quote:

Now the pineal gland's an interesting topic in itself... Apparently some early amphibian ancestors of ours had a 3rd eye that watched out for danger from above, and it atrophied into what is now called the pineal gland. Scientists have been able to create 3 eyed frogs by messing around with it during embryo development.

Actually, it may not be a third eye, but a fifth eye!



(The above picture is supposed to be a case of Opabinia, but it's not a Burgess Shale specimen; caveat emptor and all that, but it was what I could find to link to). Opabinia is frequently called an "oddball" early form, but there are a few (tenuous) reasons to think it may have been representative of the early state of affairs - if you look at how eyes work out throughout the vertebrates and invertebrates, there's a frequent contrast of medial vs. lateral vs. pineal eyes, with different methods of stacking, different geometries and different opsins showing up, much of which would make more sense if the common ancestor had five eyes or so instead of only two. In any case, if you transplant a third eye into a frog, its input goes to one or the other optic lobe of the brain - what was so beautiful about that experiment is that normally a frog's eyes don't overlap and one side of the brain handles the opposite eye, but if it has a middle eye the input is interleaved with another eye in ocular dominance columns, a structure normally not seen in the frogs examined. But the brain never handles it like a "pineal eye", but just as one more out of two.

Cool stuff, Banshee. I hadn't seen anything like that before.

quote:

Originally posted by Eric:
What all does the blood take to the brain? It has to be more than just oxygen. But more oxygen is most likely the key.

I started wondering why oxygen was so important to the brain that you would die in minutes without it, whereas some tissues can be taken from a body quite a while after it's died and be transplanted successfully. What the heck is going on here? What is death, really?

Some interesting answers, and some disturbing questions. And a new word: ischemic - "A decrease in the blood supply to a bodily organ, tissue, or part caused by constriction or obstruction of the blood vessels."

From The Internet Stroke Center:

Lack of glucose and oxygen deplete the cellular energy stores required to maintain electrical potentials and ion gradients.

In ischemic brain tissue, the membrane that surrounds each affected neuron becomes "leaky," and the cell loses potassium and adenosine triphosphate (ATP), the tissue's medium for energy exchange.

Energy failure is not the immediate cause of cell death; however, since all brain cells tolerate loss of ATP for several minutes. In humans, it appears that 5 to 10 minutes of complete occlusion is required for irreversible brain damage. In actuality, most strokes do not involve a complete occlusion of blood flow, but even a partial occlusion, if allowed to continue for a sufficient time, may produce irreversible brain damage.

Once blood flow to cerebral neurons diminishes, one or more branching mechanisms may independently lead to brain cell death. These mechanisms may involve
deterioration of ion gradients including or the effects of anaerobic metabolism.

With respect to the latter, anaerobic glycotic pathways are utilized in the affected region to compensate for the loss of oxygen and provide a source of energy. However, this produces damaging by-products, including lactic acid and hydrogen ions, which accumulate in tissue in proportion to the carbohydrate stores present at the outset of ischemia. Toxicity of hydrogen ions, especially their ability to facilitate ferrous-iron-mediated free-radical mechanisms, appears to irreversibly affect neuronal integrity.

Remember that stuff about Glutamate acting as an excitotoxin? That's what they're talking about when they mention 'gylcotic pathways' and toxins being created. Now, what's interesting is that the first few stages of this process are reversible. It isn't until you get all of these free-radicals being formed that wreck all of the cells' molecular machinery that it becomes irreversible. If you can restore oxygen flow before the damage becomes irreversible (aka "reperfusion"), then the brain can recover from the initial lack of oxygen.

Room Air Appears To Do Less Brain Damage Than Pure Oxygen
When a person's heart stops, standard resuscitation includes treatment with 100 percent oxygen. Now researchers at the University of Maryland School of Medicine and George Washington University School of Medicine and Health Sciences report that regular air -- which is 21 percent oxygen -- may be a better choice in some cases, helping prevent neurological damage that can occur after the brain is deprived of oxygen.
Much of the brain damage that occurs after the heart stops pumping is what doctors call reperfusion injury. That means it occurs while the blood flow is being restored to the brain. Fiskum said it is caused by the toxic effects of free radicals, which are by-products of the process of oxidation.

Fiskum and Rosenthal compared levels of oxidation of brain lipids -- fatty acids and fat-like substances that maintain vital metabolic functions -- in animal models resuscitated after 10 minutes of cardiac arrest. In those given 100 percent oxygen, free-radical levels were significantly higher than in those resuscitated using the oxygen ratio found in room air.

