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Press Release: How We Feel What We Feel

from: 2015, 13 Oct - 09:00

Scientists in Tübingen and Trieste (Italy) have made a major

contribution to understanding the sense of touch and pain. A team around Dr

Jing Hu (Werner Reichardt Centre for Integrative Neuroscience – CIN, Tübingen)

discovered that two substances contained within nerve cell membranes have a

crucial impact on our perception of touch. They were able to show how the

interaction of these two substances can be interrupted in such a way that touch

stimuli are not transmitted and constant pain is alleviated.

How we feel what we feel: this question has kept

neuroscience busy for a long time. The problem is fundamentally interesting, in

that we know less about the sense of touch than any other of our five senses –

even though the corresponding sensory organ, the skin, covers our entire

bodies. But more importantly, millions of pain patients all over the world

could expect more efficacious help if we knew more about the origins of our

tactile sense.

Pushing, pulling, piercing, chafing – these

words can describe perceptions of touch, but in exaggerated form, they can also

become sources of pain. A mechanical contact produces an electrical impulse in

the cellular membranes of neurons that conduct touch stimuli to the brain, the

so-called mechanoreceptors. How this happens, and which biochemical and biophysical

mechanisms are at work, though, nobody was able to answer until relatively

recently. Since the 1980s we have at least known that ion channels play a major

role: when the nerve cell is deformed, this stimulates certain proteins that

run right through the cell membrane like a channel. The deformation opens this

protein channel for a specific kind of ion, which enters the cell and produces

an electrical impulse.

Dr. Hu and her team were now able to show that

this is not all: the cell membrane surrounding the ion channels is just as

important. If it is soft, it easily yields to pressure, which does not create

an impulse. But if it is more rigid, the ion channels in the area respond

strongly to the deformation.

The behaviour of these cell membranes is controlled

by two substances. That molecule of ill repute, cholesterol, has been

well-known for a long time. But Hu and her colleagues now showed that – at

least in mice – „stomatin-like protein‑3“, or STOML3, plays a decisive role

too. Only the interaction of cholesterol and STOML3 effects a stiffening of the

cell membrane under soft pressure. This makes the activation of surrounding ion

channels possible. If one of the pieces of this puzzle is not present, or if

their reaction is disrupted, there is no stimulus.

Through behavioural studies in mice, the

scientists showed that this mechanism could apply similarly in human pain

patients. If new drugs are developed following this line of inquiry, even

patients suffering from allodynia might stand to benefit in the future: this

condition turns even the slightest of touches into intense pain.

Publication:
Yanmei Qi, Laura Andolfi, Flavia Frattini, Florian Mayer,

Marco Lazzarino & Jing Hu: Membrane Stiffening by STOML3 Facilitates

Mechanosensation in Sensory Neurons. Nature Communications 6: 8512, October 7th, 2015.

www.nature.com/ncomms/2015/151007/ncomms9512/full/ncomms9512.html

 

dx.doi.org/10.1038/ncomms9512

Organization:
  • Werner Reichardt Centre for Integrative Neuroscience
Reseach Group: Sensory Mechanotransduction: Ion Channels and Mechanism
Contact: Dr. Jing Hu
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