Gary Marcus: The New Yorker "Obama's Brain" Excerpt

Magnified 400 times, this is a 2-Photon fluorescence image of glial cells in the cerebellum. Glial cells provide support for the brain's neurons. This image was made by Thomas Deerinck of the National Center for Microscopy and Imaging Research, University of California, San Diego.

At some level, the brain is a kind of computer. It takes in information, combines new information with previously acquired information, and performs actions based on the results of those computations.

Yet we know remarkably little about how the brain performs its computations and how those computations relate to behavior, especially in comparison to what we know about computers.

Computers are, for all practical purposes, entirely understood. We know what they’re made of, we know how electrons move inside of them, and we know how their basic logical functions (such as “and,” “or,” and “not”) combine to form more complex operations, such as arithmetic and control (e.g., performing process X if a password is entered correctly and process Y if the password is entered incorrectly).

 In turn, programming languages relate machine language to more abstract sets of instructions that are more readily understood by human beings. An unbroken chain of inference connects the plans of the programmer to the actions of the electrons that ultimately implement them.

When it comes to the brain, we know comparatively little, in part because the brain is considerably less straightforward. By some counts (though the exact number remains elusive), there are hundreds of different kinds of neurons, each with different physical properties and ways of interacting with other neurons.

We don’t, for example, even know whether the basic unit of computational currency in the brain is digital (e.g., a set of zeroes and ones, like in virtually all modern computers) or analog (like the continuously moving second hand in an old-fashioned clock, an approach that was commonly used in some pre-Second World War computers).

Likewise, although we know something about which brain regions participate in the processing and storage of memories, we still don’t understand how the brain encodes those memories. And we know very little about how the brain’s basic units organize into larger-scale circuits, and how those circuits, often in physically disparate parts of the brain, work together to produce unified behavior.

Modern biology was launched in large part by three discoveries: Oswald Avery’s discovery of DNA; Watson and Crick’s deciphering of the physical structure of the DNA; and the discovery, by several researchers in the early nineteen sixties, of the code by which different triples of RNA nucleotides are turned into amino acids. All three of these discoveries were made possible in part by Mendel’s experiments with peas, in which he identified what we now know as genes.

The brain will finally give up its secrets when we do something similar, by constructing an inventory of the brain’s basic elements—the neural analogs to transistors, logic gates, and microprocessors — and relating those basic elements to broader-scale cognitive computations.

To connect brain to behavior, we don’t need to build a whole brain, as the E.U. aims to do; we need to understand how the brain’s parts work together.

And new techniques, like optogenetics (which allow experimenters to control brain activity—and hence an animal’s behavior—by exposing neurons to light) and fluorescent imaging (which makes it possible to monitor the responses of thousands of neurons simultaneously in awake, behaving animals), make addressing such questions potentially feasible for the first time.

Read more: http://www.newyorker.com/online/blogs/newsdesk/2013/02/obamas-brain.html#ixzz2LwNwZm7I

Hermona Soreq Blog: Stress Reactions: Acetylcholine

by Hermona Soreq, Professor of Molecular Neuroscience, The Hebrew University’s Edmond and Lily Safra Center for Brain Sciences

Do the Stress Reactions of Our Brain Control the Immune System -- Or Is It the Other Way Around?

In the well-known 17th-century text Le Malade Imaginaire, Molière (Jean-Baptiste Poquelin) wrote, "the mind has great influence over the body, and maladies have their origin there."

Since Molière, we now know that a diseased body and malfunctioning immune system also affect the mind.

Inflammation of the nervous system has been increasingly recognized as an important factor in multiple conditions, including Alzheimer's and Parkinson's disease. New technologies in genetic engineering and drug development are rapidly progressing to implement this knowledge for early diagnosis and creative treatment strategies that take into consideration both the brain and the body.

One area that has benefited considerably from these developments is the study of anxiety.

Historically, human stress reactions enabled our ancestors to survive attacks and protect the body from injury. But even though these reactions aren't necessities like they were for our ancestors, the same response patterns have continued to the present. An unpleasant discussion at work rarely leads to physical attacks, but our body nevertheless prepares for such attacks; it elevates the blood pressure to prepare for running, and produces more white blood cells as protection from anticipated injury.

