Sensory Systems · Unit 4: Proprioception and interoception

Proprioception: Sensing the Body's Own Position

Spindles, tendon organs and joint receptors all report on the body, but what each one actually signals, which channel carries the current and what a person loses without it were worked out over decades, the channel and the human loss only in 2015 and 2016. This lesson starts where the core course stops, at transduction and taxonomy: human recordings and vibration illusions, Piezo2 in mice and in two people who lack it, two competing mouse atlases of proprioceptor types, and the skeleton's dependence on proprioceptive neurons. Afterwards you can read a mechanically activated current as a decay curve and design an experiment that separates a developmental window from continuous need.

Watch first Position Is an Estimate · 2:55

Close your eyes, and a vibrator pressed on your biceps tendon at 100 Hz can make you misjudge where your elbow is, by as much as 40 degrees when the muscle is contracting, though the joint has not moved. Your sense of limb position is a computed estimate, built from sensors you cannot feel. This lesson asks what those sensors report, what channel turns stretch into current, and what happens to people and mice that lack it.

Motor units and reflexes already covered spindle anatomy, the Ia afferent, the tendon organ, the stretch reflex and gamma drive, and touch and pain mentioned that two people lacking PIEZO2 are poor at sensing limb position. We start at what is left: transduction, taxonomy and consequences. For how adaptation is measured, see sensory coding.

What each ending actually reports

Human limb position is not read from one receptor type. A review of the human literature concludes that limb-position information is generated by populations of afferents, not by one receptor (Proske and Gandevia, 2012). Here are the main members, with the common mistakes removed.

A muscle spindle has encapsulated intrafusal fibres with two sensory endings, a primary (Ia) and a secondary (II). Both signal static muscle length, and Ia endings add sensitivity to the rate of change of length. So “Ia is velocity and II is position” is wrong: Ia carries both, and the difference is that Ia endings are the more sensitive to the rate of change, while II endings also respond to it, though less. Gamma motor neurons on the polar ends of the intrafusal fibres set the gain of the afferent signal. Human microneurography, in which an electrode in a nerve records single afferents, separates the two classes by vibration: Roll and Vedel (1982) recorded 15 primary and five secondary endings from tibialis anterior and extensor digitorum longus in healthy people, and the secondary endings were less sensitive to low-amplitude tendon vibration.

A Golgi tendon organ sits at the myotendinous junction and has one Ib afferent. It is highly sensitive to contraction of the motor units in series with it, so it reports force from those units. It is not an injury alarm that waits for dangerous tension.

AI-generated illustration: a schematic muscle with a muscle spindle lying along its fibres, showing a primary Ia ending, a secondary II ending and gamma motor neuron inputs at its ends, and a Golgi tendon organ with an Ib afferent at the junction between muscle and tendon. An inset states what each ending reports.
A muscle spindle has a primary Ia and a secondary II ending, set in gain by gamma motor neurons at its polar ends. Both signal static muscle length and Ia adds sensitivity to its rate of change. A Golgi tendon organ at the myotendinous junction reports force from the motor units in series with it.

Joint receptors were once credited with signalling joint angle. Burke, Gandevia and Macefield (1988) recorded from the median and ulnar nerves at the wrist of six conscious people while their finger and thumb joints were rotated passively. Most joint afferents fired near the limits of rotation, not across the range. One afferent from the thumb interphalangeal joint responded in one direction throughout the physiological range, so the correction is “mostly near the limits, with exceptions”. Proske (2023) proposed that near elbow extension, joint signals combine with spindle signals to carry joint-limit information. Treat that as a hypothesis.

Spindle endings are not passive. Bewick, Reid, Richardson and Banks (2005) worked in adult rat hindpaw lumbrical nerve-muscle preparations ex vivo. The dye FM1-43 was taken up and released at primary endings in a calcium-sensitive way, which indicated recycling of synaptic-like vesicles about 50 nm across. Added glutamate raised the excitability of Ia endings to stretch, and the compound PCCG-13 lowered it even with no glutamate added. The authors interpreted this as an endogenous peripheral glutamatergic system. The pharmacology did not establish the receptor (the authors suggested a phospholipase D-linked metabotropic one), and it was done in rat.

