Glider

Capsaicin "is slightly soluble in water, but very soluble in alcohol, fats, and oils." (http://www.fiery-foods.com/dave/capsaicin.asp). I don't know about the sugar. I haven't heard of any reason for it, but then, I haven't looked for one either. It's intriguing though. I'll have to try it next time I have a chilli.

I doubt adding salt makes much of a difference at the molecular level, but I agee, it does seem to improve the taste. Given the nature of capsaicin (a plant alkaloid), the best way to counter the heat is to apply a mild acid. Citric acid works well, lemon, orange or lime, as does tannic acid in tea. A bad thing to do is to drink water, that just puts more capsaicin into solution, spreads it around some more and generally makes things worse.

The brain uses so much energy because it is constantly active. Plus' date=' there are around 146,000 neurons per square mm in the cortical surface which has a total surface area of ~2,200 cm^2. All these cells require energy. Because synapses allow information processing to take place. One long neuron is capable of transmitting information from one point to another, but that's it. Most (though not all) sensory pathways consist of three neurons; one from the receptor to the dorsal horn of the spinal cord (this neuron can have an axon over a meter in length), from the dorsal horn to the thalamus and from the thalamus to the appropriate area of the cerebral cortex. But the function of this pathway is simply to get information from the receptor to the brain. Once in the brain, the information needs to be processed. This requires synapses. The action at synapses can be varied. Synaptic transmission can be excitatory, resulting in an excitatory post synaptic potential (EPSP) or inhibitory, resulting in an inhibitory post synaptic potential (IPSP). Each cortical cell has many synapses. On a single cortical pyramidal cell there can be between 20,000 and 1,000,000 synapses (there are around 6x10^8 synapses per square mm in the cortex). Each cell requires input from many synapses in order reach its firing threshold. This input can take the form of many incoming signals from a few cells in a short time (temporal summation), or incoming signals from many diverse cells to dendrites all over the cell body (spatial summation). Given that the incoming signals can also be either excitatory or inhibitory, you can begin to see the potential for processing at this level. When you add to all that the different actions of different transmitter substances (which are only released at synapses), you can begin to see the potential for truly huge processing power, and why synapses are necessary.

And all before breakfast too

There is an application called Ring Central that acts as a phone & fax. You could check that out.

Thre isn't a type of nerve for each sensation. There are only a few types of afferent neuron A-alpha, A-beta (large, fast, myelinated fibres), A-delta (smaller, thinly myelinated) and C fibres smallest, slow, non-myelinated). What differentiates their functions is their axon terminals. Differenk kinds of touch receptors mediate different mechanical sensations; vibration, steady indentation, deep pressure and so-on. These are all mediated by speciallised receptors such as Pacinian corpuscles, Meissner's corpuscles, Ruffini corpuscles and Merkel receptors. Only two fibres mediate thermal sensation; A-delta and C fibres. These are primary afferents, also known as nociceptive afferents, becauce they also mediate pain sensation. A-delta fibres are associated with both thermal and mechano-thermal receptors. They mediate warmth, non-noxious cold and mechanical senstation, and are also associated with sharp-pricking pain. C fibres are also accociated with thermal and mechano-thermal receptors. C fibres are polymodal and have a wide dynamic range in that they are not as specific as A-delta fibres in the range of stimulus intensity they respond to. C fibres respond to noxious heat and cold, and are associated with slow, burning or aching pain. So, in answer to the original question "are there 2 types of nerves for this (one for hot and one for cold) or is it the same nerve that gives off a different signal to the brain", there are two types of nerve that mediate thermal sensation. Both mediate hot and cold, but the wide dynamic range C fibres also mediate painful heat and cold. "what "chems" are released.... When a receptor is subjected to the stimulus it is specific to it depolarises. The chemical action of depolarisation is more or less the same in every nerve cell. There is a sodium influx raising the potential of the fibre from -70mv to around +40mv. The sodium influx is followed by an efflux of Potassium, and the sodium potassium pump also helps to repolarise the cell. However, C fibres release Substance P as a neurotransmitter. Substance P, once released contributes to oedema and hyperalgesia (increased sensitivity to pain) by causing vasodilation and the release of histamine from mast cells. ...and or how does the signal to the brain differ if it`s only an electrical signal?" An action potential is an action potential, and they are all pretty much the same. The reality is that if you cause depolarisation in a cold receptor, then the sensation will be perceived as cold, even if you used electricity to depolarise the cell. This is lablelled-line coding. Activity in a specific sensory fibre will always be perceived as the sensation the fibre is specific to. So, if by some means you could use sound to exite rod & cone cells in the retina, then that sound would be perceived as light. In reality, rod and cone cells will only respond to light, but all sensory receptors can be depolarised by mechanical deformation. If you push the side of your eyeball, you deform a part of the retina and this will be perceived as light. A more common example is eating chilli. The active ingredient in capsaicin, this is a crystalline alkaloid and is neither hot nor cold. However, it does quite specifically target C fibres (it is toxic to them and causes in influx of calcium, which eventually kills the cell. This is why people can adapt to hotter and hotter chilli/curry). So, although capsaicin is neither hot nor cold, it does trigger receptors that mediate hot & cold sensation. It triggeres them a lot, causing high frequency volleys of action potentials, which are perceived as noxious heat, although there is no actual noxious tempterature involved.

