Sentences with phrase «a pain signal»

Researchers aren't sure why it works on headaches, but suspect it helps to block pain signals in the brain.

The effectiveness of chiles on sore throat probably involves the depletion of substance P, the neurotransmitter that sends pain signals to the brain.

Repeated use of capsaicin also prevents the nerve endings from making more substance P, and thus further pain signals from the skin are greatly diminished or completely eliminated as long as the capsaicin is applied.

One theory is that this stimulation depletes the nerves of Substance P, a neuropeptide that transmits pain signals to the brain, which then reduces pain and irritation in a treated area.

«The pain signals, or the cumulative fatigue, are nonlinear,» according to Jimmy Dean Freeman, an ultrarunner and L.A. - based endurance coach.

He's about to experience a lot of nonlinear pain signals, with a planned six 100 - mile ultras in the next 13 weeks.

When these pain signals are blocked, it becomes more difficult for the brain to register the sensation of pain (or it opts for the more pleasant pulsing sensation).

It utilizes the Gate Theory of Pain Control by gently stimulating your sensory nerves to suppress or block the pain signal to the brain.

Teething babies need to overwhelm the sensory receptors on their gums to help stop the (Nociceptive) pain signal that is sent to the brain that says «OUCH!».

It may also involve pain signals from sensitised nerves in the gut.

TENS encourages the release of endorphins (the body's own natural pain killing chemicals) whilst also blocking the pain signals from getting to the brain.So what's the de...

My understanding is that they inject a small amount of water into four points in the lower back that block the pain signals to the brain.

It is these sensations that block the pain signals from reaching the brain.

Used medicinally, these toxins block pain signals from reaching the brain, yielding pain relievers more powerful than morphine.

Serotonin and norepinephrine can stifle pain signals traveling from the brain to the rest of the body.

Chronic pain may be due to an overabundance of a protein, which amplifies the pain signal to the brain.

Also found in nociceptors, these channels can become blocked when exposed to acid, dampening the pain signal.

Researchers already knew that even without opioids, some people with chronic pain from nerve damage or fibromyalgia, for example, experience hyperalgesia when normal pain signaling gets reinforced and amplified over time.

(It's also possible that a patient's underlying condition has changed, or that the chronic pain itself has kicked their pain signaling into high gear.)

But when the immune system becomes activated in response to an illness or injury, glia in regions associated with pain processing seem to take on another role: They release inflammatory molecules that interact with nearby neurons to amplify pain signals.

Animal studies have revealed several ways in which opioids may amplify pain signals in the central nervous system, suggesting targets for drugs that could counter the effect.

The results suggested that opioids may trigger glia to set off system - wide pain signaling that both counteracts the pain relief from the drug and makes the body generally more sensitive to pain.

A team led by Peggy Compton of Georgetown University in Washington, D.C., meanwhile, is investigating a pain and antiseizure drug called gabapentin that may block neural transmission to reduce excessive pain signals.

The drug works to block release of substances at nerve endings, which, from effects in different nerves, will lead to reduced muscle contraction and less transmission of pain signals.

The researchers doused nociceptors from naked mole rats and mice in acid, and found the strength of the pain signal passing through the NaV1.7 channels dropped by 42 per cent in mice, but by 63 per cent in the mole rats.

In mice, the balance tips in favour of the acid signal making it to the brain — but in naked mole rats the balance tips the other way and the pain signal dissipates.

In a study published in the April issue of the Journal of Neuroscience, Saint Louis University scientists led by professor of pharmacological and physiological sciences Daniela Salvemini, Ph.D., discovered that drugs targeting the A3 adenosine receptor can «turn off» pain signals in the spinal cord to provide relief from chronic pain.

However, with repeated short - term exposure to capsaicin, those calcium ions essentially close the receptor door behind them, inhibiting further transmission of pain signals.

Normally, pain signals begin somewhere in the body and work their way to the thalamus, deep in the brain, and then to the prefrontal cortex, producing conscious perception of pain.

Moreover, the pharmacologists were able to demonstrate that neurons on the superficial layers of the spinal cord, where the relay of the pain signals takes place, are primarily inhibited by glycine signals.

Now, new research from the Salk Institute shows how a protein called p75 is critical for pain signaling, which could one day have implications for treating neurological disorders as well as trauma such as spinal cord injury.

Prostaglandins are best known for their role in pain signaling.

The spinal cord transmits pain signals to the brain, where they are consciously perceived.

Members of the GDNF family support the survival of sensory neurons that transmit the pain signal and p75 enhances this survival - promoting effect by interacting with Ret.

Chronic pain can be viewed as a learned memory: In the way that repetition of a piano piece enables you to learn it by facilitating transmission of the appropriate signals through your neurons, pain that persists can become chronic because your neurons become more efficient at transmitting pain signals.

That's because pain signals travel along separate cables at a low - priority speed of just 3 mph.

Neurons keep firing, and even pain signals travel their normal routes.

The device uses electrical stimulation to block the pain signals from reaching the brain.

Similarly, mechanoreceptor fibers that project to the spinal cord from a missing limb might spur erroneous pain signals.

In a major breakthrough, a team led by researchers at the Salk Institute and Harvard Medical School have identified an important neural mechanism in the spinal cord that appears to be capable of sending erroneous pain signals to the brain.

But when you have a weak pain signal, it doesn't trigger the brake and the signal can go through.»

Advances in understanding the cells and molecules that transmit pain signals are providing new targets for drugs that could relieve various kinds of pain — including those poorly controlled by existing therapies

Scientists have long theorized that pain signals are sent from sensory neurons in the limbs and other extremities to transmission neurons in the spinal cord, which then relay the information to the brain.

At the same time, GRP neurons are not the only group of spinal cord neurons that receive and forward pain signals toward the brain, and the brain itself plays a central role in translating signals from peripheral neurons into experienced sensation.

The inhibitory neurons they identified appear to control whether touch activates the excitatory neurons to send a pain signal to the brain.

«Normally, only pain receptors are involved in sending pain signals to the brain, but when the spinal dynorphin inhibitory neurons are lost, touch sensation are now perceived as painful,» says Goulding, holder of Salk's Frederick W. and Joanna J. Mitchell Chair.

By charting the spinal circuits that process and transmit pain signals in mice, the study, published online November 20, 2014 in Cell, lays the groundwork for identifying ways to treat pain disorders that have no clear physical cause.

Studies in animals indicated that in branches of the nerve that exit from the back of the brain and wrap around various parts of the face and head, overactive cells would respond to typically benign lights, sounds and smells by releasing chemicals that transmit pain signals and cause migraine.

Ironically, subsequent drug studies show that they actually disrupt the transmission of pain signals in the brain and that constricting blood vessels is not essential.

Most people think of pain as something that happens in the body — I twist my head too far, and my neck sends a «pain signal» to the brain to indicate that the twisting hurts.