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Do neurons fire at a faster rate during dreaming?

Do neurons fire at a faster rate during dreaming?


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When I dream it seems that the (subjective) time is slower than the objectively passed time as seen on my clock radio. Is this because neurones fire collectively at a faster rate, so you can "put an hour of dream time in a minute of objective time"? If they fire at a faster rate, then this does not mean that you perceive the events in your dream as going faster, as you adapt to your experience of time in the real world.


In REM sleep, the EEG is remarkably similar to that of the awake state (Purves et al., 2001). Although the EEG represents the synchronized activity of many neurons in the cortex, it does give us a clue whether they are firing faster or not.

Wakefulness is mainly dominated by beta and gamma waves (source: Scholarpedia), i.e. 12 - 100 Hz. REM sleep is characterized by low-amplitude mixed-frequency brain waves, quite similar to those experienced during the waking state - theta waves, alpha waves and even the high frequency beta waves more typical of high-level active concentration and thinking, i.e. 4-30 Hz (table 1) (source: Sleep).


Table 1. EEG bands. source: Neurosky

So if anything, I would say REM sleep, being largely devoid of the gamma band, is associated with slightly lower-frequency oscillations and hence lower neural activity overall.

References
- Purves et al. (eds). Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates (2001)


Is this because neurons fire collectively at a faster rate, so you can "put an hour of dream time in a minute of objective time"?

I believe it has more to do with what information becomes available to the association cortex and ncc (or consciousness) in the waking/sleep brain.

In the waking brain the neocortex is connected to the environment, so things tend to progress smoothly and for the most part we have contextual references to measure the passing of time,in sleep there is a varying degree of a disconnect both internal and external culminating in REM sleep, where thalamocortical connections (a switchboard/router for the senses) are at it's lowest, so cut off from the environment an cues, the thalamus- neocortex interplay stimulates only neocortical areas ( presumably those recently active through interplay with the hippocampus ) which in turn activate related areas through plasticity. So you could be in one scene where the only measurement of time is internal followed by another one without, the passage of time thus becomes hard to gauge. 1

The firing rate specifically as it pertains to cycles I believe is a wrong measure to focus on, for one, even in the waking gamma ( 30 >htz ) we top at something like 24 fps comprehending a scene and it takes about 200ms to bind information2,there is little to no information ( although if I am wrong please point it out), that we increase our comprehension and perception rates as information presents itself faster, rather we drop frames, and so even at a faster rate the information available to consciousness in the sleeping or waking brain seems to be capped.

Notes, reference & sources:

1. An excellent and readable overview of dream and it's data components is : The Secret World of Sleep (Lewis).

2. Rhythms of the brain (buzsaki) deals in depth with EEG measurements as they relate to information exchange in the brain. In search of consciousness (Koch)looks at the binding problem and ncc in detail.


What happens during REM sleep?

Sleep involves five distinct phases, which the brain and body cycle through several times during the night. The first four phases involve a transition from shallow to deep sleep, while the fifth phase, REM sleep, involves heightened brain activity and vivid dreams.

REM sleep stages tend to be relatively short during the first two-thirds of the night as the body prioritizes deeper, slow-wave sleep. And because longer periods of REM sleep only happen during the final hours of sleep (in the early morning, for most people), it can get cut off when you don&rsquot spend a full seven or eight hours in bed, says psychologist Rubin Naiman, a sleep and dream specialist at the University of Arizona Center for Integrative Medicine and the author of a recent review about dreaming published in the Annals of the New York Academy of Sciences.

During REM sleep, there is more activity in the visual, motor, emotional and autobiographical memory regions of the brain, says Matthew Walker, professor of psychology at the University of California, Berkeley and author of the new book Why We Sleep. But there is also decreased activity in other regions, like the one involved in rational thought &mdash hence the reason for extremely lucid, but often nonsensical, dreams. (The dreams you remember when you wake up are only part of REM sleep, says Walker in reality, the brain is highly active throughout the entire phase.)


Detailed visuomotor and other sense modality information that constitutes the representational structure of awareness. Such awareness must involve the interaction and integration of emotion.

Subjective awareness including perception and emotion that is enriched by abstract analysis (thinking) and metacognitive components of consciousness (awareness of awareness).