Vibrating a tendon moves the limb you feel

Goodwin, McCloskey and Matthews (1972) vibrated the biceps or triceps tendons of human subjects at 100 Hz and asked them to judge elbow position. The subjects perceived a position consistent with stretching the vibrated muscle. During contraction the errors could reach 40 degrees. That figure is the error under contraction in that experiment, not a standard size of the illusion. In the leg, Roll and Vedel found primary endings more sensitive to low-amplitude vibration than secondary endings, and in their elbow illusions the perceived velocity of movement rose up to about 70 to 80 Hz in a 10 to 120 Hz series before falling. Those two sets of data come from different limbs and were not recorded together.

AI-generated illustration: a side view of a bent human arm resting on a table, with a vibrator pressed on the biceps tendon at the elbow. The real forearm stays fixed, while a dashed outline of a second forearm shows the position the subject feels.
Vibrating the biceps tendon at 100 Hz, Goodwin, McCloskey and Matthews found that subjects judged a position consistent with stretching the vibrated muscle, though the joint had not moved. The illusion shows that muscle afferent signals bias the percept.

Read the result with care. The illusion shows that muscle afferent signals bias the percept. Primary endings are the likely carriers, since they are the more vibration-sensitive, but the experiments do not show that only they act. The same argument is what the next section applies to a channel.

Piezo2: the mouse current and the human loss

Which protein turns stretch into current at a spindle ending? Piezo2 is a mechanically activated channel, covered in Piezo channels and the physics of force. Woo and colleagues (2015) supplied three kinds of evidence in mouse:

  • Where it is. A Piezo2-GFP reporter showed the protein in proprioceptor endings that innervate spindles and tendon organs of postnatal hindlimb muscle.
  • What current it carries. Whole-cell patch clamp with mechanical indentation of dissociated adult DRG cell bodies, labelled with a parvalbumin-driven Cre line, recorded rapidly adapting currents.
  • Whether the ending needs it. Conditional deletion of Piezo2 with Pvalb-Cre or with HoxB8-Cre sharply reduced stretch-evoked firing in an isolated extensor digitorum longus muscle with its deep peroneal nerve, from postnatal male mice.

A small stretch response remained after deletion (in the paper, one of eight muscles for each Cre line still increased its firing on stretch), so the careful word is principal transducer, not the transducer. Whether the pore is Piezo2 itself in every subtype, and what carries the rest, were not settled by this paper.

AI-generated illustration: three schematic panels from a mouse study of Piezo2. First, a sensory ending around a spindle capsule marked by a green reporter. Second, a dissociated neuron with a patch pipette and an indentation probe. Third, an isolated muscle with its nerve being stretched while a recording electrode hooks the nerve.
Woo and colleagues used three setups in mouse: a Piezo2-GFP reporter for where the protein sits, patch clamp with mechanical indentation of dissociated neurons for the current it carries, and stretch of an isolated muscle with its nerve for whether the ending needs it. A small stretch response remained after deletion, so Piezo2 is the principal, not the only, transducer.

Worked problem: reading the soma current

In the cell-body recordings, 23 of 25 labelled neurons had rapidly adapting mechanically activated currents, and the inactivation time constant of those rapidly adapting currents was reported as 5.6 ± 0.33 ms (the paper’s notation, which I leave as it is).

Step 1, a fraction. 23/25 = 0.92, so 92% of this sample of 25. Parvalbumin labels proprioceptors and some other neurons, so this is not 92% of proprioceptors.

Step 2, a decay. Assume the current decays as a single exponential from its peak with tau = 5.6 ms. That is our assumption, not the paper’s. The fraction left at time t is exp(-t/tau).

fraction remaining = exp(-t / tau)

At 10 ms, exp(-10/5.6) = exp(-1.786) = 0.168, about 17%. At 20 ms, exp(-20/5.6) = exp(-3.571) = 0.028, about 3%.

