There are many explanations for why individuals acquire peripheral neuropathy and, unfortunately, only a few reliable strategies for reducing the discomfort and other symptoms associated with it. There are a minimum number of different types of prescription drugs that have proven therapeutic success. An example of these types of drugs works by increasing the amount of a neurotransmitter called GABA. This substance, GABA, works as a braking mechanism on the nervous system. GABA is believed to decrease neuropathic pain by decreasing or decreasing the pain impulses that travel from the hands and feet to the brain. An additional class of drugs works by increasing the neurotransmitters serotonin and norepinephrine. It is not known exactly how this inhibits neuropathic pain. Another important additional neurotransmitter, glutamate acts much like the gas pedal inside the nervous system. It speeds up the signaling of pain transmission in sensory neural fibers. In nerve damage that includes neuropathy associated with chemotherapy, glutamate concentrations may be increased or their transport pumps depressed. The net consequence is an increased action of the function of glutamate, which, due to the excitatory nature of glutamate, in due course results in neural hypersensitivity in the pain pathways. Drug treatments that reduce glutamate or block glutamate receptors may help decrease pain signaling. Even though neuropathy is a common and debilitating disease, and huge sums of money have already been invested in studying its treatment, no single method is universally successful in helping people who have to endure neuropathy. Each patient responds to these drugs differently, and unfortunately none of them offer exceptional benefits for most patients with peripheral neuropathy.
Since the various types of prescription drugs used to treat different types of neuropathy render insufficient or daunting benefits overall, there is still an ongoing search for unique and perhaps more potent biological pathways to treat them. signs or symptoms of neuropathy.
Another neurotransmitter and its receptor are particularly catching the attention of the neuropathy research community. The amino acid glycine is what is called an inhibitory neurotransmitter. It works at the junction between neural cells known as a synapse. Each time glycine is introduced into the junction between two nerves, it decreases or stops the transmission of impulses (such as pain signals) that travel to the brain. For this reason, glycine is labeled as an inhibitory neurotransmitter. However, inhibition of pain signaling by glycine does not last long because the nerve ending at the synapse junction has pumps that push glycine out of the space between the nerves and sequester it in the cell. neural. When it returns to the cell, glycine is less active and no longer generates inhibition of nerve signaling.
Therefore, pain impulses like those seen in neuropathy can start again along their way from the toes and fingers to the head, making life dark for people with neuropathy. At least one group of experts has confirmed that substantial levels of glycine consumed orally can dramatically increase blood and cerebrospinal glycine levels. On the other hand, due to the glycine transporter positioned between nerve cells, we cannot be sure that glycine concentrations in the synapse, where it is effective in reducing neurological impulses, can be achieved by glycine supplementation. by herself.
So providing excess glycine in the diet may not be the optimal strategy for reducing the discomfort associated with neuropathy. Since the glycine transport pump can be so efficient that it might require large doses of oral glycine, and yet it might be difficult to obtain adequate glycine in the synapse between the nerves and the hold back long enough to achieve significant reductions in pain associated with the nerves.
If only we are able to inhibit the glycine transporter?
The investigation of pharmaceutical development intended to inhibit the glycine transporter is exploding. Undoubtedly, preliminary research shows that increasing the effects of glycine by slowing the removal of this neurotransmitter out of the gap between nerve cells reduces pain-related patterns in animal models of neuropathy. Therapies created to block the glycine transporter are an exciting new avenue and offer something truly unique in the treatment of patients with neuropathy.
The use of pharmacognosy concepts to address this problem suggests fascinating opportunities. For hundreds of years and on many cultures, various varieties of ash have been used for therapeutic applications. Native American herbalists used the bark of the Barbary ash for many ailments. One of the most intriguing conditions in neuropathy is toothache. It seems that the ability of the bark of this prickly ash was so recognized for its dental pain relieving qualities that it was often referred to as toothache tree or toothache bush. Most recently, scientists studying the effects of the compound of various species of ash on the transmission of pain signals in a nerve complex known as the trigeminal ganglion (the nerve complex associated with toothaches and other facial pain ), discovered that the chemicals contained therein are ash bark. nerve pain suppressed in this system. Their research further implied that the mechanism for this nerve pain relief was related to the ability of the prickly ash constituents to inhibit the glycine transport pump.
This raises the prospect of using compounds derived from prickly ash to control the glycine transporter at the synapse level while supplementing the diet with oral glycine, methylglycine or trimethylglycine, which are different forms. of the natural amino acid glycine.
Make sure you don’t try this or any other treatment recommendations posted on the net. This short article should be used for educational purposes only. Each patient is a unique individual, and medical treatments should truly be tried using the advice, approval and supervision of a qualified physician.