Rapid eye movement (REM) sleep

Sleep with electroencephalographic evidence of brain activation (similar to that of waking) but with inhibition of muscle tone (as measured by electromyography) and involuntary saccadic eye movements (the REMs).

Subjective awareness of perception and emotion.

Subjective awareness of the world, the body and the self, including awareness of awareness.

A brain state associated with electroencephalographic activation (similar to that of REM) but with the muscle tone enhancement (as measured by electromyography) that is necessary for posture and movement.

Non-rapid eye movement (NREM) sleep

Sleep with electroencephalographic evidence of brain deactivation spindles and slow waves characterize this brain state.

The subjective awareness that one is dreaming and not awake (as is usually incorrectly assumed).

A science of consciousness must explain how so many aspects of our experience are integrated. The binding of perception, emotion, thought and memory requires a physical explanation at the level of brain function.

A primordial state of brain organization that is a building block for consciousness. In humans, protoconsciousness is proposed to develop as brain development proceeds in REM sleep in utero and in early life.

(A). In behavioural neurobiology and cognitive science, the term activation is used to express the level of energy of the brain and its constituent circuits. The analogy to a power supply with an on–off switch conveys the essence of this idea.

(I). The process that facilitates or inhibits, as the brain changes state, access to the brain of sensory information (input) from the outside world and the transmittal of motor commands from the brain (output) to the musculature.

(M). The chemical microclimate of the brain is determined largely by neurons in the brainstem, which send their axons widely to the forebrain, spinal cord and cerebellum. Among the chemicals released by these cells are dopamine, noradrenaline, serotonin, histamine and acetylcholine.


When Your Brain Talks, Your Muscles Don't Always Listen

Have your neurons been shouting at your muscles again? It happens, you know.

As we grow older, neurons--the nerve cells that deliver commands from our brains--have to &ldquospeak&rdquo more loudly to get the attention of our muscles to move, according to University of Delaware researcher Christopher Knight, an assistant professor in UD's College of Health Sciences.

&ldquoAs a result of age-related changes in muscle and neurons, elderly people are often frustrated by poor control during precision tasks, and slowed physical responses contribute to more falls as people grow older,&rdquo Knight said.

Knight and co-author Gary Kamen, who directs the Exercise Neuroscience Laboratory at the University of Massachusetts, recently published the results of a study on motor-unit firing rates in the Journal of Applied Physiology, and Knight is now beginning a new project focusing on motor-control mechanisms in the elderly. Both studies are sponsored by the National Institutes of Health.

The ultimate goal of the research, Knight said, is to improve movement quality in older adults, as well as patients with disorders such as cerebral palsy or multiple sclerosis, or who are recovering from strokes.

Every move you make is made possible through a miraculous communications network involving the brain at the command center, the spinal cord, billions upon billions of nerve cells, and thousands of muscle fibers.

&ldquoMuscles are the driving force behind our movements,&rdquo Knight said. &ldquoEvery time they get a command from the neurons, the muscle fibers contract. In the generation of muscular force, the smallest controllable unit consists of an individual neuron and the muscle fibers it stimulates. We believe that our research is very important to our understanding of motor-control mechanisms in general and impaired control in patient populations.&rdquo

Shedding light on the communication between neurons and muscles, and how it changes as we age, may lie right at our fingertips, according to Knight's research.

Using an experimental apparatus he and his students created in UD's Human Performance Lab, Knight has been examining muscular force on a very small scale in the index finger, specifically, the first dorsal interosseous muscle. Located between the index finger and the thumb, this muscle contains 120 &ldquomotor units&rdquo--in other words, 120 individual neurons, or nerve cells, and the muscle fibers they activate.

&ldquoIt's a relatively simple muscle, so you get to see more of a one-to-one relationship between the activity of the neurons and the resulting muscular force,&rdquo Knight said.

Twenty-three subjects, ranging from 18 to 88 years of age, participated in Knight's recent study.

In a virtually painless procedure, a small needle-like electrode with four tiny wires was embedded in the muscle of an index finger of each subject. The electrode was hooked up to a computer to record the electrical impulses as they travel from neurons to the muscle fibers.

As the index finger was held steady in a small harness, each subject was asked to use the finger to follow the outline of a sinusoidal curve, with its peaks and valleys, on a computer screen.

