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Does every nerve ending send information to the brain separately?

Does every nerve ending send information to the brain separately?



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Does every nerve ending send information to the brain separately? Is there a nerve path (I don't know their scientific name) from every nerve ending to the brain; or are they sent to brain from the same paths in the dorsal root ganglion? If not, how can we determine the (almost) exact location of pain in our hand?

I am not very familiar with the biology except the lessons I had taken in the high school. So please try to use daily language explaining this.


There are two main structures in the human nervous system:

  • The central nervous system, which includes the brain and spinal cord
  • The peripheral nervous system, which is all of the nerves in the rest of the body (fingers, arms, feet, etc.)

The signals taken by the peripheral nerves mainly travel to the brain through the spinal cord, and the brain sends signals back to the peripheral nerves through the central nervous system.

There are a lot more complex mechanisms and various exceptions, but essentially: the nervous system is a vast network of signals, and the majority of these signals travel through the spinal cord to the brain and from the brain to the target nerves.

The signals travel via different nerve "branches" - think of it like a tree of nerves, with the common root being the brain.

For more information please see:

Overview of the nervous system for dummies

Wikipedia (with strong references and lots of detailed information)


As commented, a nerve ending is really the ending of a neuron, some sensory neurons travel directly to the brain, some form synapses in the spinal cord (most touch and pain neurons from the body), then spinal cord neurons carry the information to the brain. (Note that facial sensation is carried by cranial nerves from the brain stem).

Some, e.g. in the retina undergo some quite intensive processing before ganglion cells carry any information to the brain.


The Vagus Nerve: Your Body's Communication Superhighway

The vagus nerve serves as the body's superhighway, carrying information between the brain and the internal organs and controlling the body's response in times of rest and relaxation. The large nerve originates in the brain and branches out in multiple directions to the neck and torso, where it's responsible for actions such as carrying sensory information from the skin of the ear, controlling the muscles that you use to swallow and speak and influencing your immune system.

The vagus is the 10th of 12 cranial nerves that extend directly from the brain, according to the Encyclopedia Britannica. Although we refer to the vagus nerve as singular, it's actually a pair of nerves that emerge from the left and right side of the medulla oblongata portion of the brain stem. The nerve gets its name from the Latin word for wandering, according to Merriam-Webster, which is appropriate, as the vagus nerve is the largest and most widely branching cranial nerve.

By wandering and branching throughout the body, the vagus nerve provides the primary control for the nervous system's parasympathetic division: the rest-and-digest counterpoint to the sympathetic nervous system's fight-or-flight response. When the body is not under stress, the vagus nerve sends commands that slow heart and breathing rates and increase digestion. In times of stress, control shifts to the sympathetic system, which produces the opposite effect.

The vagus nerve also carries sensory signals from internal organs back to the brain, enabling the brain to keep track of the organs' actions.


Naked Body: Our sense of touch

When I stroke a cat, I am aware of the softness of its fur, I can feel the ridges of its spine (unless it’s very fat cat) and I know in which direction the fur is moving, with respect to my hand. This is all information that I can obtain through my touch. Voluntary movement is key to the lives of most of us, and touch is a key in guiding our movements. But how does our skin relay the information? How has the pressure applied on this cat’s back been interpreted in my brain?

Like most of your senses, touch works through a sensory pathway that consists of an external stimulus, in this case the cat’s fur, detected by a receptor in your skin, transmitted through nerve cells to the brain where the information will be broken down and analysed. Cat petting is serious biological business.

The stimulus is perceived by a sensory neuron with a long, thin process called an axon which extends into the skin. The sensory stimulus leads to the neuron firing, and the resulting change in the electric flow within it codes for the information and sends it to the brain. Depending on the frequency of this firing and how it interacts with other incoming signals, the sensation will be interpreted in different ways.

But how do I know I am stroking the cat and not the carpet next to it? What causes specific neurons to become activated?

When force is applied to a nerve fibre, the tip of the nerve fibre, the bit within your skin, deforms with the force applied. This makes special channels open, which changes the electric flow, activating the neuron.

Neurons tend to be selective with the signal they respond to. What type of touch information is detected (whether it’s pressure, tension, stretch, ‘stickiness’, etc.) depends on what structures are surrounding the nerve ending in the skin.

Some of these accessory structures resemble elastic, onion-like cushions: these are called Pacinian corpuscles. Because of the elasticity of the capsule, the shape of the cushion after applying pressure is restored rapidly. So the associated nerve endings detect changes and respond well to vibration.

They are the receptors in my fingers that would detect whether the cat is purring when I stroke it, even if I could not hear the purring.

Other receptors signal skin tension and are particularly sensitive to edges. They probably tell you when you feel the spine as you stroke the cat along its back. The higher the density of receptors in an area, the better the tactile acuity, as in hands, in contrast to our back. Please note the Naked Scientists do not advocate using your back to pet a cat.

So I can detect different elements of the cat’s back using different neurons and receptors. But how does the body know how to put them all together?

The information sent by neurons is ferried up via the spinal cord to the brain, where it is processed in the thalamus and a specific part of our cortex: the somatosensory cortex.