Reading the soma current as a decay curve⚙ original · interactive
Time constant τ (a computed curve; the 5.6 ms is reported, the other two are what-ifs) The ± 0.33 is the paper’s, its statistic not stated in the lesson.
Fraction of peak remaining
0.168
As a percent of the peak
about 17%
Arithmetic
exp(−10.0/5.6) = exp(−1.786) = 0.168

In this sketch: one exponential from the peak, τ from Pvalb-labelled adult mouse DRG cell bodies in culture (Woo and colleagues, 2015), no rise phase, no spikes, no ending.

Rule to keep: fraction remaining = exp(−t/τ), and it is a current in cultured cell bodies under indentation, not a spindle afferent firing spikes. The 25 dots are a count in one sample, not part of the curve.

Step 3, the limits. This is a current in a cell body in culture, not a current at a spindle ending. It says how fast the channel population inactivates under indentation, not how a spindle afferent adapts when it fires spikes.

Humans

Chesler and colleagues (2016) reported two unrelated females with compound inactivating PIEZO2 variants, who presented at 18 and 8 years and were last examined at 19 and 10. In a forced-choice task with 10-degree angular joint movements, and in reaching with and without sight, proprioceptive ataxia and dysmetria became markedly worse without visual cues. Their report says they could still perform tasks such as walking, talking and writing, though one walked only with support. Delle Vedove and colleagues (2016) described ten affected people in four consanguineous families, with homozygous variants in each family (three frameshifts and one two-exon deletion), and a picture that included arthrogryposis, muscular atrophy, perinatal respiratory distress and scoliosis. Two people are a clinical series, not a prevalence. The human data show that loss of the gene goes with the deficit, and they do not show which endings account for each part.

An older case shows what such loss feels like in practice. Cole and Sedgwick (1992) studied an adult man, known as I.W., with a complete loss of large-fibre sensation below the neck that had lasted more than 16 years. He lacked light touch and proprioception below the neck but kept pain, heat, cold and the sense of muscular fatigue, and in their testing no novel movement was possible without visual feedback. That separates sensory loss from motor loss. The participant’s cause and onset are not needed for the point and are not given here.

Eight groups, or five: proprioceptor atlases and their disagreement

The classical picture has three classes: Ia, II and Ib. In 2021 two papers asked what single-cell RNA sequencing finds (for the method, see sequencing and genomes).

Wu and colleagues (Nature Communications 12:1026) sorted proprioceptors from the C5 to T1 dorsal root ganglia of adult mice (postnatal day 54, PV-Cre crossed to Ai14), sequenced them by Smart-seq2, kept 1,109 neurons after quality control and reported eight molecular subgroups. The analysis first found seven clusters, and one heterogeneous cluster was subdivided to give eight. Oliver and colleagues (Nature Communications, Molecular correlates of muscle spindle and Golgi tendon organ afferents) sampled neurons labelled by an intersection of PV-Cre and Runx3-FlpO, at all segmental levels in adults of at least P56, and reported five clusters. They validated Ia (calretinin, calbindin 1, vGlut2) and Ib (Pcdh8, Pou4f3) by markers and tissue, and assigned the rest to group II only provisionally, proposing Nxph1 as a possible group II marker that needs more validation.

Do the counts conflict? Not necessarily. They differ in labelling, age range, sampling depth and how clusters were cut, and Wu’s eight include a choice to split one cluster. Neither is a human atlas. A cluster is a molecular class, not a proven function, and the number of groups depends on the data set and the method. The practical lesson is to cite the paper with the count. Related atlases are in the sensory neuron atlas; for how proprioceptors depend on neurotrophin signalling in development, see Trk and p75.

