Glider

Well, the maths works only if you assume that each synapse plays a unique part in a single memory. However, if you assume that each single synapse may be involved in many related memories, then the equasion becomes a lot more plastic.

It comes from random firing of the affected nerve. If the nerve feeds an area of epidermis then the signals will be interpreted by the brain as having originated in the epidermis. Nerves are very sensitive to oxygen deprivation. If the blood flow is restricted, the nerves will very quickly become non-responsive. When blood flow is restablished, the nerves begin to function again and begin to fire randomly, resulting in parasthesia (pins and needles). It doesn't really matter where along their length the activity occurs. If a nerve innervates your little finger, activity in that nerve at any point along its length will 'feel' like it's coming from your little finger. A good example of this is when you bang your 'funny bone'. This is sudden compression of the ulnar nerve and the site of compression (the elbow) is the origin of the activity in response to the insult, but this nerve innervates your little finger (and ring finger) and that's why you feel the tingling there. See above Not really. In phantom limb pain, the nerve endings no longer exists. The parasthesias associated with the phantom limb could originate anywhere along the sensory pathway, from the terminated nerve ending, the dorsal horn of the spine or even in the primary somatosensory cortex. There is a surgical procedure designed to alleviate phantom limb pain called a 'Drezotomy'. This involves isolating the afferent nerves from the missing limb at the dorsal root, and cutting them. However, this is not always successful, and even when it is, the sensation sometimes returns and is often worse, resulting in a really painful burning sensation. Tghis would suggest that the sensation does not (in these cases) originate in the nerve itself, but higher up, possibly in the thalamus.

Hehe, that reminds me of an essay I marked once. It contained the enlightening phrase; "Pavlov, the father of salivating dogs...". I can't see the phrase "...the father of..." now without laughing. How very Pavlovian

I'm a bit vague on this, but both cheese and chocolate contain substances that trigger particular CNS function. Chocolate contains substances that trigger reward. Cheese contains tryptophan, which a 5-hydroxytriptamine precurser (hence the so-called 'cheese effect' which is the term given to the mild antidepressant effect of cheese in many cases). Cheese also contains substances that affect vasal responses (tyramine), and it is one of the reasons that cheese is thought to be a trigger for migraine. Tyramine is structurally similar to catecholamines so tyramine could act as a 5-HT (serotonin) agonist causing vasoconstriction, followed by longer term vasodilation. This is likely to be the substance that results in sweating as vasodilation in the face will trigger a sweat response. Capsaicin does the same thing.

The most basic trigger for a neuron to fire is the previous neuron firing. However, if it was as simple as that, every time one neuron fired, they all would. To allow processing, there are a number of mechanisms which control activity. For example, not all neurons are exitatory. Many are inhibitory and their firing inhibits the next neuron by raising its firing threshold (creating an inhibitory post synaptic potential, or IPSP). Further, many neurons won't fire in response to a single incoming action potential. They require many incoming impulses, each creating an exitatory post synaptic potential (EPSP), each of which which lowers the firing threshold, but on their own can't trigger the cell. These cells require the summation of many incoming impulses to trigger them. Sometimes it's the number of impules within a certain period of time (temporal summation), that triggers them. There is also spatial summation. This is where of the huge numbers of inhibitory and exitatory synapses contacting one cell, sufficient numbers of exitatory synapses trigger at once in the same region to outweigh the inhibitory activity and the membrane depolarises at that point. There is also long-term potentiation (a key factor in learning). This is where chains of cells that fire frequently are reinforced, i.e. the firing threshold of the cells in the chain is lowered and that particular combination of cells becomes more likely to fire in sequence when one is triggered. Beyond the single cell events, there are also group phenomena, for example, where the activity of a cell or group of cells inhibits activity in the cells around it (this can be seen in retinal ganglion cells), and so-on. So, the brain is full of positive and negative feedback systems. If you take combinations of the four basic modifiers I've outlined above; IPSPs, EPSPs, temporal summation and spatial summation you can see that there are a huge number of possible modulatory effects. If you include the more subtle modulatory effects of neurotransmitters and NT receptors (for example 5-HT has four or five known receptors, each of which responds differently to serotonin) and differences in NT effect according to location then you have a mindblowing number of possible modulatory mechanisms. The brain does generate an electrical field. It is detectable using EEG, however, EEG it quite a 'blunt' instument (it lacks resolution) and detects only the net field associated with higher areas of activity on the cortex. This field occurs as a direct result of neuronal actvity and so both dependent and related to that activity, which is quite handy as EEG is a useful diagnostic tool and if the field was independent of activity, then EEG would be pretty useless.