In that special area of the brain, the entire body is mapped out such that specific areas of this cortex correspond to particular regions of the body surface. So in our case we know the cat is at the end of my fingertips because the ‘fingers’ part of my cortex is activated.

So I know my fingers are feeling the fur because the pattern of the neurons which are active in my cortex depends on what kind of thing I’m touching.

When you touch something, each feature of the touch is broken down and analysed separately.

The brain then puts it all together: Am I moving? Do I need to pay particular attention to this information? Have I accurately sensed what is going on? Why is the cat biting me now?


Our sense of touch

When I stroke a cat, I am aware of the softness of its fur, I can feel the ridges of its spine (unless it’s very fat cat) and I know in which direction the fur is moving, with respect to my hand. This is all information that I can obtain through my touch. Voluntary movement is key to the lives of most of us, and touch is a key in guiding our movements. But how does our skin relay the information? How has the pressure applied on this cat’s back been interpreted in my brain?

Like most of your senses, touch works through a sensory pathway that consists of an external stimulus, in this case the cat’s fur, detected by a receptor in your skin, transmitted through nerve cells to the brain where the information will be broken down and analysed. Cat petting is serious biological business.

The stimulus is perceived by a sensory neuron with a long, thin process called an axon which extends into the skin. The sensory stimulus leads to the neuron firing, and the resulting change in the electric flow within it codes for the information and sends it to the brain. Depending on the frequency of this firing and how it interacts with other incoming signals, the sensation will be interpreted in different ways.

But how do I know I am stroking the cat and not the carpet next to it? What causes specific neurons to become activated?

When force is applied to a nerve fibre, the tip of the nerve fibre, the bit within your skin, deforms with the force applied. This makes special channels open, which changes the electric flow, activating the neuron.

Neurons tend to be selective with the signal they respond to. What type of touch information is detected (whether it’s pressure, tension, stretch, ‘stickiness’, etc.) depends on what structures are surrounding the nerve ending in the skin.

Some of these accessory structures resemble elastic, onion-like cushions: these are called Pacinian corpuscles. Because of the elasticity of the capsule, the shape of the cushion after applying pressure is restored rapidly. So the associated nerve endings detect changes and respond well to vibration.

They are the receptors in my fingers that would detect whether the cat is purring when I stroke it, even if I could not hear the purring.

Other receptors signal skin tension and are particularly sensitive to edges. They probably tell you when you feel the spine as you stroke the cat along its back. The higher the density of receptors in an area, the better the tactile acuity, as in hands, in contrast to our back. Please note the Naked Scientists do not advocate using your back to pet a cat.

So I can detect different elements of the cat’s back using different neurons and receptors. But how does the body know how to put them all together?

The information sent by neurons is ferried up via the spinal cord to the brain, where it is processed in the thalamus and a specific part of our cortex: the somatosensory cortex.

In that special area of the brain, the entire body is mapped out such that specific areas of this cortex correspond to particular regions of the body surface. So in our case we know the cat is at the end of my fingertips because the ‘fingers’ part of my cortex is activated.

So I know my fingers are feeling the fur because the pattern of the neurons which are active in my cortex depends on what kind of thing I’m touching.

When you touch something, each feature of the touch is broken down and analysed separately.

The brain then puts it all together: Am I moving? Do I need to pay particular attention to this information? Have I accurately sensed what is going on? Why is the cat biting me now?


HOW TASTE RECEPTORS IN THE GUT INFLUENCE EATING BEHAVIOR 5

Taste cells in the tongue are among the first cells in the GI tract that come into contact with food. Only recently have scientists discovered taste-like cells in the gut as well. Robert Margolskee provided an overview of taste receptors in the oral cavity and discussed recent research on taste-like receptors in the gut.

Taste Receptors in the Oral Cavity

Oral taste buds𠅌ollections of about 50 to 100 specialized epithelial cells𠅊re scattered throughout the oral cavity, primarily in papillae 6 on the front, sides, and back of the tongue. Although oral taste buds are not neurons, they have a number of neuronal properties. Much of the taste transduction cellular machinery is contained within the fingerlike microvilli coating the apical end of each taste bud cell.

Margolskee explained that scientists have identified several different types of taste receptors in the oral cavity, each having a unique taste receptor molecule or set of molecules underlying the taste response (Lindemann, 2001). Over the past decade, work from Margolskee's laboratory, as well as the laboratories of Linda Buck, Nick Ryba, and Charles Zucker, has led to identification of many of the different taste quality receptors. Today, researchers know that the bitter taste receptors involve a family of about 25 to 30 G protein-coupled receptors 7 called the T2Rs (type 2 taste receptors). Sweet receptors, in contrast, involve a dimeric or multimeric combination of T1R2 (type 1 receptor 2) and T1R3 (type 1 receptor 3) receptors, which together respond to a number of sweet compounds, both sugars and noncaloric sweeteners. A related receptor, the umami receptor, involves a combination of T1R1 (type 1 receptor 1) and T1R3 receptors and responds to “savory” tastes such as monosodium glutamate.