&ldquoMore force--which is indicated by a corresponding higher firing rate of neurons--is exerted just before you begin the upturn toward one peak and then it eases off again in the downturn toward a valley,&rdquo Knight noted.

Once recordings were completed at one site in the muscle, the electrode was repositioned to sample from other motor units within the muscle.

Knight and graduate student Dhiraj Poojari and undergraduate researchers Maria Bellumori and Christopher Martens then analyzed the firing-rate data for frequency and amplitude in a tedious process that Knight hopes to automate in the future through the ongoing development of a software program that will help sort out the bang-bang-like &ldquodoublets,&rdquo the brief periods when the neurons fire faster, from slower periods of activity.

The results showed lower firing rates among older subjects versus younger subjects--a diminished ability of the muscle fibers to &ldquohear&rdquo and respond to the neurons' commands.

&ldquoThe repeated contraction of muscles is essential to movements such as walking,&rdquo Knight said. &ldquoHowever, our muscles have a reduced capacity to contract or 'twitch' as we grow older. We lose fast-twitch muscle fibers as we age.&rdquo

However, there are steps we can take to preserve this critical motor capacity, according to Knight.

&ldquoAfter power training with weights, we see an increase in firing rates,&rdquo Knight said. &ldquoFor safety, we're commonly advised to do things slowly when exercising, but it's important to also do some fast exercises. You need a fast movement to prevent a fall. Even in the frail elderly, it is possible to use exercise bands for manual resistance to improve the speed of movement.&rdquo

Knight has always been interested in how the body adapts to exercise. When he entered college years ago, his goal was to become an elite track-and-field athlete. While he competed well, he realized that his dreams lay elsewhere, and his attention focused full force on academics.

At the University of Connecticut, a class on the biology of the brain introduced him to the nervous system and movement, and he was hooked. His interests were further piqued during a summer research experience, where he had the opportunity to work with wheelchair athletes.

&ldquoPeople with severe spinal cord injuries have limited cooling because they can't perspire below the site of injury,&rdquo Knight said, &ldquoso their core body temperature can reach dangerous levels.&rdquo

In graduate school, he decided to pursue motor control research, and he's never looked back.

&ldquoMy early interests were based on sport, but my career in this field now allows me to address a much larger population that needs our knowledge,&rdquo Knight said. &ldquoExercise is still the means for improvement, and aging is a process that unites us all.&rdquo

Knight is now recruiting healthy, older subjects, ages 70 and up, as well as individuals with Parkinson's disease or multiple sclerosis for his next motor-control study. For more information, please contact him at [.edu] or (302) 831-6175.

Story Source:

Materials provided by University of Delaware. Note: Content may be edited for style and length.


You lose muscle tone

Have you ever tried to move your body during a dream, but couldn't? Well it turns out, that paralyzing feeling is because of REM. "In REM sleep, there is loss of almost all muscle tone, except for the diaphragm and eye muscles," according to Psychology Today. You literally can't move a muscle during REM sleep (except for the muscles that control your eyes). So, for the most part, when you dream your body remains very very still.


The neural correlates of dreaming

Consciousness never fades during waking. However, when awakened from sleep, we sometimes recall dreams and sometimes recall no experiences. Traditionally, dreaming has been identified with rapid eye-movement (REM) sleep, characterized by wake-like, globally 'activated', high-frequency electroencephalographic activity. However, dreaming also occurs in non-REM (NREM) sleep, characterized by prominent low-frequency activity. This challenges our understanding of the neural correlates of conscious experiences in sleep. Using high-density electroencephalography, we contrasted the presence and absence of dreaming in NREM and REM sleep. In both NREM and REM sleep, reports of dream experience were associated with local decreases in low-frequency activity in posterior cortical regions. High-frequency activity in these regions correlated with specific dream contents. Monitoring this posterior 'hot zone' in real time predicted whether an individual reported dreaming or the absence of dream experiences during NREM sleep, suggesting that it may constitute a core correlate of conscious experiences in sleep.


Footnotes

↵ ¶ To whom reprint requests should be addressed. e-mail: a.herzbiologie.hu-berlin.de .

This paper is a summary of a session presented at the third annual German-American Frontiers of Science symposium, held June 20–22, 1997 at the Kardinal Wendel Haus in Munich, Germany.