Exactly.

Nothing is ever 'proven', especially when we are dealing with a subjective experience. I take your point. And if this were a purely epistemological area I would agree with you. However, there is a huge clinical overlap where levels of consciousness, or assessment thereof, is critical to tratment and outcome. There are objectively observable differences in the correlates of consciousness; awareness, responsivity, cognitive cohesion, cognitive ability and so-on. Whilst you are quite right when you say these may not relate to subjective experience so, if a person feels there are no levels, then there are no levels, you would have to reconcile this with, for example, a patient with Alzheimer's coming into a period of lucidity who then shows distress at the realisation of what they're losing. There are states in which an individual is at a lower level of consciousness, but retains sufficient functionality to realise it. Well, as I have said (twice) "A thermostat was never aware, either of itself, nor of the concept of temperature. The flexion of a bimetal strip cannot be said by any means to represent a conscious response to increasing temperature, any more than the expansion of a stone in the sun.". Responsivity is only an observable correlate of consciousness, it is not in and of itself consciousness, nor is it an acceptable definition of consciousness. I think this is where our respective arguments begin to come together I see your point, but then this is where the difference between objective observation and subjective experience conflict. Subjectively it will always be the case that reality is what you percieve it to be. Objective observation would show that your level of consciousness it very different to that of your waking state. This is exactly the same problem as exists in pain management. Hospitals work to the philosophy that "The patient's pain is what they say it is", simply because, as with consciousness, nobody can ever know the pain of another. We can make inferences based on observations of pain correlates; antalgic gait, shielding, grimacing, verbal report etc., but none of these are pain. Pain has no physiological indices and is purely subjective. As with consciousness, there are different levels of pain. In this case, although only the sufferer is aware of the different levels, they can report changes. Nonetheless, as with our discussion of consciousness, we can debate the nature of pain on an epistemological level for ever, but it doesn't help the sufferer. Reality requires that we make best use of flawed measures of pain correlates in order to manage pain effectively. Again, I take your point. The difference between objective observation and subjective experience will always exist. However, as I say, there are cases where a person retains awareness of another level of consciousness. In cases where a healthy and bright individual suffers some physical trauma resulting in lowered levels of conciousness, the objective signs of which are (for example) impaired cognition and responsivity, i.e. the person cannot perform simple calculations, does not know who the prime minister is, cannot remember the date etc., it is not unusual to see such a person presented with a simple test question (e.g. a basic addition calculation) respond (albeit very slowly) with "I should know this...why can't I do this?". This suggests that on some level, despite their subjective experience being all there is for them, they retain some knowledge of their previous state or abilities. It is not unusual for such individuals to become quite distressed at the differences they can perceive between their current 'lowered' state of consciousness and their 'normal' level.

Sisyphus was speculating, but is quite right. Cuts involve edges of healthy tissue. Burns involve areas of damaged tissue. The damaged tissue breaks down and new tissue has to granulate in from the outer edge of the damaged area. You can get problems when the damaged tissue remains which impedes granulation so surgical debridement (very painful) is needed to 'clear the way', or when the damaged area dries out, killing a further layer. In burns, you also have the problem of eschar, which won't allow new tissue to form and has to be cut away.

Not offhand, but I know they're a lot higher at this time of year.

You won't find them in clinical psychology either. You may still find them used allegorically by Freudian Psychoanalytic therapists, but they are from a different area of psychology. Psychologists who work with clinical populations, e.g. clinical psychologists and health psychologists, have to use workable models.