The sour and salty taste transduction channels are not as well understood as the bitter, sweet, and umami channels, said Margolskee. Although ENaC 8 certainly plays a role in salty taste transduction, it is involved more with low concentrations of salt. There is likely at least one other transduction channel, as yet unidentified, for high concentrations of salt. The sour taste receptor has a number of candidate channels, including acid-sensing ion channels (ASICs), hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, and polycystic kidney disease (PKD) family member channels, but no one channel has yet been definitively identified.

Taste-Like Cells in the Gut (and Pancreas)

As summarized by Margolskee, researchers recently have identified taste-like cells in the gut that play an important role in integrating physiological responses during digestion. Taste-like cells in the gut are not actual taste cells, although they have a number of characteristics in common with true oral taste cells: they are morphologically similar under both light and electron microscopy and produce many of the same taste signaling proteins. Indeed, the signaling process that occurs in certain types of endocrine cells in the gut is very similar to the transduction process that occurs in oral taste cells (Cummings and Overduin, 2007) (see Figure 2-3). In both types of cells, when G protein-coupled receptors at the apical surface of the cell couple with gustducin and other taste-associated G proteins, they initiate a signal transduction cascade involving multiple signaling enzymes, second messengers (e.g., inositol triphosphate), and channels (e.g., the calcium-activated TRPM5 channel), ultimately leading to neurotransmitter or, in the case of taste-like cells, neuropeptide release. Margolskee explained that one of the differences between taste receptors in the oral cavity and taste-like receptors in the gut is that instead of releasing a true neurotransmitter, taste-like receptors in the gut release neuropeptide hormones, such as GLP-1 (glucagon-like peptide-1).

FIGURE 2-3

Oral taste cells (“taste cell”) and gut taste-like cells (𠇎ndocrine cell”) share similar signaling processes. SOURCE: Modified from Cummings and Overduin, 2007. Reprinted with permission of the American Society for Clincial (more. )

Margolskee went on to explain that the idea that taste signaling molecules exist in the gut dates back to the mid-1990s, when Dirk Hr discovered alpha-gustducin (the alpha subunit of the heterotrimeric gustducin protein) being expressed in stomach and intestinal cells that had the general appearance of taste receptor cells (Hr et al., 1996). Subsequently, Enrique Rozengurt's group identified a number of T2R bitter taste receptors in the stomach and small intestine (Wu et al., 2002). Later, Soraya Shirazi-Beechey found T1R receptors in the gut (Dyer et al., 2005).

In more detailed microscopic studies, Shirazi-Beechey and Margolskee collaborated and found that both T1R2 and T1R3, the two components of the sweet receptor, are present in a small subset of cells lining the small intestinal mucosa and that the cells have the typical appearance of enteroendocrine cells (Margolskee et al., 2007). Margolskee and his team also collaborated with Josephine Egan at the National Institutes of Health and identified several taste signaling proteins in both human and mouse tissues. They also found essentially the entire taste transduction pathway as it was known to exist in oral taste cells, in gut endocrine cells, and particularly in L cells expressing GLP-1 (Jang et al., 2007).

More recently, Yan Li in Margolskee's laboratory examined co-expression of gustducin-positive endocrine cells from various locations in the small and large intestines and found a roughly equal level of L, K, and L/K co-expression 9 with gustducin in the colon but mainly only K or L/K cells co-expressing with gustducin in other areas (Li et al., 2013). Li also found a number of short chain fatty acids co-expressed with alpha-gustducin in endocrine cells in the colon, including cells activated by the G protein-coupled receptors GPR43 and GPR41. Curious about the potential physiological role of gustducin in the colon, she turned to gustducin knockout mice and found that short chain fatty acid–stimulated GLP-1 secretion from colon endocrine cells requires alpha-gustducin.

In other collaborative work between Margolskee's laboratory and Shirazi-Beechey's group, the researchers examined SGLT1 (sodium glucose co-transporter 1) expression in two types of knockout mice (Margolskee et al., 2007). SGLT1 is a protein that co-transports glucose and sodium from the gut lumen across the absorptive enterocytes and into the epithelial cells. According to Margolskee, this is typically the rate-limiting step for glucose uptake in the small intestine. Margolskee, Shirazi-Beechey, and colleagues found that SGLT1 mRNA (messenger RNA), SGLT1 protein expression, and glucose uptake activity in wild-type mice all increased when the mice were treated with a high-carbohydrate diet compared with a low-carbohydrate diet. But in knockout mice missing T1R3, a component of both the sweet and umami receptors, there was no difference in SGLT1 between the low- and high-carbohydrate diets. Likewise with gustducin knockout mice, the research revealed no difference in SGLT1 mRNA or protein or glucose uptake activity between the low- and high-carbohydrate diets. According to Margolskee, the evidence suggests that both T1R3 and gustducin are necessary to elicit an increase in SGLT1 in response to dietary carbohydrate and a subsequent increase in glucose uptake activity.

Margolskee described a similar effect observed in knockout mice fed either a low-carbohydrate diet alone or a low-carbohydrate diet supplemented with a noncaloric sweetener (i.e., sucralose) (Margolskee et al., 2007). Wild-type mice showed an increase in SGLT1 mRNA, SGLT1 protein, and glucose uptake activity when their low-carbohydrate diet was supplemented with a noncaloric sweetener, but knockout mice did not. These results indicate a chemosensory detection pathway in the gut that responds to luminal sugars and luminal sweeteners and leads to the up-regulation of SGLT1 and an increase in glucose uptake activity across the gut.

