Only From a Pre-Med

Where medicine, studying, and having a life collide.

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neurosciencestuff: Some Autism Behaviors Linked to Altered Gene Scientists at Washington University School of Medicine in St. Louis have identified a genetic mutation that may underlie common behaviors seen in some people with autism, such as difficulty communicating and resistance to change. An error in the gene, CELF6, leads to disturbances in serotonin, a chemical that relays messages in the brain and has long been suspected to be involved in autism. The researchers identified the error in a child with autism and then, working in mice, showed that the same genetic alteration results in autism-related behaviors and a sharp drop in the level of serotonin circulating in the brain. While the newly discovered mutation appears to be rare, it provides some of the first clues to the biological basis of the disease, the scientists report Feb. 13 in the Journal of Neuroscience. “Genetically, autism looks very complicated, with many different genetic routes that lead to the disease,” says lead author Joseph D. Dougherty, PhD, an assistant professor of genetics at Washington University. “But it’s not possible to design a different drug for every child. The real key is to find the common biological pathways that link these different genetic routes and target those pathways for treatment.” Autism is known to have a strong genetic component, but the handful of genes implicated in the condition so far explain only a small number of cases or make a small contribution to symptoms. This led Dougherty and senior author Nathaniel Heintz, PhD, a Howard Hughes Medical Institute investigator at Rockefeller University, to speculate that some of the most common behavioral symptoms of autism may be caused by disruptions in a common biological pathway, like the one involved in serotonin signaling.

neurosciencestuff:

Some Autism Behaviors Linked to Altered Gene

Scientists at Washington University School of Medicine in St. Louis have identified a genetic mutation that may underlie common behaviors seen in some people with autism, such as difficulty communicating and resistance to change.

An error in the gene, CELF6, leads to disturbances in serotonin, a chemical that relays messages in the brain and has long been suspected to be involved in autism.

The researchers identified the error in a child with autism and then, working in mice, showed that the same genetic alteration results in autism-related behaviors and a sharp drop in the level of serotonin circulating in the brain.

While the newly discovered mutation appears to be rare, it provides some of the first clues to the biological basis of the disease, the scientists report Feb. 13 in the Journal of Neuroscience.

“Genetically, autism looks very complicated, with many different genetic routes that lead to the disease,” says lead author Joseph D. Dougherty, PhD, an assistant professor of genetics at Washington University. “But it’s not possible to design a different drug for every child. The real key is to find the common biological pathways that link these different genetic routes and target those pathways for treatment.”

Autism is known to have a strong genetic component, but the handful of genes implicated in the condition so far explain only a small number of cases or make a small contribution to symptoms.

This led Dougherty and senior author Nathaniel Heintz, PhD, a Howard Hughes Medical Institute investigator at Rockefeller University, to speculate that some of the most common behavioral symptoms of autism may be caused by disruptions in a common biological pathway, like the one involved in serotonin signaling.

106 notes

neurosciencestuff: Stopping cold: USC scientists turn off the ability to feel cold USC neuroscientists have isolated chills at a cellular level, identifying the sensory network of neurons in the skin that relays the sensation of cold. David McKemy, associate professor of neurobiology in the USC Dornsife College of Letters, Arts and Sciences, and his team managed to selectively shut off the ability to sense cold in mice while still leaving them able to sense heat and touch. In prior work, McKemy discovered a link between the experience of cold and a protein known as TRPM8 (pronounced trip-em-ate), which a sensor of cold temperatures in neurons in the skin, as well as a receptor for menthol, the cooling component of mint. Now, in a paper appearing in the Journal of Neuroscience on February 13, McKemy and his co-investigators have isolated and ablated the neurons that express TRPM8, giving them the ability to test the function of these cells specifically. Using mouse-tracking software program developed by one of McKemy’s students, the researchers tested control mice and mice without TRPM8 neurons on a multi-temperature surface. The surface temperature ranged from 0 degrees to 50 degrees Celsius (32 to 122 degrees Farenheit), and mice were allowed to move freely among the regions. The researchers found that mice depleted of TRPM8 neurons could not feel cold, but still responded to heat. Control mice tended to stick to an area around 30 degrees Celsius (86 degrees Fahrenheit) and avoided both colder and hotter areas. But mice without TRPM8 neurons avoided only hotter plates and not cold — even when the cold should have been painful or was potentially dangerous. In tests of grip strength, responses to touch, or coordinated movements, such as balancing onto a rod while it rotated, there was no difference between the control mice and the mice without TRPM8-expressing neurons. By better understanding the specific ways in which we feel sensations, scientists hope to one day develop better pain treatments without knocking out all ability to feel for suffering patients. “The problem with pain drugs now is that they typically just reduce inflammation, which is just one potential cause of pain, or they knock out all sensation, which often is not desirable,” McKemy said. “One of our goals is to pave the way for medications that address the pain directly, in a way that does not leave patients completely numb.”