While such reactions are useful for immediate protection -- since alertness can assist us in reacting to stressful experiences faster and more efficiently -- the consequences of stress responses may also entail long-term damages spanning muscle and nerve cells malfunctions, neurodegenerative diseases like Alzheimer's and Parkinson's, and inflammatory diseases.

The long-term and disease-provoking consequences of stress responses may take years to develop. This was not a concern for early humans, whose life span was shorter than ours (by the time stress could take its toll, they were no longer alive). But today, humans live much longer, and as a result, stress-associated diseases -- especially in the elderly -- have become a major social and financial burden.
*** Over the past two decades, I, along with my colleagues at the Edmond and Lily Safra Center for Brain Sciences (ELSC) at The Hebrew University of Jerusalem, have pioneered and developed innovative strategies for investigating the consequences of traumatic experiences and designed new strategies to combat neurodegenerative diseases.

Our work has proven that in both brain neurons and blood cells, the genetic information that processes events are vulnerable to changes under stress. Moreover, we've discovered that both inherited and acquired defects in neurons, as well as traumatic experiences or exposure to a contaminated environment, contribute to delayed susceptibilities to stress-associated diseases.

The consequences may be seriously harmful, affect seemingly unrelated functions (e.g. learning and memory, the day-and-night cycle, muscle fatigue, inflammation), and last over the life spans of individuals and communities.

A good portion of our research has been devoted to a small chemical called acetylcholine, the first known neurotransmitter (a small chemical compound which is capable of activating neurons to send electrical signals) and the primary communicator between the body and the brain.

Discovered 100 years ago by the Nobel laureate Otto Loewi, acetylcholine comes from the brain through the vagus nerve and is responsible for muscle twitching. We've discovered that acetylcholine signals produced in the brain affect psychological stress responses, inflammation, aging, and the recovery from acute ischemic stroke.

As part of our research, we isolated the genes controlling acetylcholine degradation in humans and identified stress-induced changes in their expression in brain neurons and blood cells alike.

To pinpoint the physiological role of these genes, we engineered mice with excess or deficient amounts of the genes' protein products and watched their learning, muscle functioning and behavior. We learned three basic things:

1) Either too much or too rapid degradation of acetylcholine may cause cognitive deterioration, which intensifies anxiety reactions and can also intensify them, creating a vicious cycle;

2) The mice with excess breakdown of acetylcholine suffer constant inflammation, demonstrating the power of brain-to-body communication for our immune system and showing that individuals who carry inherited small changes in these genes are at increased risks for Parkinson's and Alzheimer's disease;

3) Different products of these genes may either enhance the progression of brain pathology in Alzheimer's and Parkinson's disease or help protect against them, and they also determine one's prospects to survive and recover from ischemic stroke. Measuring such changes by a simple blood test can hence predict one's prospects for recovery and the risks for post-traumatic stress disorder.

New discoveries in stress-related pathologies are occurring at a quickening pace. Just recently, we've developed a synthetic DNA-based drug for treating patients with inflammatory bowel disease.

With the help of a $5 million grant approved by the Leona M. and Harry B. Helmsley Charitable Trust, we hope that such developments will bring us closer to finding more permanent treatments for neurodegenerative and other diseases that have, unfortunately, become all too common.

Jonah Lehrer: Meta-Lessons - Fail Big, Grit, and Growing Up

For Jonah Lehrer: First we smirk, then we work.

by Don Mangus

“When I walked into the classroom of Silas Cooper, a drama teacher at the school, I couldn’t help but notice the handwritten banner hanging above the door. This is what it said: FAIL BIG.” – Jonah Lehrer, “The Shakespeare Paradox,” Imagine How Creativity Works

I greatly enjoyed Jonah Lehrer’s first two popular science books, Proust Was a Neuroscientist and How We Decide. These were written in a breezy Malcolm Gladwellesque style -- quick and fun reads, peppered with intriguing research-based observations.

I was dealt quite a surprise when I surfed over to Amazon to order his latest, Imagine How Creativity Works. Instead of finding a nicely discounted copy as expected, I found instead that the book ”was no longer available.” Frantically searching eBay and abe.com, the few copies I found listed were listed at sky-high collectible prices. How could this be? This was a brand new publication. Could the title really be that popular?

