Slashdot Mirror

http://www.jneurosci.org/content/35/48/15800
"Thus, the hypothesis that the propagation of neural activity can be carried out solely by electric fields is consistent with experimental data as well as computer simulations. The fact that the speed of the propagation remains constant under different experimental conditions can be explained by the presence of an electric field effect associated with neural firing generated by the network configuration and not by the properties of individual cells. This electrical field effect is revealed when synaptic transmission is blocked and both pathologic and normal propagation can exist simultaneously with field effect governing short range or local propagation, where synaptic transmission may govern long-range propagation and communication."

You want a cite? Start with the link you posted! See the part on MONAMINE OXIDASE. YOU read that, didn't you?

Of course, the entire article is ABOUT the role of nicotine in sustaining the behavior of SMOKING. OP is looking for information on nicotine not consumed as part of tobacco consumption.

As for your second link reading the non-paywalled part, it is about nicotine in smokers and a long list of references to other works about nicotine in the context of smoking. In other words, nothing about nicotine not in the context of smoking.

You say it's easy to find, but you failed.

Try this one. They administered nicotine as a freebase to rats. One group got just nicotine and the other got nicotine and MAOI. The second group showed a dramatically increased habituation. Guess which group smokers are in? Now guess which group vapers are in.

So yeah, there is a real question about how addictive nicotine is when divorced from the MAOIs present in cigarette smoke.

It's not, see the journal abstract. http://www.jneurosci.org/conte...

The OP is 100% correct. Taking "normal" people, people who have not committed violent acts, DOES NOT tell you this procedure would stop someone who WOULD commit violent acts. Obviously there's a difference between someone who commits a violent act and someone who doesn't.

Unless this article is mistaken, this sounds like an extension of a known phenomenon. And I can't remember where I read it, but I also remember reading another article years ago theorizing that in some cases this effect could be the brain sort of "redistributing" its load to areas that are underutilized and can handle it. There was no proof, but I thought it was an interesting theory.

In short, just because you don't have a functioning sensory organ, that doesn't mean the brain will completely stop using the main area the organ would have used to interpret its input.

Nope. It's very real and the neurological mechanism is indeed scrutinized in peer reviewed papers

http://www.fuenterrebollo.com/...

http://www.jneurosci.org/conte...

http://www.ptsdforum.org/c/gal...

The vascular part I am guessing / noting / observing.. it's a ,thing I noted a long time ago is all.

  The rest of it is information readily available . The general topic goes by the name of neural plasticity which is broken down into functional and structural .

It's not the thing I research specifically so I am not loaded down with bookmarks for you but I know all about it from undergrad

For people with no neuroscience background there's books like The Brain That Changes Itself and of course it's a big area of research- pulled from the web without much effort:

http://education.jhu.edu/PD/newhorizons/Neurosciences/articles/Response%20of%20the%20Brain%20to%20Enrichment/

http://www.jneurosci.org/content/29/10/3019.full.pdf

http://psyserv06.psy.sbg.ac.at:5916/fetch/PDF/21906988.pdf

http://www.medicaldaily.com/talk-therapy-reverses-biological-structural-brain-changes-ptsd-patients-264229

Some notes on one methodology:

http://dbm.neuro.uni-jena.de/pdf-files/May-TICS11.pdf

Aside from that, what exactly do you think phenomena like PTSD are? Purely disembodied psychological issues? If you've were or have ever repeatedly sustained hard study, you'd notice that your whole "self" changes in response to your efforts. You're smarter, your experience of everyday life is richer etc etc. This goes on as long as you're willing to inflict a good measure of discomfort on yourself.

By the same token, leaving your studies for a time then coming back is an extraordinarily punishing affair. Along with feelings of inadequacy and bewilderment when faced with the same material you left even a few short weeks ago, there's a sense of awe at your own former self's output and level of functioning.

Like the song says:

When you're up / looks like a long ways down
When you're down / looks like a long ways up

Cheers

If you check out the actual reporting from the authors (here for abstract http://www.jneurosci.org/content/33/33/13251.abstract?sid=bb49e635-09a9-4719-8462-cf027b122652) you can see that they tested three predictors for dyslexia on children who had not yet received reading lessons. Without making any claims of observing dyslexia, they noted that the size of the arcurate fasciculus is positively correlated with scores of 'phonological awareness' and no correlation with 'rapid naming' or 'letter knowledge.' Perhaps a linguist or clinician could help elucidate what those tests are actually measuring.