neurosciencestuff:

Stopping cold: USC scientists turn off the ability to feel cold

USC neuroscientists have isolated chills at a cellular level, identifying the sensory network of neurons in the skin that relays the sensation of cold.

David McKemy, associate professor of neurobiology in the USC Dornsife College of Letters, Arts and Sciences, and his team managed to selectively shut off the ability to sense cold in mice while still leaving them able to sense heat and touch.

In prior work, McKemy discovered a link between the experience of cold and a protein known as TRPM8 (pronounced trip-em-ate), which a sensor of cold temperatures in neurons in the skin, as well as a receptor for menthol, the cooling component of mint. Now, in a paper appearing in the Journal of Neuroscience on February 13, McKemy and his co-investigators have isolated and ablated the neurons that express TRPM8, giving them the ability to test the function of these cells specifically.

Using mouse-tracking software program developed by one of McKemy’s students, the researchers tested control mice and mice without TRPM8 neurons on a multi-temperature surface. The surface temperature ranged from 0 degrees to 50 degrees Celsius (32 to 122 degrees Farenheit), and mice were allowed to move freely among the regions.

The researchers found that mice depleted of TRPM8 neurons could not feel cold, but still responded to heat. Control mice tended to stick to an area around 30 degrees Celsius (86 degrees Fahrenheit) and avoided both colder and hotter areas. But mice without TRPM8 neurons avoided only hotter plates and not cold — even when the cold should have been painful or was potentially dangerous.

In tests of grip strength, responses to touch, or coordinated movements, such as balancing onto a rod while it rotated, there was no difference between the control mice and the mice without TRPM8-expressing neurons.

By better understanding the specific ways in which we feel sensations, scientists hope to one day develop better pain treatments without knocking out all ability to feel for suffering patients.

“The problem with pain drugs now is that they typically just reduce inflammation, which is just one potential cause of pain, or they knock out all sensation, which often is not desirable,” McKemy said. “One of our goals is to pave the way for medications that address the pain directly, in a way that does not leave patients completely numb.”