A quick fact-finding search on google revealed just the opposite. The book was now somewhat of a literary scandal – ashamedly recalled, and thus made in short supply. Apparently, according to his peers, Mr. Lehrer had taken unconscionable “journalistic shortcuts.” He “fabricated and fabulized” many of his quotes, and was also guilty of egregious blogging transgressions dubbed “self-plagarism.” Undaunted, I ordered the cheapest copy of the book I could find online. I wanted to read this book more than ever.

When it arrived, the back of the hard cover boasted two of the highest back-of-the-dust jacket accolades possible:

“Jonah Lehrer’s new book confirms what his fans have known all along – that he knows more about science than a lot of scientists and more about writing than a lot of writers.” – Malcolm Gladwell author of The Tipping Point and Outliers

“Jonah Lehrer may be the most talented explainer of science that we’ve got. His engrossing investigation of creativity and its sources makes Imagine his best book yet.” – Joshua Foer author of Moonwalking with Einstein

Ouch! After the scandal broke, such ringing endorsements might now feel a bit embarrassing to two of my all-time favorite science writers. As I read Imagine, I searched the text for clues as to what went through Jonah Lehrer’s mind -- why he took the “literary liberties” that led to his fall from grace. I think I found a few in these passages, mostly gleaned from his chapter titled “The Shakespeare Paradox” (bold emphasis mine).

(page 221) – “… But Shakespeare didn’t just read these texts and imitate their best parts: he made them his own, seamlessly blending them together in his plays. Sometimes this literary approach got Shakespeare into trouble. His peers regularly accused him of plagiarism, and he was often guilty, at least by contemporary standards. What these allegations didn’t take into account, however was that Shakespeare was pioneering a new creative method in which every conceivable source informed his art. For Shakespeare the art of creation was inseparable from the act of connection…”

(pages 246-7) -- “…But Dylan wasn’t just copying these tunes; his close study was an essential part of his creative method – learning an old song meant he was on the version of inventing a new one...

…One consequence is that virtually all of Dylan’s first seventy compositions from ’Blowin’ In the Wind’ to ‘The Times They Are a-Changin’, have clear musical precursors….

…T. S. Eliot said it best: ‘Immature poets imitate. Mature poets steal.’ Even at the age of twenty-one Dylan was a mature poet. He was already a thief.”

…What kind of culture have we created? Is it a world full of ideas that can be connected? Are we willing to invest in risk takers? Do our schools produce students ready to create?...

… We have to make it easy to become a genius.”

(pages 252-3) – “…The mystery is this: although the imagination is inspired by the everyday world – by its flaws and beauties – we are able to see beyond our sources, to imagine things that exist only in the mind. We notice an incompleteness and we can complete it; the cracks in things become a source of light…

…Every creative story is different. And every creative story is the same. There was nothing. Now there is something. It’s almost like magic.”

So it seems Jonah Lehrer took the “poetic license” and “incompleteness” parts of the creative process to heart with his “fabulized” quotes and research. He engaged in creative storytelling rather than hard-and-fast journalism or science. I for one, forgive him this sin. He certainly has FAILED BIG in the eyes of his peers.

However, I sincerely hope Mr. Lehrer will learn and recover from this “scandal” and write again. Science is always being revised anyway. I never regarded these popular science books as other than a stimulating source of wonder and inspiration.

In the grand scheme of things I prefer to save my slings and arrows for other “system gamers” such as self-serving, exempt-from-the-law Congressmen, do-nothing government watchdog agencies, and corrupt financial power brokers.

I will close my Imagine essay with some passages about persistence (or grit) and growing up from Jonah Lehrer’s book that I hope he will also take to heart.

(page 56) -- “…The reality of the creative process is that it often requires persistence, the ability to stare at a problem until it makes sense, It’s forcing oneself to pay attention, to write all night and then fix those words in the morning. It’s sticking with a poem until it’s perfect; refusing to quit on a math question…

… The answer won’t arrive suddenly, in a flash of insight. Instead, it will be revealed slowly, gradually emerging after great effort.”

(page 232-3) -- “…It doesn’t matter if people are playing jazz or writing poetry – if they want to be successful, they need to learn how to persist and persevere, how to keep working until the work is done…”

And finally,

(page 109) -- ‘’Picasso once summarized the paradox this way: ‘Every child is an artist. The problem is how to remain an artist once we grow up.”

Don’t quit, and keep writing, Mr. Jonah Lehrer. Remain an artist.