When neurological deficits were measured, the animals resuscitated with 21 percent oxygen showed less brain damage than those resuscitated with 100 percent oxygen, the researchers report.

"It was reasonable to expect that pure oxygen would be good for a brain that has been deprived of oxygen," Fiskum said. "But we found that was not necessarily the case. After oxygen levels reached normal levels in the blood, continuing to administer pure oxygen actually was damaging the metabolic mechanism in the brain."

It appears that the 'reperfusion injury' can be reduced by inhibiting a specific signaling pathway (more...).

Even more encouraging, studies of how Alaskan ground squirrels are able to hibernate in freezing temperatures with almost no oxygen flow to their brain are pointing to the fact that reducing the temperature of the brain allows it to survive without oxygen for long periods of time. The ground squirrels also have adapted ways to use Vitamin C to avoid the free-radical damage that results from oxygen being re-introduced to the brain (article).

Now, this is where it starts getting wierd. Some scientists have shown that you can do head transplants by lowering the temperature of the head to 10-15 degrees C that it can go without blood flow for an hour, and then re-connecting up the arteries. If/when nerve splicing becomes reality, then this may start becoming a viable way to treat massive body injuries.
From the article:
Where would the bodies come from? The same place that individual organs come from, says White. At the trauma unit at the Metro Health Medical Center in Cleveland, where White has worked, many people with damage to their brains – but with their bodies otherwise intact – are brought in and pronounced brain-dead. Instead of using the body's organs separately for individual organ transplants among many people, the whole body could be used for one person.

And this is where things get really disturbing. It appears that one of the tests that is used to pronounce someone brain dead (testing to see if breathing has stopped) can actually cause brain death in brains that would normally have recovered.
Apnea testing may induce rather than diagnose death:

Evolution of brain blood flow (BBF) in three hypothetical cases of intracranial hypertension: influence of hypotension induced by apnea testing at 24-h survival. Whilst BBF is unaffected in case 1, apnea testing hastens and sets the clinical outcome to irreversible brain damage in cases 2 and 3 by inducing collapse of intracranial vessels.

The data reviewed here suggest the possibility that a global reduction of blood supply to the whole brain or solely to the infratentorial structures down to the range of ischemic penumbra for several hours or a few days may lead to misdiagnosis of irreversible brain or brain stem damage in a subset of deeply comatose patients with cephalic areflexia. The following proposals are advanced: 1) the lack of any set of clinically detectable brain functions does not provide a safe diagnosis of brain or brain stem death; 2) apnea testing may induce irreversible brain damage and should be abandoned; 3) moderate hypothermia, antipyresis, prevention of arterial hypotension, and occasionally intra-arterial thrombolysis may contribute to good recovery of a possibly large subset of cases of brain injury currently regarded as irreversible; 4) confirmatory tests for brain death should not replace or delay the administration of potentially effective therapeutic measures; 5) in order to validate confirmatory tests, further research is needed to relate their results to specific levels of blood supply to the brain. The current criteria for the diagnosis of brain death should be revised.

yikes.

This message has been edited. Last edited by: DIT,

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from DIT post above: 3) moderate hypothermia, antipyresis, prevention of arterial hypotension, and occasionally intra-arterial thrombolysis may contribute to good recovery of a possibly large subset of cases of brain injury currently regarded as irreversible

I always love it when something is again considered reversible.


Chromosome 1 from Nature article

quote:

from Nature: The explosion of parallel investigations using this resource to characterize features of genomic biology, such as sequence variation, disease-causing mutations, recombination, and replication, provide a new level of information with which to annotate chromosome sequences.

Two of the diseases caused by the mutations in chromosome 1 are Altheimer's and Parkinson's disease.

I was googling for the neurobiological basis of cognitive dissonance because of the discussion over in theIntriguing perspective on religion thread and found this:

quote:

A Principle of Dissonance Reduction
The central hypothesis of our proposal is that the discrepancy in the network between expected and actual outcomes (actions and affect)reflects cognitive dissonance, while the adjustments in the connection weights (determined by the delta algorithm) reflect dissonance reduction through attitude change. Among the several possible sources of cognitive dissonance that Festinger (1957) outlined in his book, one of them is close in spirit to the present proposal. Festinger stated that behavior is guided by accurate information
about the environment and the self, and that dissonance can arise when this information disconfirms cognitions or expectations (Festinger et al., 1956). Therefore, any
discrepancy between one's predictions (based on relevant input) and one's behavior or emotion would be psychologically disturbing to the person and will be avoided. As Festinger (1957) noted:

quote:

