Researchers at the University of California, San Francisco, have been tingling the spidey senses of their lab mice in order to learn about the roots of pain. By injecting tarantula venom into their rodent “volunteers”, the researchers have honed in on one of the neural mechanisms underpinning the sensation of pain, potentially opening the door to new treatments for certain disorders of the central nervous system (CNS).
Most of the body’s afferent nerve fibers – which carry sensory impulses from the skin to the CNS – operate using voltage-gated sodium (Nav) channels. These are tiny passages on the nerve cell membrane through which sodium ions can pass, altering the electrical charge of the nerve fiber in order to generate an impulse.
However, because there are so many different types of Nav channel, we still don’t really have a precise idea which ones are specifically involved in the detection and transmission of pain. Local anaesthetics, therefore, work by blocking all Nav channels in a particular region of the body, hedging their bets and guaranteeing that patients will feel no pain.
Yet by learning which of these channels are responsible for which effects, it may be possible to gain a more precise understanding of exactly why we feel certain types of pain.
To try and achieve this, the researchers isolated two protein toxins in the venom of the Heteroscodra maculata spider, which they then injected into the feet of mice. This immediately caused the mice to feel pain, as signified by their distressed licking and biting of the affected area.
Jazz hands tarantula. Lucas Foglia
An analysis of the nerve activity in the mice’s feet revealed that the proteins had specifically acted upon a type of Nav channel called Nav1.1. After infecting the mice with these isolated proteins, the researchers then conducted a range of experiments to determine which types of pain the animals were particularly sensitive to.
Results – which are published in the journal Nature – show that the activation of the Nav1.1 channel caused the mice to become hypersensitive to touch but not heat. As such, the researchers believe that Nav1.1 channels may play a key role in mechanical pain but not thermal pain.
Since Nav1.1 channels are highly abundant in the sensitive nerve fibers of the gut, the study authors decided to test whether or not this particular channel plays a role in the abdominal pain often reported by those who suffer from irritable bowel syndrome (IBS). By stimulating the nerve fibers in the mice’s guts with the tarantula venom proteins, they discovered that activity in these neurons spiked, suggesting that the activation of Nav1.1 channels in these nerves was indeed responsible for this pain.
Based on these findings, the team conclude that “pharmacological blockade of Nav1.1 represents a novel therapeutic strategy for diminishing the chronic pain in IBS, and perhaps other pain conditions associated with mechanical sensitization.”