Mega Savant: Kim Peek, The Mount Everest of Memory




Mega Savant Kim Peek.

 
From yee Wiki:

Laurence Kim Peek (1951 –2009), known as a "megasavant", he had an exceptional memory, but he also experienced social difficulties, possibly resulting from a developmental disability related to congenital brain abnormalities. He was the inspiration for the character of Raymond Babbitt, played by Dustin Hoffman in the movie Rain Man. Unlike Babbitt, Peek had FG syndrome (a rare genetic syndrome linked to the X chromosome which causes physical anomalies such as hypotonia (low muscle tone) and macrocephaly).

Early life

Peek was born in Salt Lake City, Utah with macrocephaly, damage to the cerebellum, and agenesis of the corpus callosum, a condition in which the bundle of nerves that connects the two hemispheres of the brain is missing; in Peek's case, secondary connectors such as the anterior commissure were also missing. There is speculation that his neurons made unusual connections due to the absence of a corpus callosum, which resulted in an increased memory capacity.

According to Peek's father, Fran Peek, Kim was able to memorize things from the age of 16–20 months. He read books, memorized them, and then placed them upside down on the shelf to show that he had finished reading them, a practice he maintained. He could speed through a book in about an hour and remember almost everything he had read, memorizing vast amounts of information in subjects ranging from history and literature, geography and numbers to sports, music and dates. According to an article in the Times newspaper, he could accurately recall the contents of at least 12,000 books. Peek lived in Murray, Utah.

Peek did not walk until the age of four and then in a sidelong manner. He could not button up his shirt and had difficulty with other ordinary motor skills, presumably due to his damaged cerebellum, which normally coordinates motor activities. In psychological testing, Peek scored below average (87) on general IQ tests.

Rain Man

In 1984, screenwriter Barry Morrow met Peek in Arlington, Texas; the result of the meeting was the 1988 movie Rain Man. The character of Raymond Babbitt, although inspired by Peek, was portrayed as having autism. Dustin Hoffman, who played Babbitt, met Peek and other savants to get an understanding of their nature and to play the role accurately and methodically.

The movie caused a number of requests for appearances, which increased Peek's self-confidence. Barry Morrow gave Kim his Oscar statuette to carry with him and show at these appearances; it has since been referred to as the "Most Loved Oscar Statue" as it has been held by more people than any other. Kim also enjoyed approaching strangers and showing them his talent for calendar calculations by telling them on which day of the week they were born and what news items were on the front page of major newspapers. Peek also appeared on television. He travelled with his father, who took care of him and performed many motor tasks that Peek found difficult.

Scientific investigation

In 2004, scientists at the Center for Bioinformatics Space Life Sciences at the NASA Ames Research Center examined Peek with a series of tests including computed tomography and magnetic resonance imaging. The intent was to create a three-dimensional view of his brain structure and to compare the images to MRI scans done in 1988. These were the first tentative approaches in using non-invasive technology to further investigate Kim's savant abilities.

Brain Plasticity: How Learning Changes Your Brain

Plas makes it look easy. The New Yorker April 17 1999. Art Spiegelman cover.

by Dr. Pascale Michelon

You may have heard that the brain is plas­tic. As you know the brain is not made of plas­tic. Neu­ro­plas­tic­ity or brain plas­tic­ity refers to the brain’s abil­ity to change through­out life. The brain has the amaz­ing abil­ity to reor­ga­nize itself by form­ing new con­nec­tions between brain cells (neurons).

In addi­tion to genetic fac­tors, the envi­ron­ment in which a per­son lives, as well as the actions of that per­son, play a role in plasticity.

Neu­ro­plas­tic­ity occurs in the brain:

1– At the begin­ning of life: when the imma­ture brain orga­nizes itself.
2– In case of brain injury: to com­pen­sate for lost func­tions or max­i­mize remain­ing functions.
3– Through adult­hood: when­ever some­thing new is learned and memorized

Plas­tic­ity and brain injury

A sur­pris­ing con­se­quence of neu­ro­plas­tic­ity is that the brain activ­ity asso­ci­ated with a given func­tion can move to a dif­fer­ent loca­tion as a con­se­quence of nor­mal expe­ri­ence, brain dam­age or recovery.