Wu and colleagues also tested what experience does. Adult C57BL/6J males started four weeks of free-wheel or locked-wheel housing at eight weeks of age. Running changed the marker-defined composition of Ia subtypes, but the total number of brachial Ia proprioceptors was unchanged. That could be marker regulation, conversion of subtype, or something else, and lineage tracing would be needed to choose among them.

A sense that shapes bone: proprioceptor Piezo2 and postnatal alignment (2020)

If a muscle sensor is removed, would the spine notice? Assaraf and colleagues (2020) used Pvalb-Cre to delete Piezo2 in mice. Serial in vivo CT at P40, P60 and P90 showed scoliosis by P60 in some of these animals, and hip histology showed signs of dysplasia by P14. Spine histology at P10 showed no apparent differences from controls in bone, cartilage or surrounding soft tissue. When Piezo2 was deleted instead with Col1a1-Cre or Col2a1-Cre, which target osteogenic and chondrogenic lineages, the spinal deformities did not appear in the tested ages. The authors interpreted the results as a non-autonomous role: proprioceptive Piezo2 acts on the skeleton through a route that does not need Piezo2 inside the bone cells tested.

What the paper does not show is the intervening pathway, and a human family with scoliosis and PIEZO2 variants shows association, not the causal tissue. Parvalbumin-driven Cre also labels cells that expressed parvalbumin at some time, and not only proprioceptors.

Design problem

In the Assaraf mice, proprioceptor-directed Piezo2 deletion gave scoliosis in some animals by P60 and hip dysplasia signs by P14, while the tested collagen-I and collagen-II deletions did not reproduce the spinal phenotype. Design experiments that decide whether the skeletal phenotype needs proprioceptive feedback in a postnatal window or continuously in adults.

One way to do it

Timing. Use an inducible deletion of Piezo2 in proprioceptors and open it at two times: early, before alignment is established, and later, after it. Image the same animals with serial CT at matched ages. If only the early deletion gives scoliosis, a postnatal window is needed. If the late deletion also curves the spine, feedback is needed continuously.

Channel versus cell. Compare Piezo2 deletion with a generic reversible silencing of the same neurons, and with loss of the proprioceptor population itself. A result that follows the channel deletion and silencing alike points to lost activity, while one that needs the cells to disappear points to something the cells provide beyond transduction.

Controls and scope. Use littermate controls and a second, independent driver, because one Cre line labels cells that expressed it at some time and not a pure type. Keep the ages tested in the claim.

Limit. Even a clean answer shows the requirement in the mouse. Human PIEZO2 families show association, so they do not name the causal tissue.

How we measure it

Microneurography

A fine electrode is inserted through the skin into a peripheral nerve of an awake person and records the spikes of single afferents while the limb is moved or the muscle is vibrated. It gives the firing of identified endings in humans but samples few units, from accessible nerves.

Tendon-vibration psychophysics

A vibrator is held against a tendon and the person reports or matches where the limb seems to be. A systematic error in the direction expected from stretching the muscle shows that muscle afferent signals bias the percept, but it does not by itself show which ending class did it.

Conditional gene deletion with ex vivo muscle-nerve recording

A Cre driver removes a floxed gene in chosen cells, and an isolated muscle with its nerve is stretched while sensory firing is recorded. It tests whether the gene is needed for the ending's response, only in the cells the driver reached and at the ages tested.

Single-cell RNA sequencing of labelled proprioceptors

Genetically labelled neurons are dissociated, sorted and their transcripts read cell by cell. Clustering then groups neurons by expression. A cluster is a molecular class, and it becomes a functional type only when anatomy, physiology or behaviour is tied to it.

Finish line

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Next · Lesson 16

Vagal Sensory Neurons: The Body Reports to the Brain

Light on one set of vagal sensory axons stops an anaesthetized mouse breathing, and light on another set makes it breathe fast and shallow. What does each set report, and how would you know?

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Seung-Hyun Woo

Seung-Hyun Woo

First author of the 2015 Nature Neuroscience paper from Ardem Patapoutian's group that placed Piezo2 in mouse muscle spindle and tendon organ endings and showed that its conditional deletion sharply reduced stretch-evoked firing.