1,543 notes

bekindplzrewind: fyeahchemistry: (photo credit) via Rajini Rao on Google+, for #ScienceSunday: ‘Smallest rotary motor in biology, the ATP synthase. All the work done in your body is fueled by breaking a chemical bond in ATP, the “currency of energy”. Did you know that you convert your body weight (or an estimated 50 kg) of ATP per day?! Where does this ATP come from? It is synthesized by an incredibly sophisticated molecular machine, the ATP synthase, embedded in the inner membrane of our mitochondria. Energy from the oxidation of food results in protons being pumped across the membrane to create a proton gradient. The protons drive the rotation of a circular ring of proteins in the membrane that in turn move a central shaft. The shaft interacts sequentially with one of 3 catalytic sites within a hexamer, making ATP (little butterflies in the movie!). The ATP synthase rotates about 150 times/second To visualize the rotation under a microscope, a very long fluorescent rod (actin filament) was chemically attached to the central shaft. Watch real movies (not animations!) of the enzyme spinning here: http://www.k2.phys.waseda.ac.jp/F1movies/F1long.htmNotice the rotation is slower with longer rods. The rotor produces a torque of 40 pN nm (40 pico Newtons x nanometer), irrespective of the load. This would be the force you would need to rotate a 500 m long rod while standing at the bottom of a large swimming pool at the rate shown in the movie. How did this amazing rotor evolve? The hexameric structure is related to DNA helicases that rotate along the DNA double helix, using ATP to unzip the two strands apart. The H+ motor has precedence in flagella motors that use proton gradients to drive rotation of long filaments, allowing bacteria to tumble through their surroundings. At some point, a H+ driven motor came together with a helicase like hexamer to create a rotor driving the hexamer in reverse, to synthesize ATP. The 1997 Nobel prize in Chemistry was awarded to John Walker and Paul Boyer for solving the structure and cyclical mechanism of the ATP synthase, respectively. This amazing enzyme was also the subject of my own Ph.D. thesis, and my first love!’For #ScienceSunday curated by +Allison Sekuler and +Robby Bowles ATP synthase is an amazing little thing. It was, personally, what got me hooked on biochemistry. LOOK AT THAT. JUST LOOK AT IT GO. Amazing.

bekindplzrewind:

fyeahchemistry:

(photo credit)

via Rajini Rao on Google+, for #ScienceSunday:

‘Smallest rotary motor in biology, the ATP synthase.

All the work done in your body is fueled by breaking a chemical bond in ATP, the “currency of energy”. Did you know that you convert your body weight (or an estimated 50 kg) of ATP per day?!

Where does this ATP come from?

It is synthesized by an incredibly sophisticated molecular machine, the ATP synthase, embedded in the inner membrane of our mitochondria. Energy from the oxidation of food results in protons being pumped across the membrane to create a proton gradient. The protons drive the rotation of a circular ring of proteins in the membrane that in turn move a central shaft. The shaft interacts sequentially with one of 3 catalytic sites within a hexamer, making ATP (little butterflies in the movie!). The ATP synthase rotates about 150 times/second

To visualize the rotation under a microscope, a very long fluorescent rod (actin filament) was chemically attached to the central shaft. Watch real movies (not animations!) of the enzyme spinning here: http://www.k2.phys.waseda.ac.jp/F1movies/F1long.htm

Notice the rotation is slower with longer rods. The rotor produces a torque of 40 pN nm (40 pico Newtons x nanometer), irrespective of the load. This would be the force you would need to rotate a 500 m long rod while standing at the bottom of a large swimming pool at the rate shown in the movie.

How did this amazing rotor evolve?

The hexameric structure is related to DNA helicases that rotate along the DNA double helix, using ATP to unzip the two strands apart. The H+ motor has precedence in flagella motors that use proton gradients to drive rotation of long filaments, allowing bacteria to tumble through their surroundings. At some point, a H+ driven motor came together with a helicase like hexamer to create a rotor driving the hexamer in reverse, to synthesize ATP.

The 1997 Nobel prize in Chemistry was awarded to John Walker and Paul Boyer for solving the structure and cyclical mechanism of the ATP synthase, respectively. This amazing enzyme was also the subject of my own Ph.D. thesis, and my first love!’

For #ScienceSunday curated by +Allison Sekuler and +Robby Bowles

ATP synthase is an amazing little thing. It was, personally, what got me hooked on biochemistry.

LOOK AT THAT. JUST LOOK AT IT GO.

Amazing.