It could be that dyslexia is a grouping of somewhat different brain/processing abnormalities that have similar behaviors. If that is the case, then brain imaging of the size of arcurate fasciculus could predict whether treatment aimed at increasing phonological awareness would have any effect. If you haven't had an intro neuropsych course you may not have heard that the arcurate fasciculus is a primary connection between auditory cortex and motor representations - thought to translate hearing into replying. Folk who have damage to this fiber tract are typically unable to repeat back to you what they just heard. The auditory and visual conduits run in parallel in this part of the brain, so it may have bearing on sequencing of writing, not just spoken words.

Could also cure breathing.

Been done many times

Could also cure breathing.

Been done many times

What do you mean by no pharmacological effect though?

See: "Neurobiological Mechanisms of the Placebo Effect"
http://www.jneurosci.org/content/25/45/10390.full

In an experimental model of pain (Amanzio and Benedetti, 1999), the placebo response could be blocked by naloxone if it was induced by strong expectation cues, whereas if the expectation cues were reduced, it was insensitive to naloxone. In the same study, if the placebo response was obtained after exposure to opioid drugs, it was naloxone reversible, whereas if it was obtained after exposure to non-opioid drugs, it was naloxone insensitive.

Placebos and nocebos have only EVER been shown to affect SUBJECTIVE factors.

Not true.

Placebos can affect healing of duodenal ulcers:
http://www.jstor.org/discover/10.2307/649462?uid=3737496&uid=2&uid=4&sid=21100974892383
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014313/

Naloxone can block the effects of pain-reduction placebos in some cases.
http://www.jneurosci.org/content/25/45/10390.full

The mind affects the body in many ways.
http://www.sciencedirect.com/science/article/pii/S0889159112001936

The protein structures behind memory are beginning to be understood:

(Discovery of mBDNF) http://news.bbc.co.uk/2/hi/health/3747716.stm
(CaMKII association) http://www.jneurosci.org/content/31/25/9170.abstract?sid=e8ce0965-4b50-4ee4-913b-16d422f25230
(RNA handling of the proteins) http://www.newswise.com/articles/making-memories-how-one-protein-does-it

We're now very close to understanding how memories form and are activated.

Anyone have a link to the actual study, so we can find out what "better than chance" really means?

http://www.jneurosci.org/content/31/26/9599.full?sid=9fc54d71-af27-4f59-b121-747e942411a9

my bad. the above link is just a release by the center. Actual study is not freely available. Here is the abstract - http://www.jneurosci.org/content/31/26/9599.abstract

A peer-reviewed publication in The Journal of Neuroscience suggests that it is, in fact, science.

Despite that, I have watched too much Star-Trek and know too little about neuroscience to be able to read about "cortical excitability" via "theta-burst stimulation" or about "enhanced spontaneous neuronal firing and EEG gamma band power" and not feel that I'm reading a sci-fi screenplay.

When I read that headline my immediate reaction was, "Uh oh... pseudo-science incoming". However this comes from a paper published in the Journal of Neuroscience and the European Journal of Neuroscience. So perhaps we can enhance our brain through the (in a 1950's movie scientist voice) POWER OF MAGNETS!

It wasn't linked to in the article, so here's the actual abstracts for the two papers:

http://www.jneurosci.org/cgi/content/abstract/31/4/1193
http://onlinelibrary.wiley.com/doi/10.1111/j.1460-9568.2010.07425.x/abstract

Theta-Burst Transcranial Magnetic Stimulation Alters Cortical Inhibition

Human cortical excitability can be modified by repetitive transcranial magnetic stimulation (rTMS), but the cellular mechanisms are largely unknown. Here, we show that the pattern of delivery of theta-burst stimulation (TBS) (continuous versus intermittent) differently modifies electric activity and protein expression in the rat neocortex. Intermittent TBS (iTBS), but not continuous TBS (cTBS), enhanced spontaneous neuronal firing and EEG gamma band power. Sensory evoked cortical inhibition increased only after iTBS, although both TBS protocols increased the first sensory response arising from the resting cortical state. Changes in the cortical expression of the calcium-binding proteins parvalbumin (PV) and calbindin D-28k (CB) indicate that changes in spontaneous and evoked cortical activity following rTMS are in part related to altered activity of inhibitory systems. By reducing PV expression in the fast-spiking interneurons, iTBS primarily affected the inhibitory control of pyramidal cell output activity, while cTBS, by reducing CB expression, more likely affected the dendritic integration of synaptic inputs controlled by other classes of inhibitory interneurons. Calretinin, the third major calcium-binding protein expressed by another class of interneurons was not affected at all. We conclude that different patterns of TBS modulate the activity of inhibitory cell classes differently, probably depending on the synaptic connectivity and the preferred discharge pattern of these inhibitory neurons.