Elements of cognition correspond for the most part with what the person actually does or feels or with what actually exists in the environment. In the case of opinions, beliefs, and values, the reality may be what others think or do; in other instances the reality may be what is encountered experientially or what others have told him. But...persons frequently have cognitive elements which deviate markedly from reality....Consequently, the major point to be made is that the reality which impinges on a person will exert pressures in the direction of bringing the appropriate cognitive elements
into correspondence with that reality. (p. 11,
original italics)

Our idea of dissonance as error in the network reflects a novel, perhaps somewhat counterintuitive view on the imbalance in the structure or relationships among the relevant cognitions. Dissonance is captured in our model by the fact that as long as no attitude adjustments are made, activation of the causal nodes will always create error at output (see also Lord, 1992). The amount of this error (averaged over all output nodes) can be taken as measure of the degree of dissonance. Our model thus specifies how an initially dissonant system can evolve to achieve greater coherence and less dissonance. By changing weights and decreasing the network's error, the network effectively strives for cognitive consistency and reduces cognitive dissonance.

This is interesting because of this last part, that an initially dissonant system can evolve to achieve less dissonance.

quote:

Originally posted by Eric:
This is interesting because of this last part, that an initially dissonant system can evolve to achieve less dissonance.

It seems that one of the key ways a child's brain matures is through a similar mechanism - we start off life with a 'fully connected' set of neurons and, through experience (e.g. through what we see, hear, learn), neural pathways and synapses that are consistently useful are re-inforced and those that are 'dissonant' or under-utilized are 'pared away'. One of the theories of what happens in Down syndrome children is that, because there are 3 copies of chromosome 21 (the smallest chromosome) instead of the normal 2 copies, this 'paring down' process happens half as fast as normal in the first 3 years. (SciAm Mind Vol. 16 No 3)

Have you noticed how few memories you have from when you were, say, age 6 or younger? This may apparently be a side-effect of the pruning that's going on: (from Chris Chatham's DevelIntel blog):
Adult networks that undergo synaptic pruning actually lose the ability to retrieve the earliest memories. In humans, this phenomenon is known as "childhood amnesia," in which memories before the age of 5 are hazy, and those before 3 are almost completely inaccessible. This amnesia emerges from the networks because the earliest memories are stored in a highly distributed fashion, relying on many different neurons, while later memories are stored in a more sparse format. Therefore, early memories are more degraded by the pruning strategy because of sheer probability: more neurons participate in their representation, so they are more easily affected by changes to the network.

I'm half-way through a very cool book: "Endless Forms Most Beautiful" by Sean B. Carroll. Remember all of that stuff about morphogenesis and Sonic Hedgehog and the Spemann Organizer? Well, this book takes off from there, describes the 'genetic toolkit' of signaling proteins and regulatory 'switches' that control which genes are turned on or off during development, and the cascade of events that effectively define the blueprint for the embryo's development. It then goes into how this knowledge has led to the whole 'evolutionary-development' (evo-devo) field that is providing a lot of cool insights into how life has evolved from the Cambrian explosion of life forms up to now. Very readable, although it does get kind of frustratingly vague at points.

I'm going to be signing off for a while - take care and I hope you all have a great summer.

This message has been edited. Last edited by: DIT,

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In humans, this phenomenon is known as "childhood amnesia," in which memories before the age of 5 are hazy, and those before 3 are almost completely inaccessible.

Unless some type of trauma was associated with the memory, this is true for me. I have vivid memory of a dog attack to my face that happened when I was three but thats about it. Maybe thats why teachers used scare tatics on children. Pack a memory in with adrenaline and it stays in tight less likely to be pruned.

Have a good one DIT. Drop a post in if you run across an open line.

hey here's some neurobliology news...
Today I had an eye appt and I had 20/25 in one eye and not bad in another. I was way over 20/50 a year ago. I couldn't see any of the hidden numbers in the color blothches, today I could see almost all of them...

go figure.

You weren't drinking sodium santoninate last time were you

quote:

Acquired colour blindness can be the result of disease, such as multiple sclerosis, optic neuritis, anaemia, lukaemia, vitamin B1 deficiency, or the result of poisioning by carbon disulphide, lead, sulfanilamide, iodoform, thallium, tobacco and alcohol. These causes attack the conducting paths of the optical system, and can be temporary or permanent. They can progress as far as monochromatism if the poisoning or disease continues. If the rod-cone mechanism is damaged, acquired tritanopia may occur, in which there is a reduced discrimination between blue and yellow. This may be stable and localized in small regions of the retina. A dose of half a gram to a gram of sodium santoninate produces temporary violet-blindness (accompanied by nausea and visual hallucinations). A violet haze is seen over the visual field.

