Light touch plays a critical role in everyday tasks, like picking up a glass a playing a musical instrument. This sensation is an essential part of the body’s protective defence system, alerting us to objects in our environment that could cause us to fall or injure ourselves. This detection system is since evolved to protect us from biting insects, such as those that cause malaria and Lyme disease, by eliciting a feeling of an itch when an insect lands on your skin.
Salk researchers have discovered how neurons in the spinal cord help transmit such itch signals to the brain. Researchers have also found that this mechanical itch sensation is distinct from other forms of touch and it has this specialised pathway within the spinal cord.
Goulding and his colleagues had previously discovered a set of inhibitory neurons in the spinal cord that act like cellular brakes, keeping the mechanical itch pathway in the spinal cord turned off most of the time. Without these neurons, which produce the neurotransmitter neuropeptide Y (NPY), the mechanical itch pathway is constantly on, causing chronic itch. It was then found that the itch signal, under normal circumstances is suppressed by the NPY neurons, is transmitted to the brain to register the itch sensation.
The Goulding team then showed that the NPY neurotransmitter controls the level of Y1 neuron excitability. Hence, NYP signalling acts as a kind of thermostat to control our sensitivity to light touch. Data from other labs found that some people with psoriasis have lower than average levels of NPY. This might mean that their brakes on mechanical itching are less effective than other people’s, a potential cause of their itching.
Researchers seek to understanding which mechanical itch is signalled under normal circumstances, the researchers might then be able to address what happens in the chronic itch.
Source material from Science Daily