A new approach to pain relief in neuropathy, the glycine transporter

A new approach to pain relief in neuropathy, the glycine transporter

There are numerous explanations as to why people develop peripheral neuropathy, and unfortunately only a few reliable strategies to reduce the discomfort and other associated symptoms. There are a minimal number of different types of prescription medications that have been recognized for treatment success. An example of this type of medication is increasing the amount of a neurotransmitter called GABA. This substance, GABA, acts as a braking mechanism on the nervous system. GABA is believed to reduce pain in neuropathies by reducing or reducing the pain impulses that travel from the hands and feet to the brain. An additional category of drugs works by increasing the neurotransmitters serotonin and norepinephrine. Exactly how this inhibits neuropathy pain is uncertain. Another important additional neurotransmitter, glutamate, acts similarly to the accelerator pedal in the nervous system. It enhances pain transmission signaling in sensory nerve fibers. In nerve injuries, which include chemotherapy-associated neuropathy, glutamate concentrations may be increased or transporter pumps may be decreased. The net consequence is an increased effect of glutamate function, which in due course translates into neural hypersensitivity in pain pathways due to the stimulatory nature of glutamate. Drug treatments that reduce glutamate or block its receptors can reduce pain signals. Although neuropathy is a common and incapacitating disease and much money has been invested in studying its treatment, no method is universally successful in helping people who have to endure neuropathy. Each individual patient responds differently to these medications and unfortunately, none of them provide exceptional benefits for most patients with peripheral neuropathy.

Given that the various types of prescription drugs used to treat different types of neuropathy largely provide inadequate or discouraging benefits, there is a constant search for unique and potentially more effective biological ways to deal with signs or symptoms of neuropathy.

Another neurotransmitter and its receptor are attracting particular attention in the neuropathy research community. The amino acid glycine is called an inhibitory neurotransmitter. It works at the junction between nerve cells known as the synapse. When glycine is introduced into the connection between two nerves, it reduces or stops the transmission of impulses (such as pain signals) traveling to the brain. For this reason, glycine is labeled as an inhibitory neurotransmitter. However, the inhibition of pain signaling by glycine does not continue for long because the nerve that terminates at the synaptic junction has pumps that push the glycine out of the gap between the nerves and bind it within the nerve cell. When it returns to the cell, glycine is less active and no longer inhibits nerve signals.

Consequently, like in neuropathy, pain impulses can start again on their way from the toes and fingers to the head, making the life of those affected by neuropathy bleak. At least one group of experts has confirmed that significant amounts of oral glycine can significantly increase blood and cerebrospinal glycine concentrations. On the other hand, due to the glycine transporter positioned between nerve cells, we cannot be sure that glycine concentrations in the synapse, the place where they effectively reduce neurological impulses, can be maintained by glycine supplementation itself.

Therefore, providing excess glycine in the diet may not be the optimal strategy to reduce neuropathy symptoms. Given that the glycine transporter pump can be so effective that significant doses of oral glycine may be required, it may still be difficult to deliver sufficient glycine to the synapse between nerves and keep it there long enough to achieve a significant reduction in nerve-related suffering.

If only we can inhibit the glycine transporter?

The study of pharmaceutical development to inhibit the glycine transporter is exploding. Without a doubt, preliminary research shows that enhancing the effects of glycine by curbing the removal of this neurotransmitter from the gap between nerve cells reduces pain-related patterns in animal models of neuropathy. Glycine transporter blocking therapies are an exciting new possibility and offer something truly unique in the treatment of patients with neuropathy.

Using the concepts of pharmacognosy to solve this problem offers some intriguing possibilities. Various varieties of ash have been used for therapeutic applications for hundreds of years and across numerous cultures. Native American herbalists used the bark of the Northern Prickly Ash Tree for many different ailments. One of the most fascinating conditions related to neuropathy is toothache. It sounds like the ability of the bark from this prickly ash was so recognized for its toothache relieving properties that it was often referred to as the toothache tree or toothache bush. Recently, scientists studying the effects of compounds from various ash species on the transmission of pain signals within a nerve complex known as the trigeminal ganglion (the nerve complex associated with toothache and other facial pain) found that the chemical substances contained in ash bark suppressed nerve pain in this system. Their research further implied that the mechanism for this relief from nerve pain was related to the ability of prickly ash components to inhibit the glycine transporter pump.

This raises the prospect of using prickly ash-derived compounds to control the glycine transporter at the synapse while supplementing the diet with oral glycine, methylglycine, or trimethylglycine, which are different forms of the naturally occurring amino acid glycine.

Remember not to try these or any other treatment recommendations posted on the Internet. This short article should be used for educational purposes only. Each patient is a unique individual and medical treatments should only be undertaken with the advice, approval and supervision of a qualified healthcare practitioner.

Inspired by George Kukurin D.C.