The Frontiers of Science symposia is the latest in the series “From the Academy,” which is presented occasionally to highlight work of the Academy, including the science underlying reports of the National Research Council.


RAS Dysfunction

If the RAS becomes damaged in any way, it can affect both wakefulness and sleep.   Such damage is often the result of a traumatic brain injury, such as an ischemic stroke or a severe blow to the head injury.

A coma is one such example, characterized by a deep state of unconsciousness in which are you unable to move or respond to external stimulus.  

Another disorder associated with the RAS is narcolepsy, a chronic disorder characterized by poor control of sleep-wake cycles.   This disruption of the cycle can manifest with extreme and uncontrollable bouts of sleepiness, causing you to suddenly fall asleep without notice. Narcolepsy is a dangerous condition that can place you at risk of injury while walking, driving or operating machinery.

Parkinson's disease also can affect RAS function. As neurons break down as a result of the disease, they fire less frequently. Not only does this affect motor function, it can affect sleep quality by disrupting the REM cycle.

Progressive supranuclear palsy (PSP),   a degenerative brain disease often mistaken for Parkinson's or Alzheimer's disease, is also believed linked to RAS dysfunction.

With PSP, neurons in the brainstem and cerebral cortex develop abnormal clumps of protein called tangles. These tangles interfere with RAS pathways and contribute to cognitive impairment and sleep-wake dysregulation in people with PSP.  


'Good' Chemical, Neurons In Brain Elevated Among Exercise Addicts

PORTLAND, Ore. &ndash Exercise enthusiasts have more reasons to put on their running shoes in the morning, but an Oregon Health & Science University scientist says they shouldn't step up their work-outs just yet.

A study published today in the journal Neuroscience, journal of the International Brain Research Organization, confirmed that exercise increases the chemical BDNF &ndash brain-derived neurotrophic factor &ndash in the hippocampus, a curved, elongated ridge in the brain that controls learning and memory. BDNF is involved in protecting and producing neurons in the hippocampus.

"When you exercise, it's been shown you release BDNF," said study co-author Justin Rhodes, Ph.D., a postdoctoral fellow in the Department of Behavioral Neuroscience at OHSU's School of Medicine and at the Veterans Administration Medical Center in Portland. "BDNF helps support and strengthen synapses in the brain. We find that exercise increases these good things."

Mice bred for 30 generations to display increased voluntary wheel running behavior &ndash an "exercise addiction" &ndash showed higher amounts of BDNF than normal, sedentary mice. In fact, the BDNF concentration in the active mice increased by as much as 171 percent after seven nights of wheel running.

"These mice are more active than wild mice," Rhodes said, referring to the mice as small and lean, and seemingly "addicted" to exercise. "Wheel running causes a huge amount of activity in the hippocampus. The more running, the more BDNF."

In a study Rhodes also co-authored that extends these findings, to be published in the October edition of the American Psychological Association journal Behavioral Neuroscience, scientists demonstrated that not only do the mice display more of this "good" BDNF chemical in the hippocampus, they grow more neurons there as well.

But those high levels of BDNF and neurogenesis don't necessarily mean an exercise addict learns at a faster rate, Rhodes said. According to the Behavioral Neuroscience study, the running addict, compared with the normal-running, control mice, perform "terribly" when attempting to navigate around a maze.

"These studies are focusing on the effects of exercise itself on chemicals known to protect and strengthen synapses," Rhodes explained. "But too much of it is not necessarily a good thing."

High runners tend to "max out" in the production of the BDNF and neurogenesis, Rhodes said. And that topping-out effect may be what prevents learning.

A high-running mouse's inability to learn as well as a normal mouse could be due to less biological reasons, Rhodes points out. "It is possible that they're so focused on running, they can't think of anything else," he said.

Rhodes and colleagues at the University of Wisconsin at Madison, the University of California at Riverside and The Salk Institute also emphasize that the functional significance of the exercise-induced increases in BDNF and neurogenesis is not known.

Rhodes suggests that when a high-running mouse exercises, stress is placed on its hippocampus and the development of new neurons becomes a protective response. No one has yet tested whether hyperactive wheel running exercise actually kills or damages neurons in the hippocampus, he said.

"The reason why these good things are happening is they may clean up some of the mess," he said. "Knowing that, you wouldn't expect high runners to get any benefit from it."