Woah, I just re-read my last post and realized that it could be taken as very offensive. I apollogise for that. Just joking on the absinthe.
The vision correction appears to be due to the control over the MS.

I was sitting outside yesterday evening trying to enjoy the sunset in between periodic downpours and found myself spending more time smacking at mosquitoes than anything. Do they serve some purpose? Some hidden DNA exchange? A population control? Are they just an encapulation device for bacteria and viruses like cars, planes and helicopters are for us?What drives these blood suckers...

quote:

Olfaction plays a major role in host preference and blood feeding, integral behaviors for disease transmission by the malaria vector mosquito Anopheles gambiae sensu stricto (henceforth A. gambiae). We have identified four genes encoding candidate odorant receptors from A. gambiae that are selectively expressed in olfactory organs, contain approximately seven transmembrane domains, and show significant similarity to several putative odorant receptors in Drosophila melanogaster. Furthermore, one of the putative A. gambiae odorant receptors exhibits female-specific antennal expression and is down-regulated 12 h after blood feeding, a period during which substantial reduction in olfactory responses to human odorants has been observed. Taken together, these data suggest these genes encode a family of odorant receptors in A. gambiae, whose further study may aid in the design of novel antimalarial programs.

Olfaction plays a critical role in many insect behaviors, including host preference selection, among agricultural pests and disease vectors (1, 2). These vectors include several species of mosquitoes that transmit numerous parasitic and viral diseases, including malaria, dengue, West Nile encephalitis, and yellow fever. Although all of these diseases pose significant threats to human health, malaria, which is transmitted by female adults of several species of anopheline mosquitoes, remains one of the leading causes of worldwide morbidity and mortality. The World Health Organization estimates that, in Africa alone, malaria is responsible for more than two million deaths per year, including one million children younger than 5 years of age (3). Because of the importance of host preference in establishing the overall vectorial capacity in this system, a molecular analysis of mosquito olfaction may provide opportunities for reducing the incidence of disease transmission. As a first step in this process, the cloning and characterization of components of the olfactory signal transduction cascade from A. gambiae will facilitate molecular and biochemical studies of this mosquito's olfactory processes. Ultimately, these efforts may lead to the design of novel methods of disrupting vector–host interactions and thereby reduce the vectorial capacity of these insects.

my wife is a doctor who did a post doc in tropical medicine. At one point I knew a LOT about malaria and mosquitos. The bad news is that they do play a huge role at the bottom of the food chain. If you get rid of them you also get rid of the birds in an area, and the things that eat birds. As to humans, they just annoy us and spread diseases amonsts us.

Ya, my eyes are better because my MS is better. I kind of expected it, but you have to understand that the genius neuro you go see calls it 'permanent damage'. This is because MS doctors are mostly harmful yes-men to the pharmaceuticals who's basic knowledge of neurology hasnt been updated for a decade. Plasticity wasn't even documented a decade ago and now...well there may be no such thing as remission, just re-organization.
Good thin certain reorganizational agents are legal in Canada.

Good point about the food chain. I guess birds and bats would lose out if the mosquito was gone.

Plasticity falls right in with the human nature of high adaptability. Glad you kept seeking.

Man in coma's rewired brain.

Cool Gromit!

From JCI article:

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Very few neuroimaging studies have tackled the issue of late recovery of consciousness in severe brain damage. The most remarkable finding in the Voss et al. study (12) was the MRI assessment of transiently increased fractional anisotropy and directionality in the posterior midline cortices (encompassing the cuneus and precuneus), interpreted as increased myelinated fiber densities and novel corticocortical sprouting, paralleling the emergence of the patient from MCS. The same area of the patient's brain also showed amplified metabolic activity, as measured by PET. This finding stresses the importance of the posterior medial structures in consciousness of self and interaction with the environment (14, 15). Activity in the medial parietal cortex (i.e., precuneus) seems to show it to be the brain region that best differentiates MCS from VS patients (16). Interestingly, this area is among the most active brain regions in conscious waking (15) and is among the least active in altered states of consciousness, such as pharmacological coma (17), sleep (18), dementia (19), Wernicke-Korsakoff syndrome, and postanoxic amnesia (20). It has been suggested that this richly connected multimodal posteromedial associative area is part of the neural network subserving human awareness (21).

