....male and female created he them. Genesis 1:27
"Sorge was investigating how animals develop an extreme sensitivity to touch. To test for this response, Sorge poked the paws of mice using fine hairs, ones that wouldn’t ordinarily bother them.
The males behaved as the scientific literature said they would: they yanked their paws back from even the finest of threads.
But females remained stoic to Sorge’s gentle pokes and prods. “It just didn’t work in the females,” recalls Sorge.
The research could open the door for new medical advances, adds Tannenbaum. These are sorely needed: some 20% of people worldwide experience chronic pain — and the majority are women. Today, the pharmaceutical market offers the same pain drugs to everyone. But if the roots of pain are different, some drugs might work better in some people than in others.
Injecting a bacterial molecule called lipopolysaccharide into the spines of mice drew the attention of microglia, the nervous system’s resident immune cells. But in Sorge’s studies, this led to inflammation only in the males, explaining why they were so sensitive to the hair-prick test, Sorge and Mogil reported in 2011. The microglia remained quiet in females, which seemed to account for their indifference to Sorge poking their paws with fine hairs.
To better understand why male and female mice dealt with pain so differently, Sorge and Mogil turned to a pain source that affects all mice.
They injured the animals’ sciatic nerves, which run from the lower back down each leg. This led to a form of chronic pain that happens when the body’s pain-detecting system is damaged or malfunctioning. It caused both male and female mice to become extra sensitive to touch.
Yet even in this case, there were differences. Microglia seemed to have a prominent role in the pain of males, but not in that of female mice. Sorge and a team of collaborators from three institutions found that, no matter how they blocked microglia, this eliminated the pain hypersensitivity in males alone.
It’s not that females were immune to pain. They were just as bothered by nerve injury as the males were, but they weren’t using microglia to become hypersensitive to touch. Mogil and Sorge wondered whether another immune component, called a T cell, was behind the chronic pain in females. These cells have a known role in pain sensitization in mice.
Sorge tried the same nerve injury in female mice lacking T cells. They still became hypersensitive to the fine hairs, but the mechanism now seemed to occur through microglia. In females lacking T cells, blocking the activity of microglia prevented this pain response, just as it did in males. And when the researchers transferred T cells back to female mice that were lacking them, the animals stopped using microglia in nerve-injury pain (see ‘Two routes to pain’).
The results showed that even though everybody’s pain might look similar from the outside, scientists can’t assume it’s the same on the inside.
Mogil’s research points squarely at testosterone as the control switch for pain pathways. In the 2011 and 2015 studies, when Sorge tested castrated male mice, which have low testosterone levels, the animals exhibited a response similar to females. And when the researchers provided testosterone to castrated males, or to females, the pain pathway switched to one dependent on microglia.
But immune cells and hormones don’t fully explain pain differences. For instance, Sarah Linnstaedt has found hints that some women might have a genetic predisposition to chronic pain. Her team has identified a suite of RNA molecules in the bloodstream that are more likely to be elevated in women who develop chronic neck, shoulder or back pain after a motor-vehicle accident. Many of these RNA molecules are encoded by genes on the X chromosome, of which there are two copies in women."
Nature
"Sorge was investigating how animals develop an extreme sensitivity to touch. To test for this response, Sorge poked the paws of mice using fine hairs, ones that wouldn’t ordinarily bother them.
But females remained stoic to Sorge’s gentle pokes and prods. “It just didn’t work in the females,” recalls Sorge.
The research could open the door for new medical advances, adds Tannenbaum. These are sorely needed: some 20% of people worldwide experience chronic pain — and the majority are women. Today, the pharmaceutical market offers the same pain drugs to everyone. But if the roots of pain are different, some drugs might work better in some people than in others.
Injecting a bacterial molecule called lipopolysaccharide into the spines of mice drew the attention of microglia, the nervous system’s resident immune cells. But in Sorge’s studies, this led to inflammation only in the males, explaining why they were so sensitive to the hair-prick test, Sorge and Mogil reported in 2011. The microglia remained quiet in females, which seemed to account for their indifference to Sorge poking their paws with fine hairs.
To better understand why male and female mice dealt with pain so differently, Sorge and Mogil turned to a pain source that affects all mice.
They injured the animals’ sciatic nerves, which run from the lower back down each leg. This led to a form of chronic pain that happens when the body’s pain-detecting system is damaged or malfunctioning. It caused both male and female mice to become extra sensitive to touch.
Yet even in this case, there were differences. Microglia seemed to have a prominent role in the pain of males, but not in that of female mice. Sorge and a team of collaborators from three institutions found that, no matter how they blocked microglia, this eliminated the pain hypersensitivity in males alone.
It’s not that females were immune to pain. They were just as bothered by nerve injury as the males were, but they weren’t using microglia to become hypersensitive to touch. Mogil and Sorge wondered whether another immune component, called a T cell, was behind the chronic pain in females. These cells have a known role in pain sensitization in mice.
The results showed that even though everybody’s pain might look similar from the outside, scientists can’t assume it’s the same on the inside.
Mogil’s research points squarely at testosterone as the control switch for pain pathways. In the 2011 and 2015 studies, when Sorge tested castrated male mice, which have low testosterone levels, the animals exhibited a response similar to females. And when the researchers provided testosterone to castrated males, or to females, the pain pathway switched to one dependent on microglia.
But immune cells and hormones don’t fully explain pain differences. For instance, Sarah Linnstaedt has found hints that some women might have a genetic predisposition to chronic pain. Her team has identified a suite of RNA molecules in the bloodstream that are more likely to be elevated in women who develop chronic neck, shoulder or back pain after a motor-vehicle accident. Many of these RNA molecules are encoded by genes on the X chromosome, of which there are two copies in women."
Nature