(via drozkanandmrscary-deactivated20)

24 notes

neuromorphogenesis: A brain protein called vimentin can indicate damage to the hippocampus following binge drinking Binge drinking is known to increase the risk of developing dementia and/or brain damage. A new study used rodents to test markers of neurodegeneration to determine a threshold for brain damage. The vimentin brain protein can indicate damage to the hippocampus after 24 hours of binge-like drinking. Chronic drinking is known to have detrimental health effects such as cardiac and liver problems, cognitive impairments, and brain damage. Binge drinking in particular is known to increase the risk of developing dementia and/or brain damage, yet little is known about an exact threshold for the damaging effects of alcohol. A study using rodents to examine various markers of neurodegeneration has found that brain damage can occur with as little as 24 hours of binge-like alcohol exposure. Results will be published in the March 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View. “We know that the extent of damage following alcohol exposure depends heavily on the manner in which it is consumed,” said Kimberly Nixon, associate professor of pharmaceutical sciences at The University of Kentucky as well as corresponding author for the study. “Human studies suggest that binge-pattern drinking is more closely associated with brain damage. One study, for example, reported that binge drinking at least once per month in adulthood significantly increases the risk of developing dementia later in life. Animal models help provide the critical information that binge drinking, which produces high blood alcohol levels, directly causes damage.” “The exact threshold for the damaging effects of alcohol on the brain is unclear,” commented Fulton T. Crews, John Andrews Distinguished Professor and director of the Center for Alcohol Studies at the University of North Carolina. “It is likely that the higher the blood alcohol level the greater the damage, however, this manuscript only studies binge drinking, using vimentin and flurojade B as markers of neurotoxicity.” “People hear from multiple sources that low-moderate alcohol consumption can be beneficial, and then we come along and say that heavy alcohol use leads to detrimental outcomes,” said Nixon. “People then want to know what the line is between beneficial and detrimental Unfortunately, we don’t know exactly. However, our study suggests that it may be even less than previously thought.” Nixon and her colleagues administered a nutritionally complete liquid diet to adult male Sprague-Dawley rats that additionally contained either alcohol (25% w/v) or isocaloric dextrose every eight hours for either one or two days. The rodents were sacrificed immediately following, two days after, or seven days after alcohol exposure and their brain tissues were examined. “This was really a simple study that took advantage of some new ‘tools’ to look for evidence of brain damage,” explained Nixon. “In other words, we didn’t look for dying cells themselves, but we looked at more indirect indices of damage by looking at what happens to astroglia, one of the ‘supporting’ cells for neurons. Astroglia react to brain damage by expressing several proteins that they do not normally express under healthy, happy conditions, one of which is an intermediate filament protein called vimentin. We saw a remarkable number of cells expressing this marker It is one of those ‘here is your brain, here is your brain on drugs’ kind of findings where the expression was obvious to the naked eye in many brains with as little as 24 hours of high blood alcohol levels.” Nixon added that, because rodents metabolize alcohol significantly faster than humans do, it is important to look at the actual concentration of alcohol in the blood in order to translate this to the human condition. “These rats had blood alcohol levels that were more than four times the legal driving limit, which for humans would require excessive drinking in the nature of a 12-pack of beer, a couple bottles of wine, or half of fifth of whisky. Unfortunately, drinking self-reports and blood alcohol level data from emergency rooms confirm that this level of drinking is common in those with alcohol use disorders.” “Rodent brain damage can model human damage,” noted Crews. “Vimentin seems to be a good marker of glial activation that shows that one day of binge drinking can cause some brain damage that persists and grows after a week of abstinence. However, both rodent and human brain damage generally require long-term alcohol consumption that models alcoholism and not the acute responses studied in this manuscript.” Nixon agreed. “The lack of overt neuronal deterioration suggests that a single, short-term, high-level binge probably does not result in functional changes and/or cognitive deficits,” she said. “However, since alcoholics experience multiple binges throughout their lifetime, it is important to consider that each successive binge, starting with the very first one, affords some level of damage to the brain. Therefore, theoretically, with multiple binges comes a cumulative detrimental effect where pronounced cognitive, behavioral, and structural effects are observed.” Nixon said this study demonstrates that new discoveries are always possible. “You have to know where and when to look for some of these effects,” she said. “The reason why this discovery wasn’t made previously is merely due to groups, ourselves included, not taking the time to thoroughly investigate these lower threshold doses with some pretty specific time points. Chasing down a threshold is not a sexy topic and it was actually fairly risky in that it was possible that we would have had all negative effects. Nonetheless, the take-home message of our data is that even one short-duration binge-alcohol experience – which is unfortunately similar to what young adults may experience during spring break or weekend partying - may start a cascade that leads to brain damage.”