In his book “The Brain That Changes Itself: Sto­ries of Per­sonal Tri­umph from the Fron­tiers of Brain Sci­ence, Nor­man Doidge describes numer­ous exam­ples of func­tional shifts.
In one of them, a sur­geon in his 50s suf­fers a stroke. His left arm is par­a­lyzed. Dur­ing his reha­bil­i­ta­tion, his good arm and hand are immo­bi­lized, and he is set to clean­ing tables. The task is at first impos­si­ble. Then slowly the bad arm remem­bers how too move. He learns to write again, to play ten­nis again: the func­tions of the brain areas killed in the stroke have trans­ferred them­selves to healthy regions.

The brain com­pen­sates for dam­age by reor­ga­niz­ing and form­ing new con­nec­tions between intact neu­rons. In order to recon­nect, the neu­rons need to be stim­u­lated through activity.

Plas­tic­ity, learn­ing and memory

For a long time, it was believed that as we aged, the con­nec­tions in the brain became fixed. Research has shown that in fact the brain never stops chang­ing through learn­ing. Plas­tic­ity is the capac­ity of the brain to change with learn­ing. Changes asso­ci­ated with learn­ing occur mostly at the level of the con­nec­tions between neu­rons. New con­nec­tions can form and the inter­nal struc­ture of the exist­ing synapses can change.

Did you know that when you become an expert in a spe­cific domain, the areas in your brain that deal with this type of skill will grow?

For instance, Lon­don taxi dri­vers have a larger hip­pocam­pus (in the pos­te­rior region) than Lon­don bus dri­vers (Maguire, Wool­lett, & Spiers, 2006). Why is that? It is because this region of the hip­pocam­pus is spe­cial­ized in acquir­ing and using com­plex spa­tial infor­ma­tion in order to nav­i­gate effi­ciently. Taxi dri­vers have to nav­i­gate around Lon­don whereas bus dri­vers fol­low a lim­ited set of routes.

Plas­tic­ity can also be observed in the brains of bilin­guals (Mechelli et al., 2004). It looks like learn­ing a sec­ond lan­guage is pos­si­ble through func­tional changes in the brain: the left infe­rior pari­etal cor­tex is larger in bilin­gual brains than in mono­lin­gual brains.

Plas­tic changes also occur in musi­cians brains com­pared to non-musicians. Gaser and Schlaug (2003) com­pared pro­fes­sional musi­cians (who prac­tice at least 1hour per day) to ama­teur musi­cians and non-musicians. They found that gray mat­ter (cor­tex) vol­ume was high­est in pro­fes­sional musi­cians, inter­me­di­ate in ama­teur musi­cians, and low­est in non-musicians in sev­eral brain areas involved in play­ing music: motor regions, ante­rior supe­rior pari­etal areas and infe­rior tem­po­ral areas.

Finally, Dra­gan­ski and col­leagues (2006) recently showed that exten­sive learn­ing of abstract infor­ma­tion can also trig­ger some plas­tic changes in the brain. They imaged the brains of Ger­man med­ical stu­dents three months before their med­ical exam and right after the exam and com­pared them to brains of stu­dents who were not study­ing for exam at this time. Med­ical stu­dents’ brains showed learning-induced changes in regions of the pari­etal cor­tex as well as in the pos­te­rior hip­pocam­pus. These regions of the brains are known to be involved in mem­ory retrieval and learning.

Q and A about Brain plas­tic­ity

Q: Can hor­mones change my brain?

A: It seems that the brain reacts to its hor­monal milieu with struc­tural mod­i­fi­ca­tions.

Q: Can new neu­rons grow in my brain?

A: Yes in some areas and through­out your life­time.

Q: Where can I find more information?

A: Read The Sharp­Brains Guide to Brain Fit­ness: 18 Inter­views with Sci­en­tists, Prac­ti­cal Advice, and Prod­uct Reviews, to Main­tain Your Brain Sharp to pro­vide a com­pre­hen­sive and acces­si­ble entry into the research and how to apply it.

"Check out the big brain on Brad." Pulp Fiction, 1994.

A link to the SharpBrains site for those that are interested:

http://www.sharpbrains.com/blog/2008/02/26/brain-plasticity-how-learning-changes-your-brain/

Before I Forget: New Alzheimer's News

As Droopy would drawl, "Gruesome, isn't it?"

by Thomas H. Maugh II Los Angeles Times  July 11, 2012

Researchers have found the first gene mutation that protects against Alzheimer's disease, a finding that supports a now-controversial theory about the cause of the disease and that could eventually lead to the development of new drugs to treat the disorder. The gene mutation also protects against aging, suggesting that the two diseases have mechanisms in common.