Continuous and intermittent transcranial magnetic theta burst stimulation modify tactile learning performance and cortical protein expression in the rat differently

Repetitive transcranial magnetic stimulation (rTMS) can modulate cortical excitability in a stimulus-frequency-dependent manner. Two kinds of theta burst stimulation (TBS) [intermittent TBS (iTBS) and continuous TBS (cTBS)] modulate human cortical excitability differently, with iTBS increasing it and cTBS decreasing it. In rats, we recently showed that this is accompanied by changes in the cortical expression of proteins related to the activity of inhibitory neurons. Expression levels of the calcium-binding protein parvalbumin (PV) and of the 67-kDa isoform of glutamic acid decarboxylase (GAD67) were strongly reduced following iTBS, but not cTBS, whereas both increased expression of the 65-kDa isoform of glutamic acid decarboxylase. In the present study, to investigate possible functional consequences, we applied iTBS and cTBS to rats learning a tactile discrimination task. Conscious rats received either verum or sham rTMS prior to the task. Finally, to investigate how rTMS and learning effects interact, protein expression was determined for cortical areas directly involved in the task and for those either not, or indirectly, involved. We found that iTBS, but not cTBS, improved learning and strongly reduced cortical PV and GAD67 expression. However, the combination of learning and iTBS prevented this effect in those cortical areas involved in the task, but not in unrelated areas. We conclude that the improved learning found following iTBS is a result of the interaction of two effects, possibly in a homeostatic manner: a general weakening of inhibition mediated by the fast-spiking interneurons, and re-established activity in those neurons specifically involved in the learning task, leading to enhanced contrast between learning-induced and background activity.

then you are saying that exercising stroke vitcim's affected limbs doesn't improve their mobility. Which is kind of a dumb thing to say.

Yes, that's almost what I'm saying - that it doesn't necessarily improve mobility. I work on stroke therapy robots that can move people's limbs around in whatever way we feel makes a difference. Through long research, we have found that some ways make a difference, and other ways do not make a difference.

Our researchers have been working on the problem for 25 years - that is, we have research published back to the mid-1980s, for example:

http://www.jneurosci.org/cgi/content/abstract/5/7/1688

This is a seminal paper by one of our researchers, that spawned the field of rehab robotics. I have already posted other links to research earlier in this thread.

Note well, I'm not a researcher, I write software to control rehab robots. But I know that in our researchers' papers, they do experiments where one group of patients gets beneficial rehabilitative exercises on our robots, and a control group gets non-beneficial "fake" exercises on our robots, where the patient's limbs are moved by the robots, but not in a beneficial way.

So be careful when you use phrases like "It's so obviously likely to be useful."

You imply that I might have a problem with successful results from a competing method, but it's not so. I'm saying there's a difference between "shows promise" and research results, especially from research that has been going on for 25 years, and going on in earnest (it took a while to create and refine the robots) for more than 10 years.

About a year ago I came across this paper while looking into a Navy solicitation for, essentially, the Redshift/F.lux programs embedded into sailors' berth lights. Their focus was not only to help them get to sleep, but help them wake up (or more generally, help adjust to ever-changing shift times).

Action Spectrum for Melatonin Regulation in Humans: Evidence for a Novel Circadian Photoreceptor

Pawalled unfortunately, and I don't have access at home, but the gist is that blue light in the band 446-477nm encourages the "it's daytime!" melatonin response (the effect peaks around 464nm)

Some upshots:
1) It's real, and it's probably not just your computer screen.
2) Blue-light regulation could conceivably be integrated into house lights, especially if in some years LED luminaires become feasible enough to replace CFLs.
3) The effect appears to work both ways - adding some extra blue light in the mornings could conceivably help you become alert faster.
4) Some off-the-shelf LEDs produce light very close to this peak (look for "dental blue", ~460nm, used for curing certain dental adhesives). You could hack together your own active light gadgets, e.g. blue-light specs to wear on trips to reduce jetlag.