Nobody is asking you to. "A thermostat was never aware, either of itself, nor of the concept of temperature. The flexion of a bimetal strip cannot be said by any means to represent a conscious response to increasing temperature, any more than the expansion of a stone in the sun." Except that there are degrees and levels of consciousness. Well, I'm not trying to persuade you of anything. That's because, as I said, there are problems with most definitions of consciousness. The main problem is its subjectivity which means that definitions often contain descriptions of correlates, such as responsivity or EEG activity. Self awareness is a facet of consciousness, but it too is one of those pesky subjective things in that we know it only in ourselves. True, but nonetheless, for many reasons we need a working definition. The best we can do is work with the least flawed, or at least, the most reliable one we can generate. You sleep, don't you? You cease to be consciously aware of your surroundings, yet your mind still works, albeit on a different level of consciousness. Just as they cannot prove your consciousness. But that is what I said; consciousness is entirely subjective. We can know it in ourselves, but only infer it in others. Where this is necessary (e.g. in clinical situations), we do so by using observable corrolates, such as responsivity to stimuli, measures of awareness of the environment, measures of cognitive function etc.. These are not direct measures of consciousness, but as a rule, these functions don't occur without it.

The principal givaway is that no legitimate bank would ask you to do that. All banks (at least in the UK), when warning people of these scams, state quite clearly that they would never ask customers to post their account information online.

There are levels of consciousness. It's not as simple as counscious or not conscious. There have been demonstrations of learning under general anaesthesia for example. Hospitals use instruments such the Glasgow Coma Scale to assess level of consciousness. The problem in most cases is the lack of correspondence between responsiveness and awareness, insofar as lack of response does not mean unaware. This is why staff are encouraged to talk to unconscious patients; tell them what's going on, what they (the staff) are doing to them and why etc. They are also discouraged from saying things they would not say in front of 'conscious' patients. A problem in such threads as this though is definition. What do people here mean by 'conscious', self aware (as in the above thread), or responsive to stimuli or any state between the two? In humans, the default state is self-aware. A thermostat was never aware, either of itself, nor of the concept of temperature. The flexion of a bimetal strip cannot be said by any means to represent a conscious response to incresing temperature, any more than the expansion of a stone in the sun. If you relate consciousness and awareness, then humans have many levels of consciousness in normal life. People asleep are less aware, but not completely unaware of their surroundings, otherwise nothing external could wake them. People absorbed in a book are less aware of their immediate surroundings too, less unaware than people asleep, but more than people not absorbed in a task. problems occur when people are outside of the normal range of cosnciousness due to physical trauma, ilness, anaesthesia and so-on, because outside of the normal range, the generally accepted link between consciousness and awareness as signalled by responsiveness (which works for all practical purposes), breaks down and becomes a dangerous assumption. The basic rule is that one cannot know. I know I am conscious, but I cannot know whether another person is. I make an assumption based upon their responses (or lack thereof). As I say, in daily life, these assumptions serve, but still, they are only assumptions and they do break down in clinical situations. The same issues exist in the treatment of pain. You cannot know the pain of another, you can only make assumptions based upon their behaviour (which includes self-report). Usually, this is no problem, but it gets tricky in clinical situation when the prescription of effective narcotic analgesia depends upon a relatively accurate assessment.

Yep, if your tapwater smells of anything other than water I would stop drinking it and tell somebody. No kidding. It might be ok, but given what can be carried in water, I wouldn't chance it. Take samples and contact the supplier to get it checked. Don't drink it, drink bottled water for the time being.

Pretty much what the others said: O- blood can be given to anybody, because it's pretty much neutral, making O- donors 'universal donors' insofar as what they donate can be given to the entire population (more or less). People of any other type, e.g. A+ (like me) can only donate to other A types (A+, A- or AB), although A+ blood tends to be high in platelets, so A+ donors often have their blood spun down for packed cells and platelets rather than just whole blood.