neuromorphogenesis:

A brain protein called vimentin can indicate damage to the hippocampus following binge drinking

  • Binge drinking is known to increase the risk of developing dementia and/or brain damage.
  • A new study used rodents to test markers of neurodegeneration to determine a threshold for brain damage.
  • The vimentin brain protein can indicate damage to the hippocampus after 24 hours of binge-like drinking.

Chronic drinking is known to have detrimental health effects such as cardiac and liver problems, cognitive impairments, and brain damage. Binge drinking in particular is known to increase the risk of developing dementia and/or brain damage, yet little is known about an exact threshold for the damaging effects of alcohol. A study using rodents to examine various markers of neurodegeneration has found that brain damage can occur with as little as 24 hours of binge-like alcohol exposure.

Results will be published in the March 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“We know that the extent of damage following alcohol exposure depends heavily on the manner in which it is consumed,” said Kimberly Nixon, associate professor of pharmaceutical sciences at The University of Kentucky as well as corresponding author for the study. “Human studies suggest that binge-pattern drinking is more closely associated with brain damage. One study, for example, reported that binge drinking at least once per month in adulthood significantly increases the risk of developing dementia later in life. Animal models help provide the critical information that binge drinking, which produces high blood alcohol levels, directly causes damage.”

“The exact threshold for the damaging effects of alcohol on the brain is unclear,” commented Fulton T. Crews, John Andrews Distinguished Professor and director of the Center for Alcohol Studies at the University of North Carolina. “It is likely that the higher the blood alcohol level the greater the damage, however, this manuscript only studies binge drinking, using vimentin and flurojade B as markers of neurotoxicity.”

“People hear from multiple sources that low-moderate alcohol consumption can be beneficial, and then we come along and say that heavy alcohol use leads to detrimental outcomes,” said Nixon. “People then want to know what the line is between beneficial and detrimental Unfortunately, we don’t know exactly. However, our study suggests that it may be even less than previously thought.”

Nixon and her colleagues administered a nutritionally complete liquid diet to adult male Sprague-Dawley rats that additionally contained either alcohol (25% w/v) or isocaloric dextrose every eight hours for either one or two days. The rodents were sacrificed immediately following, two days after, or seven days after alcohol exposure and their brain tissues were examined.

“This was really a simple study that took advantage of some new ‘tools’ to look for evidence of brain damage,” explained Nixon. “In other words, we didn’t look for dying cells themselves, but we looked at more indirect indices of damage by looking at what happens to astroglia, one of the ‘supporting’ cells for neurons. Astroglia react to brain damage by expressing several proteins that they do not normally express under healthy, happy conditions, one of which is an intermediate filament protein called vimentin. We saw a remarkable number of cells expressing this marker It is one of those ‘here is your brain, here is your brain on drugs’ kind of findings where the expression was obvious to the naked eye in many brains with as little as 24 hours of high blood alcohol levels.”

Nixon added that, because rodents metabolize alcohol significantly faster than humans do, it is important to look at the actual concentration of alcohol in the blood in order to translate this to the human condition. “These rats had blood alcohol levels that were more than four times the legal driving limit, which for humans would require excessive drinking in the nature of a 12-pack of beer, a couple bottles of wine, or half of fifth of whisky. Unfortunately, drinking self-reports and blood alcohol level data from emergency rooms confirm that this level of drinking is common in those with alcohol use disorders.”