Seriously now, the study has some merit.
Other than getting better at the game, these youngsters were performing difficult repetitive tasks akin to musicians learning to play instruments. The key is in the age of the learning. If a child is young enough, his or her brain increases in size and density. Check out:
http://www.jneurosci.org/cgi/content/full/23/27/9240

I'm sure poor education doesn't help(though rednecks, as a stereotype, aren't known for their opposition to underage sex, so I'm not sure they are relevant here); but I suspect that it goes rather deeper than that.

For instance, it is well known that humans are typically irrational in certain aspects of financial decision making. Curiously, people with autism spectrum disorders, show much less susceptibility. Particularly for something with the emotional salience of porn and sex and involving children, I'd strongly expect the degree of emotional involvement in decision making to have a significant impact on the respondent's stated position.

>>The study you mention has since been discredited

Has it?

Here's the study (or a similar study):
http://www.jneurosci.org/cgi/content/short/25/45/10390

Post a reference showing it discredited, please.

The placebo effect is quite real, even if placebos are not.

Human Embryonic Stem Cell-Derived Oligodendrocyte Progenitor Cell Transplants Remyelinate and Restore Locomotion after Spinal Cord Injury

I'm pretty sure the fact that that trial was able to restore locomotion after a spinal cord injury would be a breakthrough.

I guess you failed reading class as well: "The tests could begin by summer, said Dr. Thomas Okarma, president and CEO of the Geron Corporation." You can't restore locomotion in patients from a test that hasn't been done yet.

Did you read what I posted? This study was being done based off the work of a previous trial. Here is the trial that was done that precedes the FDA-approved study.

Human Embryonic Stem Cell-Derived Oligodendrocyte Progenitor Cell Transplants Remyelinate and Restore Locomotion after Spinal Cord Injury

Way to fail.

And you're a real idiot if you think that the base work in embryonic stem cells has led to anything other than cancer.

HAHAHAHAHAHA. That's a good one.

I bet that there are NO cures for cancer, NO blind man seeing, and NO crippled people walking due to stem cell research, in our lifetimes. All of this talk about the immediate need to fund stem cell research is just so much hype.

[...]

The reason that stem cell research needs federal funding is because THERE ARE NO CURES IN SIGHT FOR ANYTHING FROM THEM.

Actually there are MANY current studies using stem cells, and in particular embryonic stem cells, in promising treatments for a large range of diseases. Some of them are already approved for human trials and therefore will probably see the light in mainstream medicine in very few years.

One example of such applications: restoring locomotion after spinal chord injury, a study that was cleared by the FDA for human trials a little over a month ago.

Dude, if you have no idea what you are talking about, it's better to moderate your own opinions.

• The BBC story
• Neuroscience story

Slashdot covered the story at the time, but I don't have the URL handy.

Here's the actual article.

The article is here: http://www.jneurosci.org/cgi/reprint/29/4/1046.pdf

Can I have your login so I can read it?

Could you please point to which of their inferences you think breaks down because of statistical problems caused by the sample size?

If no such problem exists, the sample size was fine.

Quantative Analysis was over six years ago now, so I'm rusty... but, let's work through this a little:

Two jersies. Two chairs. Subject sits in one chair, so there's a 50/50 chance they'll pick each jersey (assuming they randomized which jersey was closer to the door, and made everything else as even as possible). So, for 22 respondents, if there's no effect of the game experiment, your expected result would be that 11 would sit with one jersey, 11 would sit with the other.

Instead, 75% sat with one jersey. That's... 16.5. Um. Well, let's say it was 17 people, then, instead of 11. What you need is the probability of that happening *just by chance*, when there's a 50/50 probability on each trial.

Oh, hell. I can't possibly remember how to do the math, not without a lot more coffee. Someone else take over here? And if someone can do a Pearson's N or Chi Square or something, that'd be cool too. What's the margin of error? Is it larger than the deviation?

<sarcasm>Good to see they're using a nice large group of test subjects.</sarcasm>

The article is here: http://www.jneurosci.org/cgi/reprint/29/4/1046.pdf

Could you please point to which of their inferences you think breaks down because of statistical problems caused by the sample size?

If no such problem exists, the sample size was fine.

I recall reading a set of guidelines for writing psych papers (discussing and critiquing an article). They said quite explicitly that complaining about sample size was about the cheapest shot available, so don't do it unless you can really back it up.

To the mods who think my parent is insightful: could you please spell out to me what the insight is? Because I haven't seen any problems with the sample size, only an unsubstantiated claim.