Running ANOVA on SPSS will tell you only whether or not there is a significant effect. It will not tell you where the effect is. You say you have F, df & p. If p < 0.05 then there is a significant effect. The easiest way to find out where the effect is, is to generate a table of means or a bar chart of means. Either of these will show you which condition differs most from the others. If you need more detail, (i.e. the effect is not clear, or more than one condition shows an effect) then you should run post-hoc analyses (Tukey's HSD is good). Your question would be easier to answer simply, if you gave more information about the experiment, IV? Levels? DV? and so-on.

I use Waxoyl in the winter. A wipe down with a rag soaked in waxoyl is enough. The stuff goes hard (like wax) and usually lasts all winter. Not sure I'd want to scrub my chrome with ally foil. I'd like to see it done on someone else's chrome first

On my Harley I use polymer sealants (e.g. dynaglaze diamond seal or auto glym) on all chrome except the pipes. This stuff forms a very effective barrier against water and other junk you don't want building up (you can watch water just bead up and run off it). On the pipes I just use a chrome cleaner. It doesn't leave any residue to burn and discolour. For burned on stuff (happens occasionally, as you know), I use solvo autosol. It's very mildly abrasive which helps in removing the crud, but nowhere near abrasive enough to mark the chrome.

That pretty much it. The stimulus of getting hit in the leg with a football will be the same, summer or winter, but in the summer, the large, fast conducting fibres run interference. The signals they conduct dampens the signals from the slower primary afferents associated with pain (Gate Control Theory of Pain; Melzack & Wall). In the winter, when your skin temperatue drops, it knocks out these larger fibres and their dampening effect, so the majority of the signals you get is from pain associated fibres, so though the stimulus is the same, it hurts more.

This is because large sensory fibres begin to struggle with transmission at around 7 degrees C, but the primary afferents (associated with pain), particularly C fibres, don't stop until about 4 degrees C. So, put simply, when you're hands/legs whatever are very cold, the only fibres left working efficiently are pain fibres. That's why it hurts so much more to get hit in the leg with a footbal in the winter, than in the summer.

True, but do memories take up volume? Do data take up physical volume in a memory chip, or does it simply alter the state of the existing media? In the brain, similar to chips, memories change the state of the media and so do not take up volume. Further, in the brain, the media is plastic. Learning involves physical as well as chemical changes, so the capacity changes as we learn. Moreover, each individual neuron can 'store' information pertaining to many, many different memories. Therefore, for all practical purposes, you have storage media that expands as you try to fill it.

Why is it obviously finite?

A woman, without her map, is lost. There 'y go. One character changed, the sentence is now in favour of the female as it assumes map reading ability. Just kidding, honest!

Toothace and orofacial pain like myalgia aren't subject to central control mechanisms to the same degree as somatic pain. We have our own mechanisms of pain control, which originates in the periaqueductal grey area (PAG; a nucleus around the cerebral aqueduct). This projects down through the raphe magnus nucleus in the brain stem and down the raphespinal tract. It terminates in the dorsal horn of the spinal cord, which is where the incoming primary afferents enter. Stimulation of the PAG has been shown to produce profound analgesia in rats, and has also shown significant effects in humans. However, toothache and other orofacial pain is mediated by cranial nerves V & VII (Trigeminal and Facial) which don't enter the spine, but project straight to the brain, and so are not subject to this central control mechanism.

I don't know that much about the mechanisms of hypnosis, but it sounds like it might have elements in common. It actually sounds more analogous to some of the visualisation techniques used in chronic pain management.

This is not strictly true, partly because of what I explained in my previous post, and partly because there isn't really any such thing as a pain receptor. In humans, there are receptors associated with nociception, but they are not strictly speaking, pain receptors. For example, there are two classes of primary afferent fibres; A-Delta and C fibres. A-Delta are associated with sharp, fast pain (they are small diameter, thinly mielinated fibres). C fibres are associates with slow aching and burning pain (they are small diameter, non-myelinated fibres with slow conduction rates of around 0.5 meters s1). However, C fibres are polymodal, they are triggered by a wide range of stimuli and are particularly associated with detection of temperature change, as well as noxious heat (>~58 degrees C) and cold. Volleys in A-Delta and C fibres are associated with pain, but do not necessarily result in pain as they have other functions. Pain is actually based on neurological interpretation of incoming primary afferent volleys. The experience of pain is a result of the way in which the brain processes and interprets these incoming volleys. Pain itself is a psychological state and as such is sensitive to psychological intervention. Therefore, the ultimate experience of pain is more dependent on the brain and its systems than on the numbers of 'nociceptive' receptors.