Proprioceptors were hard to study because their endings sit inside muscle, and the channel that turns stretch into current was unknown. Woo and colleagues approached it from three sides. They used a Piezo2 reporter to show the protein in the endings that wrap spindles and tendon organs of mouse hindlimb muscle. They recorded mechanically activated current from dissociated adult mouse sensory neuron cell bodies labelled by a parvalbumin-driven Cre line. And they stretched an isolated extensor digitorum longus muscle with its nerve attached and recorded the firing of its sensory fibres, in mice in which Piezo2 had been deleted with either of two Cre lines. Stretch-evoked firing was sharply reduced. The paper called Piezo2 the principal channel, not the only one, and the three preparations answer different questions: where the protein is, what current it carries, and whether the ending needs it. It turned a candidate into a tested gene.

✓ verbatim Woo SH, Lukacs V, de Nooij JC, Zaytseva D, Criddle CR, Francisco A et al., Nat Neurosci 18:1756-1762 (2015), doi 10.1038/nn.4162.
Alexander T. Chesler

Alexander T. Chesler

Led the 2016 New England Journal of Medicine report of two people with compound inactivating PIEZO2 variants, whose proprioceptive ataxia and dysmetria worsened markedly without visual cues.

A mouse knockout shows what an animal loses in a defined assay; it does not show what a person loses. Chesler's group reported two unrelated females, who presented at 18 and 8 years of age, with biallelic inactivating variants in PIEZO2. The investigators tested them rather than inferring from the mouse. In a forced-choice task, joint movements of 10 degrees were used to test their sense of direction, and reaching movements were assessed with the participants able to see their limbs and with sight blocked. Proprioceptive ataxia and dysmetria, a misjudging of the distance a reach should cover, became markedly worse without vision. Yet the two could still perform tasks such as walking, talking and writing, though one of them walked only with support. The paper is a two-person clinical series, so it shows what happens when the gene is lost in people, not how common the loss is or which endings account for each deficit. It supplied the human half of the Piezo2 argument.

✓ verbatim Chesler AT, Szczot M, Bharucha-Goebel D, Ceko M, Donkervoort S, et al., The role of PIEZO2 in human mechanosensation, N Engl J Med 375:1355-1364 (2016), doi 10.1056/NEJMoa1602812.
Guy S. Bewick

Guy S. Bewick

With Robert W. Banks, co-led the 2005 Journal of Physiology study in adult rat lumbrical muscle that linked synaptic-like vesicle recycling in spindle primary endings to the excitability of those endings.

By his own 2015 account, Bewick first telephoned Robert Banks in 1999 to ask whether spindle afferent terminals contain vesicles, after a dye that marks recycling vesicles had labelled them. Vesicles are the usual machinery of a synapse, not of a sensory ending. The 2005 paper tested it in adult rat hindpaw lumbrical nerve-muscle preparations kept ex vivo. Their dye FM1-43 was taken up and released by the primary endings in a calcium-sensitive way, consistent with vesicle recycling. Adding glutamate raised the excitability of the endings to stretch, and a compound called PCCG-13 lowered it even when no glutamate had been added. The authors concluded that the ending has an endogenous peripheral glutamatergic system. The pharmacology did not establish the receptor (the authors suggested a phospholipase D-linked metabotropic one), and the work was done in rat, not human. It made the spindle ending a site of feedback, not just a transducer.

✓ verbatim Bewick GS, Reid B, Richardson C, Banks RW, J Physiol 562:381-394 (2005), doi 10.1113/jphysiol.2004.074799; Bewick GS, J Anat (2015), doi 10.1111/joa.12337 (first-person account).
Jonathan Cole

Jonathan Cole

With Ewen Sedgwick, reported in 1992 the sensory and movement testing of a man, known by the initials I.W., who lacked light touch and proprioception below the neck.