If you were smart enough to read, instead of just repeating the left's propaganda, you'd know that no cures for ANYTHING have been found using embryonic stem cells. Adult stem cells are now responsible for curing over 100 conditions.

Be careful about using absolutes like "anything" or "nothing", "always", or "never". They frequently come back to bite you. Remember, all of this research is extremely nascent, most results are just getting to the human testing phases. Further, embryonic stem cell research receives far less funding (especially in the United States) and what research does occur here is very limited. Even with one hand tied behind its back though:

• Diabetes
• Cell differentiation (think growing new organs)
• Spinal cord injury
• Brain lesion repair
• Diffuse motor injury

• Ok, I'm tired to cutting and pasting. The list is way too long. And as far as Bush not opposing embryonic stem cell research, your daft if you actually believe otherwise. He's stated as much on many occasions. 8 years ago, embryonic stem cell research was a glint in sciences eye. It's no wonder that funding didn't exist before then.

  That we have received funding despite Bush's efforts is not a sign of his support. Simply compare the funding being provided within the U.S. to that being provided in other countries. It's no wonder the U.S. is lagging far behind the rest of the world. You know what happens when a societies backwards, ignorant beliefs prevent funding into cutting edge technology? The cutting edge sciencists leave.

If you were smart enough to read, instead of just repeating the left's propaganda, you'd know that no cures for ANYTHING have been found using embryonic stem cells. Adult stem cells are now responsible for curing over 100 conditions.

Be careful about using absolutes like "anything" or "nothing", "always", or "never". They frequently come back to bite you. Remember, all of this research is extremely nascent, most results are just getting to the human testing phases. Further, embryonic stem cell research receives far less funding (especially in the United States) and what research does occur here is very limited. Even with one hand tied behind its back though:

• Diabetes
• Cell differentiation (think growing new organs)
• Spinal cord injury
• Brain lesion repair
• Diffuse motor injury

• Ok, I'm tired to cutting and pasting. The list is way too long. And as far as Bush not opposing embryonic stem cell research, your daft if you actually believe otherwise. He's stated as much on many occasions. 8 years ago, embryonic stem cell research was a glint in sciences eye. It's no wonder that funding didn't exist before then.

  That we have received funding despite Bush's efforts is not a sign of his support. Simply compare the funding being provided within the U.S. to that being provided in other countries. It's no wonder the U.S. is lagging far behind the rest of the world. You know what happens when a societies backwards, ignorant beliefs prevent funding into cutting edge technology? The cutting edge sciencists leave.

If you were smart enough to read, instead of just repeating the left's propaganda, you'd know that no cures for ANYTHING have been found using embryonic stem cells. Adult stem cells are now responsible for curing over 100 conditions.

Be careful about using absolutes like "anything" or "nothing", "always", or "never". They frequently come back to bite you. Remember, all of this research is extremely nascent, most results are just getting to the human testing phases. Further, embryonic stem cell research receives far less funding (especially in the United States) and what research does occur here is very limited. Even with one hand tied behind its back though:

• Diabetes
• Cell differentiation (think growing new organs)
• Spinal cord injury
• Brain lesion repair
• Diffuse motor injury

• Ok, I'm tired to cutting and pasting. The list is way too long. And as far as Bush not opposing embryonic stem cell research, your daft if you actually believe otherwise. He's stated as much on many occasions. 8 years ago, embryonic stem cell research was a glint in sciences eye. It's no wonder that funding didn't exist before then.

  That we have received funding despite Bush's efforts is not a sign of his support. Simply compare the funding being provided within the U.S. to that being provided in other countries. It's no wonder the U.S. is lagging far behind the rest of the world. You know what happens when a societies backwards, ignorant beliefs prevent funding into cutting edge technology? The cutting edge sciencists leave.

They've only seen reproduction in neural stem cells and glial cells. Neurons lack centrioles so they cannot reproduce. There is evidence of neural stem cells reproducing in the hippocampus and olfactory areas.

It depends on your field. All the journals I submit to want word documents. They will often explicitly tell you /not/ to submit pdf http://www.jneurosci.org/icons/ftp/JNtips.pdf

The synapse allows two neurons to communicate with one another. Each synapse involves a transmission point that sends a signal across a small gap to a receiving area.

Signals are sent in the form of a chemical substance, known as a neurotransmitter. These chemicals move across the gap and bind to receptors embedded in the receiving area.

