactile organs contains a high density of mechanosensory corpuscles tuned to detect transient pressure and vibration. These corpuscles comprise a sensory afferent neuron surrounded by lamellar cells. The neuronal afferent is thought to be the mechanical sensor, whereas the function of lamellar cells is unknown. We show that lamellar cells within Meissner and Pacinian corpuscles detect tactile stimuli. We develop a preparation of bill skin from tactile-specialist ducks that permits electrophysiological recordings from lamellar cells and demonstrate that they contain mechanically gated ion channels. We show that lamellar cells from Meissner corpuscles generate mechanically evoked action potentials using R-type voltage-gated calcium channels. These findings provide the first evidence for R-type channel-dependent action potentials in non-neuronal cells and demonstrate that lamellar cells actively detect touch. We propose that Meissner and Pacinian corpuscles use neuronal and non-neuronal mechanoreception to detect mechanical signals.

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Lamellar cells in Pacinian and Meissner corpuscles are touch sensors

10.1101/2020.08.24.265231 ◽

2020 ◽

Author(s):

Yury A. Nikolaev ◽

Viktor V. Feketa ◽

Evan O. Anderson ◽

Elena O. Gracheva ◽

Sviatoslav N. Bagriantsev

Keyword(s):

Action Potentials ◽

Afferent Neuron ◽

Transient Pressure ◽

Pacinian Corpuscles ◽

Voltage Gated ◽

Voltage Gated Calcium Channels ◽

Tactile Stimuli ◽

Electrophysiological Recordings ◽

Mechanical Sensor ◽

Channel Dependent

AbstractThe skin covering the human palm and other specialized tactile organs contains a high density of mechanosensory corpuscles tuned to detect transient pressure and vibration. These corpuscles comprise a sensory afferent neuron surrounded by lamellar cells1-3. The neuronal afferent is thought to be the mechanical sensor within the corpuscle, whereas the function of lamellar cells is unknown2,4,5. Here we show that lamellar cells within Meissner and Pacinian corpuscles detect tactile stimuli. We develop a preparation of bill skin from tactile-specialist ducks that permits electrophysiological recordings from lamellar cells and demonstrate that they contain mechanically-gated ion channels. We also show that lamellar cells from Meissner corpuscles generate mechanically-evoked action potentials using R-type voltage-gated calcium channels. These findings provide the first evidence for R-type channel-dependent action potentials in non-neuronal cells and demonstrate that lamellar cells are active detectors of touch. We propose that Meissner and Pacinian corpuscles use both neuronal and non-neuronal mechanoreception to detect mechanical signals.

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The structural biology of voltage-gated calcium channel function and regulation

Biochemical Society Transactions ◽

10.1042/bst0340887 ◽

2006 ◽

Vol 34 (5) ◽

pp. 887-893 ◽

Cited By ~ 34

Author(s):

F. Van Petegem ◽

D.L. Minor

Keyword(s):

Neurotransmitter Release ◽

Action Potentials ◽

Molecular Switches ◽

Voltage Gated ◽

Calcium Dependent ◽

Voltage Gated Calcium Channels ◽

Dependent Inactivation ◽

Voltage Dependent ◽

Soluble Calcium ◽

Molecular Framework

Voltage-gated calcium channels (CaVs) are large (∼0.5 MDa), multisubunit, macromolecular machines that control calcium entry into cells in response to membrane potential changes. These molecular switches play pivotal roles in cardiac action potentials, neurotransmitter release, muscle contraction, calcium-dependent gene transcription and synaptic transmission. CaVs possess self-regulatory mechanisms that permit them to change their behaviour in response to activity, including voltage-dependent inactivation, calcium-dependent inactivation and calcium-dependent facilitation. These processes arise from the concerted action of different channel domains with CaV β-subunits and the soluble calcium sensor calmodulin. Until recently, nothing was known about the CaV structure at high resolution. Recent crystallographic work has revealed the first glimpses at the CaV molecular framework and set a new direction towards a detailed mechanistic understanding of CaV function.

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Inhibition of Dendritic Calcium Influx by Activation of G-Protein–Coupled Receptors in the Hippocampus

Journal of Neurophysiology ◽

10.1152/jn.1997.78.6.3484 ◽

1997 ◽

Vol 78 (6) ◽

pp. 3484-3488 ◽

Cited By ~ 13

Author(s):

Huanmian Chen ◽

Nevin A. Lambert

Keyword(s):

Calcium Channels ◽

Action Potential ◽

G Protein ◽

Pyramidal Neuron ◽

Action Potentials ◽

Calcium Influx ◽

G Protein Coupled Receptors ◽

Voltage Gated ◽

Voltage Gated Calcium Channels ◽

G Protein Coupled

Chen, Huanmian and Nevin A. Lambert. Inhibition of dendritic calcium influx by activation of G-protein–coupled receptors in the hippocampus. J. Neurophysiol. 78: 3484–3488, 1997. Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein–coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx. Activation of adenosine receptors, which couple to Gi proteins, inhibited calcium influx in cell bodies and proximal dendrites without inhibiting action-potential propagation into the proximal dendrites. Inhibition of dendritic calcium influx was not changed in the presence of 50 μM nickel, which preferentially blocks T-type channels, suggesting influx through these channels is not increased by activation of G-proteins. Adenosine inhibited propagation of action potentials into the distal branches of pyramidal neuron dendrites, leading to a three- to fourfold greater inhibition of calcium influx in the distal dendrites than in the soma or proximal dendrites. These results suggest that voltage-gated calcium channels are inhibited in pyramidal neuron dendrites, as they are in cell bodies and terminals and thatG-protein–mediated inhibition of action-potential propagation can contribute substantially to inhibition of dendritic calcium influx.

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Functions of Presynaptic Voltage-gated Calcium Channels

Function ◽

10.1093/function/zqaa027 ◽

2020 ◽

Vol 2 (1) ◽

Author(s):

Annette C Dolphin

Keyword(s):

Calcium Channels ◽

Neurotransmitter Release ◽

Action Potentials ◽

Voltage Dependence ◽

Kinetic Properties ◽

Excitable Cells ◽

Single Action ◽

Voltage Gated ◽

Voltage Gated Calcium Channels ◽

Vesicular Release

Abstract Voltage-gated calcium channels are the principal conduits for depolarization-mediated Ca2+ entry into excitable cells. In this review, the biophysical properties of the relevant members of this family of channels, those that are present in presynaptic terminals, will be discussed in relation to their function in mediating neurotransmitter release. Voltage-gated calcium channels have properties that ensure they are specialized for particular roles, for example, differences in their activation voltage threshold, their various kinetic properties, and their voltage-dependence of inactivation. All these attributes play into the ability of the various voltage-gated calcium channels to participate in different patterns of presynaptic vesicular release. These include synaptic transmission resulting from single action potentials, and longer-term changes mediated by bursts or trains of action potentials, as well as release resulting from graded changes in membrane potential in specialized sensory synapses.

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