Without a sense of limb position, can a person still move? Cole worked with a participant who had a complete loss of large-fibre sensory function below the neck; in the 1992 report that loss had lasted more than 16 years. Cole's own later account dates his first meeting with the man to the mid-1980s, which is his recollection and not an independently documented date. Testing showed a dissociation. Light touch and proprioception were absent, but pain, heat, cold and the sense of muscular fatigue remained. What he could not do, in the reported testing, was make a novel movement without watching it. The case separated sensory loss from motor loss. He had limited motor memory, enough to hold a posture or continue a simple repetitive movement.

✓ verbatim Cole JD, Sedgwick EM, J Physiol (1992), doi 10.1113/jphysiol.1992.sp019099; Cole J, Oxford University Press blog, June 2016 (first-person account).
Test yourself
Question 1 of 8 Score 0 / 0

A student writes that Ia afferents signal only the velocity of stretch and group II afferents only the position. Which statement corrects this?
Sources & Integrity

Every structure, slide, simulation, and clip on this page is listed below with the source it came from. None of the 3D structures is drawn by hand or by AI: each one loads by accession ID from RCSB PDB or PubChem. This panel is generated from the lesson's own data file, so what it lists is what the page loads.

Simulations

  • How fast the soma current decays · Original interactive — Biochemistrypedia (Deppmann Lab).

Scientist profiles & quotes

  • Seung-Hyun Woo — Woo SH, Lukacs V, de Nooij JC, Zaytseva D, Criddle CR, Francisco A et al., Nat Neurosci 18:1756-1762 (2015), doi 10.1038/nn.4162.
  • Alexander T. Chesler — Chesler AT, Szczot M, Bharucha-Goebel D, Ceko M, Donkervoort S, et al., The role of PIEZO2 in human mechanosensation, N Engl J Med 375:1355-1364 (2016), doi 10.1056/NEJMoa1602812.
  • Guy S. Bewick — Bewick GS, Reid B, Richardson C, Banks RW, J Physiol 562:381-394 (2005), doi 10.1113/jphysiol.2004.074799; Bewick GS, J Anat (2015), doi 10.1111/joa.12337 (first-person account).
  • Jonathan Cole — Cole JD, Sedgwick EM, J Physiol (1992), doi 10.1113/jphysiol.1992.sp019099; Cole J, Oxford University Press blog, June 2016 (first-person account).

Quotes are verbatim from the cited source. Profile text is original to this site and was checked against the sources cited.

Animated explainer

Position Is an Estimate · narration: an AI narrator voice (Gemini, Charon) reading narration written from this lesson's text · animation: AI-generated in code (Manim) by Claude, a schematic with no drawn molecular structures, plots computed from their equations · captions from the narration script.

Images & figures

3 illustrations in this lesson are AI-generated: drawn by an image model from a written spec, then checked by a separate AI judge against the spec and the lesson text. None shows a chemical structure or data.

  • a schematic muscle with a muscle spindle lying along its fibres, showing a primary Ia ending, a secondary II ending and gamma motor neuron inputs at its ends, and a Golgi tendon organ with an Ib afferent at the junction between muscle and tendon. An inset states what each ending reports.
  • a side view of a bent human arm resting on a table, with a vibrator pressed on the biceps tendon at the elbow. The real forearm stays fixed, while a dashed outline of a second forearm shows the position the subject feels.
  • three schematic panels from a mouse study of Piezo2. First, a sensory ending around a spindle capsule marked by a green reporter. Second, a dissociated neuron with a patch pipette and an indentation probe. Third, an isolated muscle with its nerve being stretched while a recording electrode hooks the nerve.

Every 3D structure is rendered live from an accession ID, and every plot is drawn from its equation in the browser.

integrity Machines check the mechanics. The build confirms that every local file exists, that every question's answer key points at a real choice, and that any AI-generated scientific figure names the person who checked it; a weekly job re-resolves every accession ID against its database. Questions are original; MCAT-style items are written for this site and are not real AAMC questions. Banned sources (the Tymoczko textbook, publisher decks, copyrighted figures) are not used.