I'm not sure if the first link is correct -- it isn't a research paper, just an intro-level lecture to integrate-and-fire models, one of the topics covered in computational neuroscience. The actual research paper by Earnshaw & Bressloff requires a subscription, but here's the abstract:

Biophysical Model of AMPA Receptor Trafficking and Its Regulation during Long-Term Potentiation/Long-Term Depression

AMPA receptors mediate the majority of fast excitatory synaptic transmission in the CNS, and evidence suggests that AMPA receptor trafficking regulates synaptic strength, a phenomenon implicated in learning and memory. There are two major mechanisms of AMPA receptor trafficking: exocytic/endocytic exchange of surface receptors with intracellular receptor pools, and the lateral diffusion or hopping of surface receptors between the postsynaptic density and the surrounding extrasynaptic membrane. In this paper, we present a biophysical model of these trafficking mechanisms under basal conditions and during the expression of long-term potentiation (LTP) and depression (LTD). We show how our model reproduces a wide range of physiological data, and use this to make predictions regarding possible targets of second-messenger pathways activated during the induction phase of LTP/LTD.

Computational neuroscience is a great topic. If you're interested in learning more about it, there's a nice book by Gerstner & Kistler called Spiking Neuron Models, which can be purchased hard-copy or downloaded for free online. The wikipedia page is also pretty good, with plenty of links to fun neural simulation software.

(And yes, I Am A Computational Neuroscientist... or at least I'm in a computational neuroscience grad program ;)

The state-of-the-art in cryonics today is *vitrification*, not freezing. Very high quality brain preservation is possible when freezing is prevented with cryoprotectants

http://www.alcor.org/Library/html/braincryopreserv ation1.html

Changes in dendritic spines cited by one poster as evidence that 5 minutes of clinical death is irreversible are in fact known to be *spontaneously reversible*!

http://www.jneurosci.org/cgi/content/abstract/25/2 2/5333

The world record for recovery of large animals without brain damage after intervals of clinical death at normal temperature using advanced resuscitation technology is now 16 minutes, not 5 minutes.

http://www.alcor.org/Library/html/annals.html

Even just post-resuscitation hypothermia, hemodilution, and hypertension will get you to 13 minutes

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd= Retrieve&db=pubmed&dopt=Abstract&list_uids=2298837

The brain doesn't go "kaboom" after a few minutes of circulatory arrest. Foreseeable technologies will likely eventually extend the reach of resuscitation medicine to one hour or more of clinical death at normal temperatures. A person with a stopped heart is fundamentally A SICK PERSON that doesn't really die until much later.

On top of it all, all this is moot for cryonics patients who suffer attended cardiac arrest, for whom the preservation process is started immediately, the first step being restoration of blood circulation and oxygenation.

http://www.alcor.org/Library/html/CardiopulmonaryS upport.html

People should do at least some minimum checking before making confident pronouncements about the stupidity of others. There are some very sharp people behind this field

http://www.cryoletter.org/

Trouble is due to the placebo effect, it might fool the brain so well that it behaves as if it is indeed caffeinated.

See Neuropharmacological Dissection of Placebo Analgesia,The Neurobiology of Placebo Analgesia and "13 things that do not make sense".

Then there's also the homeopathy thingy - see num 4 in the newscientist article.

Because that is the blueprint of life. Life works that way in this universe, does that make sense?

Yes, it does if you just look on the surface. However the details tells a quite different picture.

I'm gonna do this brief so please excuse the (eventual) gaps in my explanation. If we make an analogy of how eyes are constructed in different animals (just to continue my previous example). You need something that focuses light, you need a shutter to prevent excessive light under "good-light" conditions, you need something to collect the light and you need a clear medium separating the focusing tissue from the collecting tissue to get a useful resolution. This is the physical "blueprint" of what simplistically is needed to construct an eye.

Now, if we zoom in on a detail of this, the actual light sensitive pigment used in the "collecting" tissue (rods etc), called rhodopsin.

Rhodopsin is derived from vitamin A and present in most species. However the protein does not have the same aminoacid sequence in all animals. http://www.jneurosci.org/cgi/content-nw/full/19/10 /3681/F1 Aminoacids can be changed without affecting the function of protein and those changes are so called neutral. When you then compare the DNA-sequence of these different variants of rhodopsin and use the differences and similarities to construct an tree/network of how these different variants are related to eachother by means of similarity then that tree/network perfectly overlays with what you would see if you compared completely unrelated morphological characters. The protein functions just fine and I'm quite certain that we could take the gene for rhodopsin in mouse, put that in a chimp eggcell and see that the chimp would see just fine (that'f be an awful experiment to actually perform tho if something goes wrong so I'd leave that to less discriminatory researchers).