“Rodent brain damage can model human damage,” noted Crews. “Vimentin seems to be a good marker of glial activation that shows that one day of binge drinking can cause some brain damage that persists and grows after a week of abstinence. However, both rodent and human brain damage generally require long-term alcohol consumption that models alcoholism and not the acute responses studied in this manuscript.”

Nixon agreed. “The lack of overt neuronal deterioration suggests that a single, short-term, high-level binge probably does not result in functional changes and/or cognitive deficits,” she said. “However, since alcoholics experience multiple binges throughout their lifetime, it is important to consider that each successive binge, starting with the very first one, affords some level of damage to the brain. Therefore, theoretically, with multiple binges comes a cumulative detrimental effect where pronounced cognitive, behavioral, and structural effects are observed.”

Nixon said this study demonstrates that new discoveries are always possible. “You have to know where and when to look for some of these effects,” she said. “The reason why this discovery wasn’t made previously is merely due to groups, ourselves included, not taking the time to thoroughly investigate these lower threshold doses with some pretty specific time points. Chasing down a threshold is not a sexy topic and it was actually fairly risky in that it was possible that we would have had all negative effects. Nonetheless, the take-home message of our data is that even one short-duration binge-alcohol experience – which is unfortunately similar to what young adults may experience during spring break or weekend partying - may start a cascade that leads to brain damage.”

(Source: medicalxpress.com)

543 notes

Beyond the Oath: A Word With First Year

aspiringdoctors:

medicalstate:

For the students out there who will soon begin their first year in medical school, let me say congratulations and welcome. There is a long road ahead of you. After reflecting on the experiences I have had and the observations I have made, I have here a list of 16 words of advice to set the course. Here is a quick guide to first year:

  1. Take some time in those first few weeks to build your network. The people in your class are the ones who will be your friends, support, and future colleagues for the next few years. You will need to find people you can count on.
  2. Do not let the white coat or stethoscope fool you. Your friend probably does not have that rare syndrome you just studied and you probably do not have a ruptured triple-A. 
  3. Study hard. Get quality studying done and avoid the distractions. Make the most of your study hours so you can…
  4. Find balance. This is your out, a way to get away from medicine and back to your old life. Take some time off for yourself and adjust it accordingly depending on how much you need to study. But always take some time for yourself, your family, friends, and partner. Always.
  5. Sleep when you need. Sleeping hours disappear quickly over time so when you have a day off, get some extra shut eye. Also, if you have to choose between an all-nighter and sleep, go with the sleep.
  6. Caffeine. It is an unavoidable fact of medical school but take it from me, put it off as long as you can. At this point in your career if you can avoid it do so. Would not want to have it lose its edge down the road now would we?
  7. Stay healthy. Stay fit and eat fresh. Part of finding balance is taking the time to keep your body in shape and have a wholesome meal every now and then that needs more than three minutes in a microwave. Your body will thank you and you will feel better.
  8. Practice interviews and clinical skills. I remember when it seemed awkward watching one classmate interview another. Take those moments seriously and learn from them. These are skills you need to carry with you forever now. Practice makes perfect so do a little bit of clinical skills every now and then with your friends and family.
  9. Anatomy labs. Working with cadavers for the first time is intimidating so avoid the hands and face, the two most human elements of a person until you feel comfortable. Also, it can be easy to forget these cadavers were people once, remember to treat them with respect.
  10. Invest in your equipment. Shoes, stethoscopes, white coat, what have you, make sure the parts that last should, and make sure you are comfortable in them.
  11. Save your money when possible. Do you really need that gratuitous Starbucks? Do you need to get the pair of jeans? Medical school is costly and saving anywhere will eventually add up, even if it only puts a small dent in your debt. Seek out free things when possible. Free lunches or food-provided seminars are great for these.
  12. Be careful of what you say, how you say it and where you say it. The world of medicine is wrought with privacy and confidentiality concerns so learn to mind your surroundings before discussing something, especially if it involves a patient, real or not.
  13. Thick skin. Generally the people who work with you are nice but you will need to develop dragon skin. Expectations run high as you go through medical school and you will constantly enter situations where you do not know or make mistakes. Try not to take what people say at you personally.
  14. In the same vein, do not be overly hard on yourself. You are still learning and at this stage of your training there will be mistakes and bad calls. Take them in stride, learn from them, and move on.
  15. Be a moderate learner. Learn what you need to and maybe a bit more out of interest but take solace in knowing that you will not be able to study everything in a year. Stay within reason. Do not be obnoxiously keen. It will end badly.
  16. On a similar note, getting into medical school is not a license to become arrogant or obnoxious. Do not falter here when you have just made it through the door; it is a reputation you do not want following you around. Keep it together.