One thing is clear: Exercise greatly activates the hippocampus. Rhodes and his colleagues have conducted research that also shows the intensity of exercise is linearly related to the number of neurons that are activated in a subregion of the hippocampus called the dentate gyrus.

In addition, they have demonstrated that when mice are kept from their normal running routine, brain regions involved in craving for natural rewards such as food, sex and drugs of abuse become activated. It is allowing Rhodes to study the relationship between natural craving, like hunger, and drug craving due to a pathological addiction.

"The point is to characterize what makes drug craving different from natural craving at the level of the genes and neuronal substrates involved so that, eventually, a pharmaceutical therapy can be designed to target the pathology," Rhodes said.


Use it or lose it We are all born with more neurons than we actually need. Typically by the age of 8, our brains do a major neuron dump, removing any neurons perceived as unnecessary, which is why it’s easier to teach language and music to younger children. “If you learn music as a child, your brain becomes designed for music,” Sugaya says.

Oldest Instrument According to National Geographic, a 40,000-year-old vulture-bone flute is the world’s oldest musical instrument.

Hairy Cells The ear only has 3,500 inner hair cells, compared to the more than 100 million photoreceptors found in the eye. Yet our brains are remarkably adaptable to music.

Sing Along In the Sesotho language, the verb for singing and dancing are the same (ho bina), as it is assumed the two actions occur together.


'Good' Chemical, Neurons In Brain Elevated Among Exercise Addicts

PORTLAND, Ore. &ndash Exercise enthusiasts have more reasons to put on their running shoes in the morning, but an Oregon Health & Science University scientist says they shouldn't step up their work-outs just yet.

A study published today in the journal Neuroscience, journal of the International Brain Research Organization, confirmed that exercise increases the chemical BDNF &ndash brain-derived neurotrophic factor &ndash in the hippocampus, a curved, elongated ridge in the brain that controls learning and memory. BDNF is involved in protecting and producing neurons in the hippocampus.

"When you exercise, it's been shown you release BDNF," said study co-author Justin Rhodes, Ph.D., a postdoctoral fellow in the Department of Behavioral Neuroscience at OHSU's School of Medicine and at the Veterans Administration Medical Center in Portland. "BDNF helps support and strengthen synapses in the brain. We find that exercise increases these good things."

Mice bred for 30 generations to display increased voluntary wheel running behavior &ndash an "exercise addiction" &ndash showed higher amounts of BDNF than normal, sedentary mice. In fact, the BDNF concentration in the active mice increased by as much as 171 percent after seven nights of wheel running.

"These mice are more active than wild mice," Rhodes said, referring to the mice as small and lean, and seemingly "addicted" to exercise. "Wheel running causes a huge amount of activity in the hippocampus. The more running, the more BDNF."

In a study Rhodes also co-authored that extends these findings, to be published in the October edition of the American Psychological Association journal Behavioral Neuroscience, scientists demonstrated that not only do the mice display more of this "good" BDNF chemical in the hippocampus, they grow more neurons there as well.

But those high levels of BDNF and neurogenesis don't necessarily mean an exercise addict learns at a faster rate, Rhodes said. According to the Behavioral Neuroscience study, the running addict, compared with the normal-running, control mice, perform "terribly" when attempting to navigate around a maze.

"These studies are focusing on the effects of exercise itself on chemicals known to protect and strengthen synapses," Rhodes explained. "But too much of it is not necessarily a good thing."

High runners tend to "max out" in the production of the BDNF and neurogenesis, Rhodes said. And that topping-out effect may be what prevents learning.

A high-running mouse's inability to learn as well as a normal mouse could be due to less biological reasons, Rhodes points out. "It is possible that they're so focused on running, they can't think of anything else," he said.

Rhodes and colleagues at the University of Wisconsin at Madison, the University of California at Riverside and The Salk Institute also emphasize that the functional significance of the exercise-induced increases in BDNF and neurogenesis is not known.

Rhodes suggests that when a high-running mouse exercises, stress is placed on its hippocampus and the development of new neurons becomes a protective response. No one has yet tested whether hyperactive wheel running exercise actually kills or damages neurons in the hippocampus, he said.