Well this is where it gets tricky, because here you have to start differentiating between nociception and pain. Nociception refers to the physiological detection, transduction and transmission of noxious stimuli (and nociceptive volleys) to the brain. Pain refers to the ultimate experience. Even then, the experience can be subclassified into to components pain and suffering (for example, morphine, the most effective known analgesic, exerts it greates influence on the suffering component of pain, rather than the nociceptive component). Believe it or not, nociception and pain are not directly linked in a rigid cause/effect relationship. They only correlate. The ultimate experience has been shown to be largely independent of the frequency of nociceptive volleys. In other words, the intensity of the stimulus (higher intensity = higher frequencly nociceptive volleys), is not directly related to the intensity of the experience. Whilst as a general rule, there is a 'working correlation', e.g. the higher the stimulus intensity, the greater the experience of pain, there are too many exceptions to accept a direct causal relationship. Examples of the dissociation exist at both ends of the continuum, e.g. at one end there are examples of pain (real pain) with no organic cause, i.e. no nociceptive activity at all (thelamic pain is an example of this). At the other end, there are examples of significant physical trauma, that does not result in pain, e.g. the Indian hook swinging ceremony, surgery under hypnosis etc.. This latter phenomenon supports YT's contention of 'there must be a way to make it go'. I believe there is, but we haven't found it yet. However, as an aside, the ultimate aim is to control pain, not to abolish it. Pain is absolutely necessary for survival.

No such rule that I am aware of. Memories are not 'overwritten' in the strict sense of the term, although they can be radicly altered by a number of factors not directly to do with the events being remembered.

Yes, but the degree would depend upon the severity. You can have mild conjuctivitis which shows as an inflammation, but is not really uncomfortable.

Not necessarily. It's going to depend on the systems within the brain/nervous system. Obviously, something with an extremely tiny brain (e.g. invertebrates) is less likley to have the mechanisms required to produce the experience of pain, but mammals all have more or less the same structures to varing degrees, so whilst the brain of a cat is a lot amller than the brain of a human, cats can experience pain very well. The problem is that pain is a psychological state, so the ultimate experience will be determined by the psychology of the organism experiencing it. Humans, for example, have expectancies concerning the meaning and probable outcomes of our situation, which many animals don't have. So, for example, take two male humans, one of whom has been warned by his doctor to quit smoking, lose weight and so-on because he is at risk of a heart attack. The other male has been given a clean bill of health. Both go to a business dinner and both subsequently suffer severe indegestion (i.e. a burning chest pain). Do you think that each of these two will experience the pain in the same way? (hint: No). The one that was warned will suffer a lot more because his pain also includes heightened anxiety, fear (of death) and so on. But they both have brains of the same size.

If you were including the entire range of sub-disciplines, I would say yes, it's a bit of both. I hesitate to just say yes without that clarification because it's misleading to those who think Psychology is a single, narrow area. Certainly the more qualitative areas of research have to be considered an art. For example, data collection there is usually by interview, and the skills and personality (and even apperance) of the interviewer will strongly influence the data you get. So, no two interviewers could hope to get exactly the same data from the same respondent. Interviewing is pretty much an art I'd say. At the other end of the range, if you are looking at the effects of (e.g.) the neurological response to subliminal exposure to valenced stimuli using EEG or fMRI, then any researcher with a good working knowledge of the kit can obtain the same measures from the same person. At this end of Psychology, there is grater scope for control, which means 'true experiments' (i.e. experiments designed to test for causal relationships between the independent and dependent variables) can be conducted. At the softer end, there is no such scope for control, so experiments are pretty much out of the question.

Theoretically, no, there is no limit to the information we can store. There used to be something called 'the leaky bucket theory', which proposed that memories were eroded over time. This was joined by the 'interference theory' which posited that older memories were 'overwritten' by newer, more salient memories. However, Wilder Penfied (Canadian brain surgeon), whilst stimulating areas of the brains of patients with a microelectrode found that in certain areas of the temporal lobes, this stimulation would elicit clear memories of entire conversations and other things like songs, that the patients had heard as children, but had subsequently 'forgotten'. The predominant belief now is that once we have encoded a memory, it stays. If we can't remember it at a later date, it's not that the memory has gone, it's that the traces to the memory have gone. It's a failure of recall rather than memory (these are different processes). If we are later exposed to something that links to the memory, it often returns; information that we thought we had forgotten can suddenly pop into our minds.

Newtonian, in what way is Aardvark contradicting himself, and where is the attempt to ridicule?