Alzheimer's affects an estimated 5.4 million Americans, and the prevalence increases with age:
13% of those older than 65 and 45% of those over the age of 85 have it.

The disease is characterized by the buildup in the brain of particles called amyloid plaque, which are composed of a protein called amyloid beta. Amyloid beta is produced by the breakdown of a larger protein called amyloid precursor protein, or APP. Researchers have so far identified at least two dozen variants of APP that produce early-onset Alzheimer's disease in people younger than 65. The new variant, reported online Wednesday in the journal Nature, is the first that protects against Alzheimer's.

The idea that breakdown of APP causes Alzheimer's has led many pharmaceutical companies to search for drugs that could delay Alzheimer's by inhibiting the breakdown. Unfortunately, clinical trials of those drugs have been almost uniformly unsuccessful, leading many critics to doubt the theory. The new findings, however, tend to place it on firmer ground.

A team led by Dr. Kari Stefansson of deCode Genetics in Reykjavik, Iceland, deciphered the whole genome of 1,795 Icelanders looking for rare variants associated with Alzheimer's and found the new mutation, which is present in about 0.45% of the population there. Unpublished data show that it is even rarer in the United States, found in only about 1 in every 10,000 people. That suggests the mutation arose relatively recently in Northern Europe, Stefansson said.

The data showed that the mutant gene was present in 0.13% of those with a diagnosis of Alzheimer's, but in 0.62% of those over 85 who did not have the disease. The variant was also present in 0.79% of those over age 85 whose brain functions were normal. Furthermore, those with the variant performed significantly better in tests of cognitive functioning.

Surprisingly, the variant also seems to protect against other risk factors for the disease. At least 90% of people with two copies of a gene called ApoE4 normally get Alzheimer's by age 80. But Stefansson observed 25 people in the study with the new variant and two ApoE4 genes, and none had Alzheimer's.

Stefansson predicted that pharmaceutical companies will now accelerate their search for new drugs that can somehow mimic the action of the gene variant.

On Screen: Antonio Damasio

This is not Antonio Damasio -- it's the fabulous Dr. R., specialist in Anxiety, Asperger's, ADHD, and more.

My psychologist Dr. R. often reminds me that most of his patients would rather watch a video than read. I enjoy the pastime of reading so much, I sometimes forget that most folks spend more time watching shows. For example, I shared with my pals that I was enjoying Michael Lewis' book, The Blind Side, and was nonplussed when they countered, "Have you seen the movie? Julia Roberts was great." The film was nominated for Academy Awards, yet until then I didn't even know it existed. The same thing happened when I finished off Niall Ferguson's Ascent of Money, only to find that it was a highly-celebrated PBS show.

Here then, is a weblink to an hour-long TV show, Antonio Damasio: This Time with Feeling. I haven't watched it yet, but I'm sure it will be worthwhile if you have an interest and take the time to view it. So, here's a show to watch instead of a book to read:

http://fora.tv/2009/07/04/Antonio_Damasio_This_Time_With_Feeling




This is the dapper Antonio Damasio. Photo Emily Shur for The Wall Street Journal, 2011.



 Here are William Oates Covington Jr.'s Notes on Feelings (made by the neuroscientist Antonio Damasio):

The term feeling should be reserved for the private, mental experience of an emotion, while the term emotion should be used to designate the collection of responses, many of which are publicly observable. (Damasio; Feeling of What Happens, 42)

The machinery of feelings is a contributor to the process of consciousness, namely to the creation of the self. (Damasio; Looking for Spinoza, 110)

Feelings of pain or pleasure or some quality in between are the bedrock of our minds. (Damasio; Looking for Spinoza, 3)

All feelings contain some aspect of pain or pleasure as a necessary ingredient. (Damasio; Looking for Spinoza, 123)

Some variation of pleasure or pain is a consistent content of the perception we call feeling. (Damasio; Looking for Spinoza, 85)

Drugs such as valium that remove the affect component of pain but leave the sensation of pain impact -- you "feel" the pain but do not care. (Damasio; Looking for Spinoza, 104)