Margolskee and others have found taste-like receptors not just in the stomach and intestine but also in the pancreas. Margolskee described unpublished data showing the expression of gustducin in pancreatic islet alpha cells and the expression of T1R3 in both alpha and beta cells. The function of these pancreas taste-like receptors is unclear. However, both in vitro data and data from wild-type versus T1R3 knockout mice suggest that these receptors play a role in sweetener-enhanced insulin release.

Oral Taste Cells and the Expression of Gut Proteins

Margolskee noted that researchers have observed a number of gut hormones, including GLP1, GIP (gastric inhibitory peptide), and CCK, expressed in multiple types of oral taste cells. Oral taste cells also express intestinal sugar sensors, such as SGLT1, and pancreatic metabolic sensors (Yee et al., 2011).

Margolskee gave an example of the expression of gut proteins in the oral cavity. Based on studies with T1R3 knockout mice showing a loss of response to noncaloric sweeteners but not to sugars (Damak et al., 2003), he and his colleagues suspected that something else in the oral cavity besides the oral sweet receptor, a T1R2 and T1R3 heterodimer, responds to sugars. They hypothesized the presence of a glucose transport pathway similar to what has been observed in pancreatic beta cells. Indeed, they found that a number of the same pancreatic pathway components were present in oral taste tissue (Yee et al., 2011). Margolskee speculated that gut-like glucose transporters in taste cells may help people and animals distinguish caloric from noncaloric sweeteners.

Taste-Like Receptors in the Gut and Pancreas: Summary of the Science

In summary, Margolskee noted that researchers have identified whole taste signaling pathways in both the gut and pancreas and in both the proximal and distal gut. In the gut, taste elements are expressed in L, K, and L/K cells. In the pancreas, both pancreatic islet alpha and beta cells express taste elements. Gustducin and T1R3 in the gut are involved in the release of GLP-1 and GIP in response to sweeteners and, in the proximal gut, in the regulation of SGLT1 levels. In the colon, gustducin appears to be involved in the release of GLP-1 and GIP in response to short-chain fatty acids. With regard to the role of taste signaling molecules in the pancreas, preliminary evidence suggests that gustducin and T1R3 are involved in sweetener detection and, under some circumstances, insulin secretion.


Beyond Pain

Patapoutian says these discoveries have taken them beyond the realm of touch into the basic function of our organs. “Internal organs also experience very profound mechanical forces,” he says. Piezo1 seems to be involved with the internal workings of the cardiovascular system, explains Patapoutian. This actually isn’t too surprising. Sensing mechanical force is important to the circulatory system that’s how blood vessels know to respond to changes in flow and constrict or dilate to keep blood pressure constant (7).

“Internal organs also experience very profound mechanical forces.”

—Ardem Patapoutian

Last year, in a project with the lab of Harvard University cell biology professor Steve Liberles, Patapoutian found a role for piezo2 in lung inflation (8). “Every breath you take, the lung, of course, expands,” he says. And with that expansion, piezo2 is stimulated in a way that can, in turn, tell the lung when to retract, thus playing a role in regulation of breathing. Mice lacking the piezo2 gene faced respiration problems such as overinflation of the lung.

But respiration is just the tip of the iceberg. There’s mechanosensation involved in stomach stretch, bladder stretch, satiation, gastrointestinal function, and more. The role of touch in internal organs remains even more mysterious than the mechanisms of touch on our skin, says Patapoutian.

Bautista’s lab, meanwhile, plans to use the star-nose mole genome to further elucidate mechanosensation. “That’s been a goldmine,” she says, “to go in and look at that.”


How can our brain distinguish the sound of a single note vs. a chord?

I wondered this when I was listening to piano chords on my computer. My headphones produced a singular sound, yet I knew it was a chord compared to when only a single note is played. How can we tell the difference if they are both just single sounds?

What will blow your mind more is when you realize that literally everything you hear is a "single sound" in the sense that there is only a single waveform being received by your ear. Think of listening to a song. the singer's voice is essentially a continuously modulated "chord" in the sense that it is comprised of a fundamental frequency (the note they are singing on) layered with "Formant frequencies" (which form vowels and which are influenced by consonants to create speech). Every instrument, even if it is only playing a single note, similarly has layers of resonant frequencies that are responsible for its timbre (how you can tell the difference between instruments playing the same note).

Our brains effortlessly group together those frequencies that belong to a single source (an instrument or voice) and separate those sources into different "auditory objects" in a process called "auditory scene segregation". It's a phenomenally difficult task and we don't really understand how it works in the brain there is some evidence that the "phase" of the component sound waves contributes.

Our perception of sound is so fascinating and surprising.

Even something as fundamental as our musical scale is not as immutable as we believe. check out the work of "William Sethares". Basically, he demonstrated that our scale is an artifact of the kind of musical instruments we play. All of them vibrate in such a way to create predictably linear resonances that are essentially the notes in our scale. However it need not be that way: you can create scales with arbitrarily many consonant notes and create strange alien-sounding music from it. The thing is that an octave, which we would normally define as the doubling of frequency, turns out to be a perception. In Sethares' artificially constructed scales, you absolutely can perceive an octave, the same way you can recognize that "C" is the same note in different octaves, even though the scale is no longer based on that doubling of frequency.