"The reason why these good things are happening is they may clean up some of the mess," he said. "Knowing that, you wouldn't expect high runners to get any benefit from it."

One thing is clear: Exercise greatly activates the hippocampus. Rhodes and his colleagues have conducted research that also shows the intensity of exercise is linearly related to the number of neurons that are activated in a subregion of the hippocampus called the dentate gyrus.

In addition, they have demonstrated that when mice are kept from their normal running routine, brain regions involved in craving for natural rewards such as food, sex and drugs of abuse become activated. It is allowing Rhodes to study the relationship between natural craving, like hunger, and drug craving due to a pathological addiction.

"The point is to characterize what makes drug craving different from natural craving at the level of the genes and neuronal substrates involved so that, eventually, a pharmaceutical therapy can be designed to target the pathology," Rhodes said.


Detailed visuomotor and other sense modality information that constitutes the representational structure of awareness. Such awareness must involve the interaction and integration of emotion.

Subjective awareness including perception and emotion that is enriched by abstract analysis (thinking) and metacognitive components of consciousness (awareness of awareness).

Rapid eye movement (REM) sleep

Sleep with electroencephalographic evidence of brain activation (similar to that of waking) but with inhibition of muscle tone (as measured by electromyography) and involuntary saccadic eye movements (the REMs).

Subjective awareness of perception and emotion.

Subjective awareness of the world, the body and the self, including awareness of awareness.

A brain state associated with electroencephalographic activation (similar to that of REM) but with the muscle tone enhancement (as measured by electromyography) that is necessary for posture and movement.

Non-rapid eye movement (NREM) sleep

Sleep with electroencephalographic evidence of brain deactivation spindles and slow waves characterize this brain state.

The subjective awareness that one is dreaming and not awake (as is usually incorrectly assumed).

A science of consciousness must explain how so many aspects of our experience are integrated. The binding of perception, emotion, thought and memory requires a physical explanation at the level of brain function.

A primordial state of brain organization that is a building block for consciousness. In humans, protoconsciousness is proposed to develop as brain development proceeds in REM sleep in utero and in early life.

(A). In behavioural neurobiology and cognitive science, the term activation is used to express the level of energy of the brain and its constituent circuits. The analogy to a power supply with an on–off switch conveys the essence of this idea.

(I). The process that facilitates or inhibits, as the brain changes state, access to the brain of sensory information (input) from the outside world and the transmittal of motor commands from the brain (output) to the musculature.

(M). The chemical microclimate of the brain is determined largely by neurons in the brainstem, which send their axons widely to the forebrain, spinal cord and cerebellum. Among the chemicals released by these cells are dopamine, noradrenaline, serotonin, histamine and acetylcholine.


When Your Brain Talks, Your Muscles Don't Always Listen

Have your neurons been shouting at your muscles again? It happens, you know.

As we grow older, neurons--the nerve cells that deliver commands from our brains--have to &ldquospeak&rdquo more loudly to get the attention of our muscles to move, according to University of Delaware researcher Christopher Knight, an assistant professor in UD's College of Health Sciences.

&ldquoAs a result of age-related changes in muscle and neurons, elderly people are often frustrated by poor control during precision tasks, and slowed physical responses contribute to more falls as people grow older,&rdquo Knight said.

Knight and co-author Gary Kamen, who directs the Exercise Neuroscience Laboratory at the University of Massachusetts, recently published the results of a study on motor-unit firing rates in the Journal of Applied Physiology, and Knight is now beginning a new project focusing on motor-control mechanisms in the elderly. Both studies are sponsored by the National Institutes of Health.

The ultimate goal of the research, Knight said, is to improve movement quality in older adults, as well as patients with disorders such as cerebral palsy or multiple sclerosis, or who are recovering from strokes.

Every move you make is made possible through a miraculous communications network involving the brain at the command center, the spinal cord, billions upon billions of nerve cells, and thousands of muscle fibers.

&ldquoMuscles are the driving force behind our movements,&rdquo Knight said. &ldquoEvery time they get a command from the neurons, the muscle fibers contract. In the generation of muscular force, the smallest controllable unit consists of an individual neuron and the muscle fibers it stimulates. We believe that our research is very important to our understanding of motor-control mechanisms in general and impaired control in patient populations.&rdquo

Shedding light on the communication between neurons and muscles, and how it changes as we age, may lie right at our fingertips, according to Knight's research.