Now, to make things a bit more interresting; squids have another unrelated photo sensitive pigment called retinochrome. http://www.jgp.org/cgi/content/abstract/67/6/791 Retinochrome that is thought to be what the squid eye use as their main light absorbing pigment. It overlaps rhodopsins absorption spectrum so there is more than just one way of constructing a protein that absorbs light.

If two people, in two different countries, without collaborating, design a car, guess what?

Yes this can be seen as the equivalent of "evolving" a wing in different types of animals.

Yes, 4 wheels, + 1 for steering. Doors, you know, for getting in and out of... gearing... lights (night affects quite a large portion of the world you know ;-) and even windscreen wipers becuase of rain.

Yes, on the surface they look just the same but if you look at the actual implementation, the actual parts that make up the details they are quite different although they both solve the (for us) primary issue of transporting objects fast.

Now, the next model they develop will build upon what they designed first as that seems logical to not having to "invent the wheel again". But you can still tell that the new modell is built from the same manufacturer.

If you just want to transport humans then you might actually design a MC instead ;)

Physics puts up certain rules that you have to follow to make an effective implementation but the details in the smallscale design can vary quite a lot and still acomplish the same results.

Just compare the fins and shape of sharks and dolphins. Water puts the limitations/rules of what is an effective solution but the actual implementations are completely different in the details (sharks have cartilage instead of bone etc). We (who study evolution) look at those details and use them and when you study

The actual scientific article (free abstract) and, in fact, the Wired article, make it clear that we're not talking about repairing a transected or severed spinal cord. It only talks about repairing an injured spinal cord. In particular, the research is on re-myelinating the neurons. Myelin is the fatty sheath that insulates a neuron so the electric nervous signal can travel faster with less cross-talk. If the neuron itself were severed, there would be nothing to re-myelinate. This is important research, but it is not what the Slashdot posting says it is.

Yeah, sorry I forgot to do that.

http://www.jneurosci.org/content/vol24/issue46/
http://www.jneurosci.org/cgi/reprint/24/46/10410

Unfortunately, unless you have a subscription to J. Neuro. Sci., or you attend a university (or other institution; or at least have access to a computer from such an institution) that does, you can only get the abstract.

Yeah, sorry I forgot to do that.

http://www.jneurosci.org/content/vol24/issue46/
http://www.jneurosci.org/cgi/reprint/24/46/10410

Unfortunately, unless you have a subscription to J. Neuro. Sci., or you attend a university (or other institution; or at least have access to a computer from such an institution) that does, you can only get the abstract.

Eytan, D., Brenner, N., and Marom, S., Selective Adaptation in Networks of Cortical Neurons. Journal of Neuroscience

The problem, though has to do with peer review. To be considered legitimate, at least in my field, having your work looked over by your peers is crucial. For one thing, they're not as close to the work. They often catch errors and suggest better experiments or controls. For another thing, when I read a reviewed journal article outside my specialization, I have more trust that someone within the specialty thinks the work is reasonable.

Someone brought up Pons and Flieshmann -- a classic case of publishing via the popular press without peer review. Direct web publishing carries similar problems.

You can view the paper Here in HTML or download the pdf Here

Three cheers for journals which make their stuff public access !!!

You can view the paper Here in HTML or download the pdf Here

Three cheers for journals which make their stuff public access !!!

You can view the paper Here in HTML or download the pdf Here

Three cheers for journals which make their stuff public access !!!
Oh, the paper has pictures also but you get a decent explanation as well.

You can view the paper Here in HTML or download the pdf Here

Three cheers for journals which make their stuff public access !!!
Oh, the paper has pictures also but you get a decent explanation as well.

Things aren't quite as bad as you imply with fMRI Nick; there's been a lot of work about this in the last ten years!

Optical imaging experiments show how you can use direct observation of the brain to interrelate the changes seen with fMRI and neural activity. There are many more similar studies, all of which suggest a close correlation between neural activity and fMRI measurements. More recently people have begun comparing similar paradigms directly in macaque and human using fMRI and electrophysiology

Geraint
geraint@klab.caltech.edu