Contents

Each nerve is covered on the outside by a dense sheath of connective tissue, the epineurium. Beneath this is a layer of fat cells, the perineurium, which forms a complete sleeve around a bundle of axons. Perineurial septae extend into the nerve and subdivide it into several bundles of fibres. Surrounding each such fibre is the endoneurium. This forms an unbroken tube from the surface of the spinal cord to the level where the axon synapses with its muscle fibres, or ends in sensory receptors. The endoneurium consists of an inner sleeve of material called the glycocalyx and an outer, delicate, meshwork of collagen fibres. [2] Nerves are bundled and often travel along with blood vessels, since the neurons of a nerve have fairly high energy requirements.

Within the endoneurium, the individual nerve fibres are surrounded by a low-protein liquid called endoneurial fluid. This acts in a similar way to the cerebrospinal fluid in the central nervous system and constitutes a blood-nerve barrier similar to the blood-brain barrier. [3] Molecules are thereby prevented from crossing the blood into the endoneurial fluid. During the development of nerve edema from nerve irritation (or injury), the amount of endoneurial fluid may increase at the site of irritation. This increase in fluid can be visualized using magnetic resonance neurography, and thus MR neurography can identify nerve irritation and/or injury.

Categories Edit

Nerves are categorized into three groups based on the direction that signals are conducted:

  • Afferent nerves conduct signals from sensory neurons to the central nervous system, for example from the mechanoreceptors in skin.
  • Efferent nerves conduct signals from the central nervous system along motor neurons to their target muscles and glands.
  • Mixed nerves contain both afferent and efferent axons, and thus conduct both incoming sensory information and outgoing muscle commands in the same bundle. All spinal nerves are mixed nerves, and some of the cranial nerves are also mixed nerves.

Nerves can be categorized into two groups based on where they connect to the central nervous system:

  • Spinal nerves innervate (distribute to/stimulate) much of the body, and connect through the vertebral column to the spinal cord and thus to the central nervous system. They are given letter-number designations according to the vertebra through which they connect to the spinal column.
  • Cranial nerves innervate parts of the head, and connect directly to the brain (especially to the brainstem). They are typically assigned Roman numerals from 1 to 12, although cranial nerve zero is sometimes included. In addition, cranial nerves have descriptive names.

Terminology Edit

Specific terms are used to describe nerves and their actions. A nerve that supplies information to the brain from an area of the body, or controls an action of the body is said to "innervate" that section of the body or organ. Other terms relate to whether the nerve affects the same side ("ipsilateral") or opposite side ("contralateral") of the body, to the part of the brain that supplies it.

Nerve growth normally ends in adolescence, but can be re-stimulated with a molecular mechanism known as "Notch signaling". [4]

Regeneration Edit

If the axons of a neuron are damaged, as long as the cell body of the neuron is not damaged, the axons can regenerate and remake the synaptic connections with neurons with the help of guidepost cells. This is also referred to as neuroregeneration. [5]

The nerve begins the process by destroying the nerve distal to the site of injury allowing Schwann cells, basal lamina, and the neurilemma near the injury to begin producing a regeneration tube. Nerve growth factors are produced causing many nerve sprouts to bud. When one of the growth processes finds the regeneration tube, it begins to grow rapidly towards its original destination guided the entire time by the regeneration tube. Nerve regeneration is very slow and can take up to several months to complete. While this process does repair some nerves, there will still be some functional deficit as the repairs are not perfect. [6]

A nerve conveys information in the form of electrochemical impulses (as nerve impulses known as action potentials) carried by the individual neurons that make up the nerve. These impulses are extremely fast, with some myelinated neurons conducting at speeds up to 120 m/s. The impulses travel from one neuron to another by crossing a synapse, where the message is converted from electrical to chemical and then back to electrical. [2] [1]

Nerves can be categorized into two groups based on function:

  • An afferent nerve fiber conducts sensory information from a sensory neuron to the central nervous system, where the information is then processed. Bundles of fibres or axons, in the peripheral nervous system are called nerves, and bundles of afferent fibers are known as sensory nerves. [1][2]
  • An efferent nerve fiber conducts signals from a motor neuron in the central nervous system to muscles. Bundles of these fibres are known as efferent nerves.

Nervous system Edit

The nervous system is the part of an animal that coordinates its actions by transmitting signals to and from different parts of its body. [7] In vertebrates it consists of two main parts, the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS consists of the brain and spinal cord. The PNS consists mainly of nerves, which are enclosed bundles of the long fibers or axons, that connect the CNS to every other part of the body.

Nerves that transmit signals from the brain are called motor or efferent nerves, while those nerves that transmit information from the body to the CNS are called sensory or afferent. Spinal nerves serve both functions and are called mixed nerves. The PNS is divided into three separate subsystems, the somatic, autonomic, and enteric nervous systems. Somatic nerves mediate voluntary movement.