Good luck and take care.

Related post: A Word With Second Year.

Also check out the lists by wayfaringmd, md-admissions, and cranquis.

I’m reblogging this as both a reminder to myself and as advice to my incoming colleagues.

Samsies! Thanks Medicalstate!

38 notes

neuroanatomyblog: Comparison of SNS (Somatic Nervous System - Voluntary) to ANS (Autonomic Nervous System - Visceral) ANS differs from the SNS in: Thier effectors SNS innervates skeletal muscle and ANS innervates smooth and cardiac muscle and glands Efferent pathways SNS - cell bodies of the motor neuron are in the CNS, and their axons extend in spinal nerves all the way to skeletal muscles ANS - two neuron chain The cell body of the first neuron (preganglionic neuron) resides in the brain or spinal cord Its axon (preganglionic axon) synapses with the second motor neuron (ganglionic neuron) in an autonomic ganglion outside the CNS The axon of the ganglionic neuron (postganglionic axon) extends to the effector organ Target organ responses - neurotransmitter effects SNS - acetylcholine released at their synapse ANS - norepinephrine, epinephrine and acetylcholine

neuroanatomyblog:

Comparison of SNS (Somatic Nervous System - Voluntary) to ANS (Autonomic Nervous System - Visceral)

ANS differs from the SNS in:

  • Thier effectors
    • SNS innervates skeletal muscle and ANS innervates smooth and cardiac muscle and glands
  • Efferent pathways
    • SNS - cell bodies of the motor neuron are in the CNS, and their axons extend in spinal nerves all the way to skeletal muscles
    • ANS - two neuron chain
      • The cell body of the first neuron (preganglionic neuron) resides in the brain or spinal cord
      • Its axon (preganglionic axon) synapses with the second motor neuron (ganglionic neuron) in an autonomic ganglion outside the CNS
      • The axon of the ganglionic neuron (postganglionic axon) extends to the effector organ
  • Target organ responses - neurotransmitter effects
    • SNS - acetylcholine released at their synapse
    • ANS - norepinephrine, epinephrine and acetylcholine