Reversing Time: Temporal Illusions

Fascinating stuff.

quote:

...
By repeatedly pairing a keypress with a flash of light, in which the light flash lagged behind the keypress by 100 ms 75% of the time, and then recording subjects' perception of whether the light flashed before or after their keypress, Stetson et al. were able to cause a reversal of perceived temporal order - at the end of the experiment, the light flashed immediately after the keypress, and subjects reliably thought the light flashed before they pressed the key!
...

No idea if the source is reliable, though...

Neat ArkanGL almost a recipe for deja vu.

quote:

an organism needs a plastic mechanism for temporally aligning its perceptions and actions.

Like plugging a guitar in at the soundboard (not a good idea) with the speakers 200ft away on stage and trying to play to the amplified sound. Has anybody done it long enough to see if your hearing adjusts to the delay? If you move forward after the adjustment would you think you are hearing the notes before you play them?

Drugs that can reverse memory loss that characterizes aging.

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Restoration of neuronal viability and synaptic plasticity through increased trophic support is widely regarded as a potential therapy for the cognitive declines that characterize aging. Previous studies have shown that in the hippocampal CA1 basal dendritic field deficits in the stabilization of long-term potentiation (LTP) are evident by middle age. The present study tested whether increasing endogenous brain-derived neurotrophic factor (BDNF) could reverse this age-related change. We report here that in middle-aged (8- to 10-mo-old) rats, in vivo treatments with a positive AMPA-type glutamate receptor modulator both increase BDNF protein levels in the cortical telencephalon and restore stabilization of basal dendritic LTP as assessed in acute hippocampal slices 18 h after the last drug treatment. These effects were not attributed to enhanced synaptic transmission or to facilitation of burst responses used to induce LTP. Increasing extracellular levels of BDNF by exogenous application to slices of middle-aged rats was also sufficient to rescue the stabilization of basal dendritic LTP. Finally, otherwise stable LTP in ampakine-treated middle-aged rats can be eliminated by infusion of the extracellular BDNF scavenger TrkB-Fc. Together these results indicate that increases in endogenous BDNF signaling can offset deficits in the postinduction processes that stabilize LTP.

the re-organizational agent I was referring too is marijuana. I destroyed all of mine a month ago (boy do my lungs feel better!) but I would still recommend it to an MS patient who needs to mellow out and lateralize.

I get a lot of email from MS patients who want to know why some people are just fucked (in wheelchairs, can't talk...) and have like one white blob on their mri, and I light an MRI up like a christams tree and really ALL issues are gone.

I think its because I have had it all my life (maybe, only diagnosed 5 years ago) and I'm all about new pathways.

When my wife and I are travelling and we walk across a town, I refuse to go back the way we came. To me that is failure. I have to make a loop, go back a different way.

When I played music as a pro, a night playing covers was failure. I was all about playing originals, and improvising jazz, and composing for ensembles...really I'm pretty shitty at remembering covers, luckily I can play by ear really well so if 1 guy knows the tune, I can follow, but as a bandleader? yikes.

My web show had to stop at 60 episodes a couple months ago. The winter was all about giving myself latitude to lateralize...reopen pathways to a creative from 20 years ago...I mean for the last 10 years I've been selling my logic...writing C++ code, so trying to act creative has been rough... (to really respect those neural clusters I'd have to practice music a lot and writing a lot etc, really I've just been trying to run some energy through those neurons)

of course smoking pot slurs my speech so the show got a little dark and wobbly...

still it worked, I really would recommend that and LDN to anyone trying to consciously reorganize...

a month later I'm really glad to have quit though...at 43 it's kind of undignified trying to be creative...painful..and ultimately it's kind of disrespectful to do creation badly and not care...

quitting solved all my digestion and sex life issues in a few days...pot creates as many issues as it solves.

I dont think I'll get back to pot, or have new ms issues...(like Michael Crighton I'm downgrading it from MS to a 'neurological incident') but I'm afraid I may have to disappear from the web too...Part of new pathways is goinh yo be new habits away from the box...

I'll miss this thread. Smart nice people who helped me heal...thanks.

Thanks for sharing your stories greendreams, amazing. Especially about the LDN, very promising. Come back and give us some updates every now and again.

This is a fascinating thread and I hope it hasn't died. I only found it recently and I am still working my way through all the links. Hopefully this post will keep it from being archived until I have caught up.