The autonomic nervous system is further subdivided into the sympathetic and the parasympathetic nervous systems. The sympathetic nervous system is activated in cases of emergencies to mobilize energy, while the parasympathetic nervous system is activated when organisms are in a relaxed state. The enteric nervous system functions to control the gastrointestinal system. Both autonomic and enteric nervous systems function involuntarily. Nerves that exit from the cranium are called cranial nerves while those exiting from the spinal cord are called spinal nerves.

Cancer can spread by invading the spaces around nerves. This is particularly common in head and neck cancer, and prostate and colorectal cancer.

Nerves can be damaged by physical injury as well conditions like carpal tunnel syndrome and repetitive strain injury. Autoimmune diseases such as Guillain–Barré syndrome, neurodegenerative diseases, polyneuropathy, infection, neuritis, diabetes, or failure of the blood vessels surrounding the nerve all cause nerve damage, which can vary in severity.

Multiple sclerosis is a disease associated with extensive nerve damage. It occurs when the macrophages of an individual's own immune system damage the myelin sheaths that insulate the axon of the nerve.

A pinched nerve occurs when pressure is placed on a nerve, usually from swelling due to an injury, or pregnancy and can result in pain, weakness, numbness or paralysis, an example being carpal tunnel syndrome. Symptoms can be felt in areas far from the actual site of damage, a phenomenon called referred pain. Referred pain can happen when the damage causes altered signalling to other areas.

Neurologists usually diagnose disorders of the nerves by a physical examination, including the testing of reflexes, walking and other directed movements, muscle weakness, proprioception, and the sense of touch. This initial exam can be followed with tests such as nerve conduction study, electromyography (EMG), and computed tomography (CT). [8]

A neuron is called identified if it has properties that distinguish it from every other neuron in the same animal—properties such as location, neurotransmitter, gene expression pattern, and connectivity—and if every individual organism belonging to the same species has exactly one neuron with the same set of properties. [9] In vertebrate nervous systems, very few neurons are "identified" in this sense. Researchers believe humans have none—but in simpler nervous systems, some or all neurons may be thus unique. [10]

In vertebrates, the best known identified neurons are the gigantic Mauthner cells of fish. [11] : 38–44 Every fish has two Mauthner cells, located in the bottom part of the brainstem, one on the left side and one on the right. Each Mauthner cell has an axon that crosses over, innervating (stimulating) neurons at the same brain level and then travelling down through the spinal cord, making numerous connections as it goes. The synapses generated by a Mauthner cell are so powerful that a single action potential gives rise to a major behavioral response: within milliseconds the fish curves its body into a C-shape, then straightens, thereby propelling itself rapidly forward. Functionally this is a fast escape response, triggered most easily by a strong sound wave or pressure wave impinging on the lateral line organ of the fish. Mauthner cells are not the only identified neurons in fish—there are about 20 more types, including pairs of "Mauthner cell analogs" in each spinal segmental nucleus. Although a Mauthner cell is capable of bringing about an escape response all by itself, in the context of ordinary behavior other types of cells usually contribute to shaping the amplitude and direction of the response.

Mauthner cells have been described as command neurons. A command neuron is a special type of identified neuron, defined as a neuron that is capable of driving a specific behavior all by itself. [11] : 112 Such neurons appear most commonly in the fast escape systems of various species—the squid giant axon and squid giant synapse, used for pioneering experiments in neurophysiology because of their enormous size, both participate in the fast escape circuit of the squid. The concept of a command neuron has, however, become controversial, because of studies showing that some neurons that initially appeared to fit the description were really only capable of evoking a response in a limited set of circumstances. [12]

In organisms of radial symmetry, nerve nets serve for the nervous system. There is no brain or centralised head region, and instead there are interconnected neurons spread out in nerve nets. These are found in Cnidaria, Ctenophora and Echinodermata.


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In an article published last month in the scientific journal Nature Communication, Zelzer and his colleagues showed how genes that influence the proprioceptive system are connected to the development of two of the most widespread orthopedic problems in children worldwide: scoliosis (curvature of the spine) and hip dysplasia (in which the hip socket does not completely cover the head of the femur, for which infants are routinely tested for flexibility of the hip joints). A previous study carried out in Zelzer&rsquos laboratory showed also how the system plays a significant role in the process of healing body fractures.

Zelzer is devoting much of his research to subjects with significant medical implications &ndash not least because of the involvement of two physicians in the project, Drs. Ronen Blecher and Eran Assaraf. The two broke off their medical residencies to pursue Phds in Zelzer&rsquos lab. However, to make progress, the group must first decipher the molecular language through which the communication between body and brain takes place. Despite the applied nature of the research, it can be linked to realms including the mind-body connection &ndash a kind of modern version of the pineal gland, which French philosopher René Descartes believed was the seat of the connection between mind and body.

&ldquoYoga practitioners are very well acquainted with the location of the muscle spindles in the body,&rdquo Zelzer notes.

Muscle binds

Aristotle stated explicitly that humans have five senses. But as in many realms of knowledge, modern science needed to liberate itself from Aristotelean notions in order to begin to move forward. The 17th-century English physician William Harvey, who played a key role in our understanding of blood circulation, was the first to notice that the muscles that move the fingers are located in the forearm. &ldquoThus we perceive and so feel the fingers to move, but truly we neither perceive nor feel the movement of the muscles, which are in the elbow,&rdquo Harvey wrote in a book published in 1628.