Feelings are at the very top of the innate automated life governance machine -- the homeostasis machine. (Damasio; Looking for Spinoza, 34)

Feelings are based on composite representations of the state of life in the process of being adjusted for survival. (Damasio; Looking for Spinoza, 130)

Contents of feelings are the configuration of body state represented in somatosensing maps. (Damasio; Looking for Spinoza, 132)

A feeling of emotion is an idea of the body when it is perturbed by the emoting process. (Damasio; Looking for Spinoza, 88)


Perceptions, Objects and Feelings

Visual perceptions correspond to external objects. (Damasio; Looking for Spinoza, 91)

In the case of feelings, the objects and events at the origin are well inside the body rather than outside of it.  Feelings may be just as mental as any other perception, but the objects being mapped are parts and states of the living organism in which feelings arise. (Damasio; Looking for Spinoza, 91)

The "object" of an emotion or a feeling -- the sight of a spectacular seascape is an emotionally competent object.  The body state that results from beholding that seascape is the actual object which is then perceived in the feeling state. (Damasio; Looking for Spinoza, 91)

Feelings are not a passive perception or a flash in time, especially not in the case of feelings of joy and sorrow. For a while after an occasion of such feelings begins -- for seconds or for minutes -- there is a dynamic engagement of the body, almost certainly in repeated fashion, and a subsequent dynamic variation of the perception.  We perceive a series of transitions. We sense and interplay, a give-and-take. (Damasio; Looking for Spinoza, 92)

All feelings are feelings of some of the basic regulatory reactions, or of appetites, or of emotions-proper. (Damasio; Looking for Spinoza, 92)

We react to most, perhaps all, objects with emotions, however weak, and subsequent feelings, however feeble. (Damasio; Looking for Spinoza, 93)


Feelings and Brain Maps

Feelings are related to neural mappings of body state. (Damasio; Looking for Spinoza, 96)

The essential content of feelings is the mapping of a particular body state.  The substrate of feelings is a set of neural patterns from which a mental image of the body state can emerge.  A feeling in essence is an idea. (Damasio; Looking for Spinoza, 88)

Feelings are a mental expression of all other levels of homeostatic regulation. (Damasio; Looking for Spinoza, 37)

Goal of the homeostasis endeavor in humans is to provide a better than neutral life state, what humans identify as wellness and well-being. (Damasio; Looking for Spinoza, 35)

Regulatory reactions that ensure our homeostasis consists of a hierarchy of simple reactions (FAPs) incorporated as the components of more elaborate ones, a nesting of the simple within the complex. (Damasio; Looking for Spinoza, 37)

Somatosensory regions are involved in the feeling process, and the insula is involved perhaps more significantly than any other structure. (Damasio; Looking for Spinoza, 105)

Class of signals most likely to represent the content of feelings -- signals related to pain states; body temperature; flush; pH; tickle; shutter;  viseral and genital sensations; the state of smooth musculature in blood vessels and other viscera; local pH; glucose; osmolality; presence of inflammatory agents; etc.. (Damasio; Looking for Spinoza, 106)

Somatosensory regions appear to be a critical substrate for feelings, and the insular cortex appears to be the pivotal region of the set. (Damasio; Looking for Spinoza, 106)
Feelings become possible because there are brain maps available to represent body states. (Damasio; Looking for Spinoza, 111)

Brain maps become possible because the brain machinery of body regulation requires them in order to make its regulatory adjustments, namely those adjustments that occur during the unfolding of an emotional reaction. (Damasio; Looking for Spinoza, 111)

Mental images we call feelings arise from the neural patterns exhibited in body maps. (Damasio; Looking for Spinoza, 123)


Background Feelings

Background feelings help define our mental state. (Damasio; Feeling of What Happens, 286)

Prominent background feelings include: fatigue; energy; excitement; wellness; sickness; tension; relaxation; surging; dragging; stability; instability; balance; imbalance; harmony; discord. (Damasio; Feeling of What Happens, 286)

Moods are made up of modulated and sustained background feelings. (Damasio; Feeling of What Happens, 286)

Background feelings -- a part of the neural signaling that goes on in the brainstem and hypothalamus is continually made conscious. (Damasio; Looking for Spinoza, 126)

Background feelings -- the way you feel when you're coming down with a cold, or better still, "on top of the world." (Damasio; Looking for Spinoza, 126)