Like I'm five

You know where your arm is even with your eyes shut. Tiny sensors inside your muscles and tendons tell your brain how long and how hard each muscle is. A special door in the sensor opens when it is stretched, and a person without that door gets clumsy when they cannot look at their hands.
High school

Proprioception is the sense of where your body parts are and how hard your muscles are working. Muscle spindles report how long a muscle is and how fast it is changing, and tendon organs report how much force a muscle is making. A protein called Piezo2 forms a channel that opens when the sensory ending is stretched. Mice and people missing it have poor body sense, and in mice the loss also changes how the spine and hips grow.
College

Both Ia and group II spindle afferents signal static muscle length and Ia afferents add sensitivity to its rate of change, while Golgi tendon organs report force through one Ib afferent each. Piezo2 is the principal mechanotransduction channel of mouse proprioceptors: it is present in the endings, carries a rapidly adapting current in labelled sensory neurons, and its conditional deletion sharply reduces stretch-evoked firing, though not completely. Two people with inactivating PIEZO2 variants had severe proprioceptive ataxia that worsened without vision. In mice, proprioceptor-targeted Piezo2 deletion also produces scoliosis and hip dysplasia, which the authors interpreted as a non-autonomous effect on the skeleton.
Graduate

Population coding across spindle, tendon organ and joint afferents, not a single receptor, specifies limb position, and the relative contributions are debated: Burke and colleagues found most human hand joint afferents fire near the ends of rotation, and Proske has proposed that joint and spindle signals combine near elbow extension, a hypothesis and not a settled replacement. Piezo2 localisation, a rapidly adapting soma current (time constant 5.6 ms in Pvalb-labelled adult neurons in culture) and reduced stretch-evoked firing after Pvalb-Cre or HoxB8-Cre deletion make it the principal mouse transducer. The residual response leaves room for other contributors. The 2021 mouse atlases (eight and five groups) differ in labelling and clustering. Open question: is the skeletal phenotype a postnatal-window effect of lost proprioceptive input, or a continuing requirement, and does it need the channel or the cells?
A telephone call about vesicles

In his own 2015 account, Guy Bewick recalls telephoning Bob Banks in 1999 to ask whether spindle afferent terminals contain vesicles, after a dye that marks recycling vesicles had labelled them. Sensory endings are supposed to turn stretch into current, and vesicles belong to synapses, so the labelling raised a question. The collaboration that followed produced the 2005 paper in adult rat lumbrical muscle: dye uptake and release suggested recycling vesicles, glutamate raised the response to stretch, and the compound PCCG-13 lowered it. Both men are authors of the paper, and the account is Bewick's recollection.

— Bewick GS, J Anat (2015), first-person account; Bewick GS, Reid B, Richardson C, Banks RW, J Physiol 562:381-394 (2005).
Eyes open, the movement returns

Two human reports with different causes describe the same pattern. The participant studied by Cole and Sedgwick lacked light touch and proprioception below the neck and could not make novel movements without visual feedback. The two people Chesler's group studied, with inactivating PIEZO2 variants, had proprioceptive ataxia and dysmetria that became markedly worse without visual cues. In each, vision stood in for a lost sense, and removing it showed how much work the missing sense had been doing.

— Cole JD, Sedgwick EM, J Physiol (1992); Chesler AT et al., N Engl J Med 375:1355-1364 (2016).
Running changed the labels, not the count

In the same 2021 atlas paper, adult male C57BL/6J mice began four weeks of free-wheel running at eight weeks of age, while a comparison group had a locked wheel. At the end, the marker-defined composition of Ia proprioceptor subtypes differed between the groups, but the total number of brachial Ia proprioceptors did not. The authors' data therefore show a change in marker-defined subtype composition in this experiment. They do not decide whether neurons switched identity, markers were regulated, or something else happened, which would need lineage tracing.

— Wu H et al., Nat Commun 12:1026 (2021), doi 10.1038/s41467-021-21173-9.

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