Using an experimental apparatus he and his students created in UD's Human Performance Lab, Knight has been examining muscular force on a very small scale in the index finger, specifically, the first dorsal interosseous muscle. Located between the index finger and the thumb, this muscle contains 120 &ldquomotor units&rdquo--in other words, 120 individual neurons, or nerve cells, and the muscle fibers they activate.

&ldquoIt's a relatively simple muscle, so you get to see more of a one-to-one relationship between the activity of the neurons and the resulting muscular force,&rdquo Knight said.

Twenty-three subjects, ranging from 18 to 88 years of age, participated in Knight's recent study.

In a virtually painless procedure, a small needle-like electrode with four tiny wires was embedded in the muscle of an index finger of each subject. The electrode was hooked up to a computer to record the electrical impulses as they travel from neurons to the muscle fibers.

As the index finger was held steady in a small harness, each subject was asked to use the finger to follow the outline of a sinusoidal curve, with its peaks and valleys, on a computer screen.

&ldquoMore force--which is indicated by a corresponding higher firing rate of neurons--is exerted just before you begin the upturn toward one peak and then it eases off again in the downturn toward a valley,&rdquo Knight noted.

Once recordings were completed at one site in the muscle, the electrode was repositioned to sample from other motor units within the muscle.

Knight and graduate student Dhiraj Poojari and undergraduate researchers Maria Bellumori and Christopher Martens then analyzed the firing-rate data for frequency and amplitude in a tedious process that Knight hopes to automate in the future through the ongoing development of a software program that will help sort out the bang-bang-like &ldquodoublets,&rdquo the brief periods when the neurons fire faster, from slower periods of activity.

The results showed lower firing rates among older subjects versus younger subjects--a diminished ability of the muscle fibers to &ldquohear&rdquo and respond to the neurons' commands.

&ldquoThe repeated contraction of muscles is essential to movements such as walking,&rdquo Knight said. &ldquoHowever, our muscles have a reduced capacity to contract or 'twitch' as we grow older. We lose fast-twitch muscle fibers as we age.&rdquo

However, there are steps we can take to preserve this critical motor capacity, according to Knight.

&ldquoAfter power training with weights, we see an increase in firing rates,&rdquo Knight said. &ldquoFor safety, we're commonly advised to do things slowly when exercising, but it's important to also do some fast exercises. You need a fast movement to prevent a fall. Even in the frail elderly, it is possible to use exercise bands for manual resistance to improve the speed of movement.&rdquo

Knight has always been interested in how the body adapts to exercise. When he entered college years ago, his goal was to become an elite track-and-field athlete. While he competed well, he realized that his dreams lay elsewhere, and his attention focused full force on academics.

At the University of Connecticut, a class on the biology of the brain introduced him to the nervous system and movement, and he was hooked. His interests were further piqued during a summer research experience, where he had the opportunity to work with wheelchair athletes.

&ldquoPeople with severe spinal cord injuries have limited cooling because they can't perspire below the site of injury,&rdquo Knight said, &ldquoso their core body temperature can reach dangerous levels.&rdquo

In graduate school, he decided to pursue motor control research, and he's never looked back.

&ldquoMy early interests were based on sport, but my career in this field now allows me to address a much larger population that needs our knowledge,&rdquo Knight said. &ldquoExercise is still the means for improvement, and aging is a process that unites us all.&rdquo

Knight is now recruiting healthy, older subjects, ages 70 and up, as well as individuals with Parkinson's disease or multiple sclerosis for his next motor-control study. For more information, please contact him at [.edu] or (302) 831-6175.

Story Source:

Materials provided by University of Delaware. Note: Content may be edited for style and length.


The neural correlates of dreaming

Consciousness never fades during waking. However, when awakened from sleep, we sometimes recall dreams and sometimes recall no experiences. Traditionally, dreaming has been identified with rapid eye-movement (REM) sleep, characterized by wake-like, globally 'activated', high-frequency electroencephalographic activity. However, dreaming also occurs in non-REM (NREM) sleep, characterized by prominent low-frequency activity. This challenges our understanding of the neural correlates of conscious experiences in sleep. Using high-density electroencephalography, we contrasted the presence and absence of dreaming in NREM and REM sleep. In both NREM and REM sleep, reports of dream experience were associated with local decreases in low-frequency activity in posterior cortical regions. High-frequency activity in these regions correlated with specific dream contents. Monitoring this posterior 'hot zone' in real time predicted whether an individual reported dreaming or the absence of dream experiences during NREM sleep, suggesting that it may constitute a core correlate of conscious experiences in sleep.