Elazar Zelzer. Few labs in the world focus on the role of muscle spindles in the proprioceptive system. His lab is the only one also examining the connection between that system and the skeleton. Tomer Appelbaum

The term &ldquosixth sense&rdquo in reference to the body&rsquos ability to sense itself, was first used by the Scottish physician, scientist and neural system researcher Charles Bell, in an essay from 1826. The muscle spindles themselves were discovered in the mid-19th century. The term &ldquoproprioception&rdquo was coined in 1906 by the man who is considered the father of neurophysiology, the British physician Charles Scott Sherrington, who won the Nobel Prize in Physiology or Medicine for his work in the field in 1932. As understanding of the sense developed, scientists were divided about whether this self-perception of the body occurs in one place &ndash the brain &ndash or throughout the body.

Today we know it occurs in both: Neural information, which is collected with the aid of the various &ldquosensors&rdquo scattered throughout the body, is transmitted to the brain. The information arrives at two separate regions of the brain, along the lines of the division between conscious and unconscious, explains Roy Salomon, who studies the boundaries of human perception in the Gonda Multidisciplinary Brain Research Center at Bar-Ilan University. The unconscious pathways, Dr. Salomon says, connects to the cerebellum, a primordial section of the brain that plays a central part in planning motoric movements and maintaining equilibrium.

The conscious pathway arrives at the central sulcus &ndash a region of the cerebral cortex located exactly between the parietal lobe and the frontal lobe of the brain. Logically, Salomon adds, these neural pathways end at the point that&rsquos located between the region that is responsible for volitional motoric movements and the region that processes the sense of touch.

How is the information collected? There are three different types of sensors in the body that send proprioceptive information: in the joints, in the connections between the tendons and the muscles, and in the muscles themselves. The question of the sensors&rsquo importance has also been a matter of scientific dispute for many years today, though, it&rsquos thought that the muscle spindles play the central role. For example, one testament to the lack of importance of the sensors in the joints is the ability of people who have undergone hip-replacement surgery to know the position of their shin relative to the hip.

A muscle spindle consists of four different nerve endings that spiral around about a dozen muscle fibers. The small sensor, less than a centimeter long, is wrapped in a spindle-shaped tissue that separates it from the rest of the muscle. The internal structure and the connection to the different neurons allow the spindle to adjust the neural signal it produces to the changes in the length of the muscle. Because of this special structure, when the muscle is motionless, the spindle also &ldquoremembers&rdquo the position it was in previously.

The number of spindles differs in each muscle, Zelzer explains all told humans and other mammals each have about 20,000 these tiny sensors. Animals of other orders, he adds, have different mechanisms that serve to create proprioception.

This understanding of the mechanical elements that make possible the body&rsquos perception of itself, was articulated in the first half of the 20th century. Since then, research into proprioception in biology and the humanities, and into muscle spindles in particular, has been neglected. According to Zelzer, this is due to the 1960s revolution in molecular biology, which included the discovery of the structure of DNA.

&ldquoUntil then, great attention was devoted to the involvement of mechanical signals in biology, with regard to development and functioning,&rdquo he explains. &ldquoWhen the molecular revolution began, to a certain extent people were captivated by three examples of molecules &ndash DNA, RNA and proteins &ndash and abandoned the mechanics. Molecular biology became mainstream those who dealt with mechanics were considered part of the old world.&rdquo

The perception that the mechanical signals were important began to coalesce at the end of the 1980s. &ldquoGradually, the fact that there is a very significant mechanical world in addition to the molecular world began to be accepted again. However, for these two worlds to connect, and for the mechanical to receive its due place, it&rsquos necessary to understand the mechanism that is capable of translating the mechanics into the molecular signals of biology,&rdquo Zelzer says.

This revolution &ndash deciphering the mechanisms that generate molecular signals &ndash took place in multiple areas of life sciences and neurobiology, he notes. As for the proprioceptive system, however, &ldquoeven though it was one of the first systems in the body to be characterized, there was no one to create the molecular language for it.&rdquo The subject was barely studied in neuroscience, Zelzer adds (and Salomon from Bar-Ilan agrees with him). From the point of view of the body, the professor points out, there are very few laboratories in the world that are studying the role of the muscle spindles in the proprioceptive system. His laboratory is the only one that is also examining the connection between the system and the body&rsquos skeleton.

&ldquoWe are trying,&rdquo he says, &ldquoto create the molecular language of this system, and by that means it will be possible to return the system to the center.&rdquo

How are the scientists uncovering this molecular language? First, the researchers in Zelzer&rsquos laboratory isolate the spindles. Subsequently, they examine which genes are expressed in them and then try to discover which proteins each gene encodes, and what the proteins do. Their principal method is to inhibit the activity of individual genes and then examine closely the changes that occur when those genes cease to function. As he puts it, &ldquoWe try to adopt systemic observation &ndash not to focus on the lone tissue but to examine how it interacts with other systems, such as the skeletal one.&rdquo

Roy Salomon. Ilan Assayag

A protein called Piezo2 is a striking example of a molecule that translates a mechanical signal (movement) of the muscle into a molecular signal. The protein, Zelzer relates, is actually a channel that resides on the membrane of the nerve cell that spirals around the muscle fiber. If the muscle&rsquos length changes, the membrane is affected, the channel opens and allows a flow of positive ions (atoms with a positive charge) into the cell. They set off a chain of molecular mechanisms that modify the condition of the neuron.