This includes the time it takes to remove their foot from the gas, change peddles and hit the break. Probably anticipation. A single trial won't give you an accurate measure of your reaction time. You need to do several trials, e.g. ~ 20 and calculate the mean. This will help iron out the variance inherent in the measure due to other factors; anticipation, concentration lapse, miss-hits and so-on. The values I present above are population norms (perameters) calculated from a huge number of trials done by a huge number of people. Do you mean emit or conduct? Large myelimated motor neurons conduct at around 300-400 metres per second. Small, non-myelinated fibres (e.g. C fibres) conduct at between 0.5 and 0.2 metres per second. There are a range of different afferent and efferent fibres that conduct at different rates between those two extremes.

The fastest reaction time is to a painful stimulus as this relies on a reflex arc rather than central processing. Mean reaction time (motor response to a simple visual stimulus e.g. a light) is between 300 - 500ms. Reaction time slows with increased levels of processing. Increasing stimulus complexity results in longer reaction times as does the inclusion of differentiation tasks, i.e. telling a red light from a green light and so-on.

O is the most common blood type (O neg is the 'universal donor'). AB is the rarest.

Three is a reasonable age. It's hard to pinpoint exactly when people start laying down solid memories (or at least, being able to recal them), but two seems popular (with a large standard deviation). The earliest memories tend to be flashbulb memories though. More pictures and less processes or scripts.

As far as I know that's the case, yes. It's also the case for other plants that can multiply asexually, although I suppose you could get bogged down in semantics. Each new 'generation' is simply a shoot from the plant, and so is simply an extension of the same plant. Take Clorophytum (spiderplant) for example. It produces long stems with new shoots at the end. These grow, pulling the stem down. Eventually they touch the ground and the shoots throw out roots and begin to take nourishment from the soil. They remain attached to the central rosette though and remain structurally a part of it. Eventually, the spread of new plants will crowd out the central rosette and it dies off, but the surrounding rosettes are, genetically, the same plant, just more spread out. However, they don't need to touch the ground. If they fail to reach the ground (say, growing on the edge of a cliff), these shoots will continue to grow, and in time will produce more shoots. This can go on and on. It's all the same plant. Eventually, one cascade will reach the ground and put out roots. There are many trees that can propogate in the same or similar ways. The crack willow is particularly good at it. It grows next to rivers and has evolved to be particularly brittle (hence the name). In moderate wind, twigs and branches snap off, float down the river and eventually stick in the bank at a bend where they root (regardless of which end sticks in). The new trees could be seen as new trees, but in reality, they are the same tree 'spreading out' to increase its chances of survival. Rhizome based plants work to the same principle. They're not strictly speaking producing new plants, it that the original plant is spreading out to take advantage of a particularly favourable patch of ground and to defend against being overwhelmed by other plants. There is (as far as I know) no constraint on how long they can live, as long as external condition remain favourable.

Not really. Trees can outgrow themselves. Eventually, their roots get too long for the efficient transport of water and nutrients to the canopy. This is why bonsai tend to live longer than trees in nature. They are regularly root-pruned. The canopies are also pruned so most of the living areas of a bonsai are actually quite young.

True, and other trees have comparatively short lifespans. One variety of larch for example, has an average lifespan of between 50 and 70 years in the wild. However, as bonsai, they can live for a lot longer.

Vibrations in air are vibrations in air. They are not sound. Sound is a sensory experience resulting from excitation of auditory centres in the temporal lobes. These two things correlate insofar as vibrations in air cause the timpanic membranes to vibrate, which in turn triggers mechanoreceptors in the cochlea which send electrochemical volleys to auditory centres. But there are exceptions. It doesn't always take vibrations in air to result in sound. Nor will vibrations in air always result in sound (e.g. congenital deafness). Examples of sound percived without vibrations in air include acute (or chronic) tinitus, or direct electrical stimulation of cochleal transducers, the auditory nerve or areas of the temporal lobes (electricity is not a mechanical stimulus). So, sound can be defined as a specific sensory experience associated with activity in auditory areas in the temporal lobes which usually, but not necessarily, results from the amplification of vibrations in air through the timpanic membranes and transduced by mechanoreceptors in the cochlea.

ctc7752: Why have you answered a thread that ended over a year ago? It's not as though you have presentd a new argument or anything. Simply adding a platitude to a dead thread is a little pointless, don't you think?