17 notes

neuromorphogenesis: Why Do We Blink So Frequently? New research indicates that the brain enters a momentary state of wakeful rest when we blink, perhaps allowing us to focus better afterward. We all blink. A lot. The average person blinks some 15-20 times per minute—so frequently that our eyes are closed for roughly 10% of our waking hours overall. Although some of this blinking has a clear purpose—mostly to lubricate the eyeballs, and occasionally protect them from dust or other debris—scientists say that we blink far more often than necessary for these functions alone. Thus, blinking is physiological riddle. Why do we do it so darn often? In a published paper in the Proceedings of the National Academy of Sciences, a group of scientists from Japan offers up a surprising new answer—that briefly closing our eyes might actually help us to gather our thoughts and focus attention on the world around us. The researchers came to the hypothesis after noting an interesting fact revealed by previous research on blinking: that the exact moments when we blink aren’t actually random. Although seemingly spontaneous, studies have revealed that people tend to blink at predictable moments. For someone reading, blinking often occurs after each sentence is finished, while for a person listening to a speech, it frequently comes when the speaker pauses between statements. A group of people all watching the same video tend to blink around the same time, too, when action briefly lags. As a result, the researchers guessed that we might subconsciously use blinks as a sort of mental resting point, to briefly shut off visual stimuli and allow us to focus our attention. To test the idea, they put 10 different volunteers in an fMRI machine and had them watch the TV show “Mr. Bean” (they had used the same show in their previous work on blinking, showing that it came at implicit break points in the video). They then monitored which areas of the brain showed increased or decreased activity when the study participants blinked. Their analysis showed that when the Bean-watchers blinked, mental activity briefly spiked in areas related to the default network, areas of the brain that operate when the mind is in a state of wakeful rest, rather than focusing on the outside world. Momentary activation of this alternate network, they theorize, could serve as a mental break, allowing for increased attention capacity when the eyes are opened again. To test whether this mental break was simply a result of the participants’ visual inputs being blocked, rather than a subconscious effort to clear their minds, the researchers also manually inserted “blackouts” into the video at random intervals that lasted roughly as long as a blink. In the fMRI data, though, the brain areas related to the default network weren’t similarly activated. Blinking is something more than temporarily not seeing anything. It’s far from conclusive, but the research demonstrates that we do enter some sort of altered mental state when we blink—we’re not just doing it to lubricate our eyes. A blink could provide a momentary island of introspective calm in the ocean of visual stimuli that defines our lives.

neuromorphogenesis:

Why Do We Blink So Frequently?

New research indicates that the brain enters a momentary state of wakeful rest when we blink, perhaps allowing us to focus better afterward.

We all blink. A lot. The average person blinks some 15-20 times per minute—so frequently that our eyes are closed for roughly 10% of our waking hours overall.

Although some of this blinking has a clear purpose—mostly to lubricate the eyeballs, and occasionally protect them from dust or other debris—scientists say that we blink far more often than necessary for these functions alone. Thus, blinking is physiological riddle. Why do we do it so darn often? In a published paper in the Proceedings of the National Academy of Sciences, a group of scientists from Japan offers up a surprising new answer—that briefly closing our eyes might actually help us to gather our thoughts and focus attention on the world around us.

The researchers came to the hypothesis after noting an interesting fact revealed by previous research on blinking: that the exact moments when we blink aren’t actually random. Although seemingly spontaneous, studies have revealed that people tend to blink at predictable moments. For someone reading, blinking often occurs after each sentence is finished, while for a person listening to a speech, it frequently comes when the speaker pauses between statements. A group of people all watching the same video tend to blink around the same time, too, when action briefly lags.

As a result, the researchers guessed that we might subconsciously use blinks as a sort of mental resting point, to briefly shut off visual stimuli and allow us to focus our attention. To test the idea, they put 10 different volunteers in an fMRI machine and had them watch the TV show “Mr. Bean” (they had used the same show in their previous work on blinking, showing that it came at implicit break points in the video). They then monitored which areas of the brain showed increased or decreased activity when the study participants blinked.

Their analysis showed that when the Bean-watchers blinked, mental activity briefly spiked in areas related to the default network, areas of the brain that operate when the mind is in a state of wakeful rest, rather than focusing on the outside world. Momentary activation of this alternate network, they theorize, could serve as a mental break, allowing for increased attention capacity when the eyes are opened again.

To test whether this mental break was simply a result of the participants’ visual inputs being blocked, rather than a subconscious effort to clear their minds, the researchers also manually inserted “blackouts” into the video at random intervals that lasted roughly as long as a blink. In the fMRI data, though, the brain areas related to the default network weren’t similarly activated. Blinking is something more than temporarily not seeing anything.

It’s far from conclusive, but the research demonstrates that we do enter some sort of altered mental state when we blink—we’re not just doing it to lubricate our eyes. A blink could provide a momentary island of introspective calm in the ocean of visual stimuli that defines our lives.


(via fuckyeahnarcotics)