&ldquoPiezo is an example that links the molecular world to the mechanical world,&rdquo Zelzer notes.

Bipedal misconception

In their new study, Zelzer et al. showed what happens when a gene like this goes awry. Mice in which the gene was inhibited in the skeleton itself did not develop medical problems. However, when the gene was inhibited in the proprioceptive system only, scoliosis developed at maturation &ndash a spinal misalignment found in about 3 percent of all people, in which the vertebrae in the spinal column curve sideways.

&ldquoThe conventional assumption in research is that scoliosis is the price we pay for being bipeds,&rdquo Zelzer says. &ldquoWe showed that this is also the case with quadrupeds &ndash and that the proprioceptive system is responsible for maintaining a straight back.&rdquo

The second problem from which the mice suffered is known as hip dysplasia, a common condition in 0.1 percent to 0.6 percent of infants every infant in Israel is checked for it within the framework of the routine checkups in hospitals and the well-baby clinics. To explain the connection between the deformation of a normal hip and proprioception, Zelzer mentions a previous project of his.

As a developmental biologist, he examines how different elements in the skeleton and the muscles develop during pregnancy and natural physical growth. In the earlier study, he relates, he showed that for the joints to develop, the fetus needs to move in the womb, and that the movement encourages joint formation. &ldquoThe significance of the new research,&rdquo he says, &ldquois that not only does there have to be movement, there has to be correct movement.&rdquo

If fetuses and children who are developing have problems with the ability to sense their body, their movement is disrupted, and the joints that are involved in those movements are also disrupted. &ldquoThat is the hypothesis: Not only is movement needed, but a particular movement is needed, so that the joint will develop properly,&rdquo Zelzer says.

This hypothesis bears deeper implications for understanding biology and evolution, he adds, and not only in pathological examples &ndash in cases where something goes wrong. What it means is that the structure of the pelvis, a central anatomical organ, is influenced not only by genetics but also by the body&rsquos own movements. If the structure of the pelvis is determined by the movements of animals, it follows that it has plasticity, that it is capable of adjusting itself to changes.

&ldquoLet&rsquos say that a mutation occurred in a certain animal that modified its muscle activity, the bone size or the connection of the bone to the muscle,&rdquo Zelzer says. &ldquoThat mutation changes the way the animal walks.&rdquo However, because the final form is determined by movement, this means that the pelvis can adjust itself to the change in walking, &ldquoand thus preserve its survivability.&rdquo Accordingly, in contrast to eye and hair color, which are genetically predetermined, the sixth sense research project presents an example of a system in the body by which activity defines structure.

&ldquoNot everything is predetermined part of the body retains plasticity for changes,&rdquo Zelzer sums up.

Another place at which activity and functioning intersect with proprioception is aging. Proprioception is one of the first mechanisms affected by growing old. Because the aging process is frequently accompanied by a deterioration of various cognitive mechanisms in the brain, it is easy to assume that the effects are partly due to the brain&rsquos getting older. But it&rsquos possible that the deterioration of the proprioceptive system, too, is related to the decline in the quality of the signal that arrives from the sensors throughout the body.

Dr. Salomon notes that when the brain feels uncertain about proprioception, it makes us move and in so doing makes the sense more precise. At present, it is impossible to state that this precision mechanism can also help curb the damage to proprioception that comes with age. In order to understand exactly how aging affects the sixth sense, Zelzer adds, it&rsquos necessary also to articulate the specific molecular language of this sense and the changes that come with age. Much research is needed to arrive at reliable conclusions, he says. However, the possible connection between physical activity and the improvement of proprioceptive ability in this sphere, including at advanced ages, is a logical hypothesis about the system that lies on the seam line between body and brain.


PHYSICAL MEDICINE APPROACHES TO PAIN MANAGEMENT

Steven Stanos , . Allison Baum , in Current Therapy in Pain , 2009

Pain Threshold

The nociceptive nerve endings that are found in skin, joints, muscles, bone make up an intricate network of pain perception controlled by the human central nervous system. Because muscle afferent nerve pathways and pain afferent nerve pathways both converge on the dorsal horn of the spinal cord, it has been proposed that pain afferents may be susceptible to some form of selective inhibition as a result of physical activity and exercise training. 22 Another hypothesis is that endogenous opioid release may be involved in exercise-induced hypoalgesia. Most likely, exercised-induced hypoalgesia is caused by a host of interrelated factors that may be partially controlled by the mode and intensity of exercise. Koltyn and coworkers’ study 23 demonstrated significant hypoalgesia after maximal isometric gripping exercise in both men and women. These researchers tested 15 males and 16 females under two isometric exercise conditions. Subjects squeezed a hand dynamometer for 2 minutes at two different intensities (40%–50% and 100% of maximal handgrip contractions [MVC]).


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