You lose muscle tone

Have you ever tried to move your body during a dream, but couldn't? Well it turns out, that paralyzing feeling is because of REM. "In REM sleep, there is loss of almost all muscle tone, except for the diaphragm and eye muscles," according to Psychology Today. You literally can't move a muscle during REM sleep (except for the muscles that control your eyes). So, for the most part, when you dream your body remains very very still.


Use it or lose it We are all born with more neurons than we actually need. Typically by the age of 8, our brains do a major neuron dump, removing any neurons perceived as unnecessary, which is why it’s easier to teach language and music to younger children. “If you learn music as a child, your brain becomes designed for music,” Sugaya says.

Oldest Instrument According to National Geographic, a 40,000-year-old vulture-bone flute is the world’s oldest musical instrument.

Hairy Cells The ear only has 3,500 inner hair cells, compared to the more than 100 million photoreceptors found in the eye. Yet our brains are remarkably adaptable to music.

Sing Along In the Sesotho language, the verb for singing and dancing are the same (ho bina), as it is assumed the two actions occur together.


What happens during REM sleep?

Sleep involves five distinct phases, which the brain and body cycle through several times during the night. The first four phases involve a transition from shallow to deep sleep, while the fifth phase, REM sleep, involves heightened brain activity and vivid dreams.

REM sleep stages tend to be relatively short during the first two-thirds of the night as the body prioritizes deeper, slow-wave sleep. And because longer periods of REM sleep only happen during the final hours of sleep (in the early morning, for most people), it can get cut off when you don&rsquot spend a full seven or eight hours in bed, says psychologist Rubin Naiman, a sleep and dream specialist at the University of Arizona Center for Integrative Medicine and the author of a recent review about dreaming published in the Annals of the New York Academy of Sciences.

During REM sleep, there is more activity in the visual, motor, emotional and autobiographical memory regions of the brain, says Matthew Walker, professor of psychology at the University of California, Berkeley and author of the new book Why We Sleep. But there is also decreased activity in other regions, like the one involved in rational thought &mdash hence the reason for extremely lucid, but often nonsensical, dreams. (The dreams you remember when you wake up are only part of REM sleep, says Walker in reality, the brain is highly active throughout the entire phase.)


RAS Dysfunction

If the RAS becomes damaged in any way, it can affect both wakefulness and sleep.   Such damage is often the result of a traumatic brain injury, such as an ischemic stroke or a severe blow to the head injury.

A coma is one such example, characterized by a deep state of unconsciousness in which are you unable to move or respond to external stimulus.  

Another disorder associated with the RAS is narcolepsy, a chronic disorder characterized by poor control of sleep-wake cycles.   This disruption of the cycle can manifest with extreme and uncontrollable bouts of sleepiness, causing you to suddenly fall asleep without notice. Narcolepsy is a dangerous condition that can place you at risk of injury while walking, driving or operating machinery.

Parkinson's disease also can affect RAS function. As neurons break down as a result of the disease, they fire less frequently. Not only does this affect motor function, it can affect sleep quality by disrupting the REM cycle.

Progressive supranuclear palsy (PSP),   a degenerative brain disease often mistaken for Parkinson's or Alzheimer's disease, is also believed linked to RAS dysfunction.

With PSP, neurons in the brainstem and cerebral cortex develop abnormal clumps of protein called tangles. These tangles interfere with RAS pathways and contribute to cognitive impairment and sleep-wake dysregulation in people with PSP.  


Footnotes

↵ ¶ To whom reprint requests should be addressed. e-mail: a.herzbiologie.hu-berlin.de .

This paper is a summary of a session presented at the third annual German-American Frontiers of Science symposium, held June 20–22, 1997 at the Kardinal Wendel Haus in Munich, Germany.

The Frontiers of Science symposia is the latest in the series “From the Academy,” which is presented occasionally to highlight work of the Academy, including the science underlying reports of the National Research Council.


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