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Key Articles 1Key articles relative to quantum consciousness theory 1.) Anaesthesia & consciousness - Hameroff 2.) Quantum & classical modes of processing - Hameroff & Tuszynski 3.) Reply to Grush & Garland - Penrose & Hameroff 4.) More neural than thou - Hameroff 5.) A neural mechanism that randomises behaviour - R.H.S. Carpenter 6.) Microtubules in memory and consciousness - Nancy Woolf 7.) Consciousness, neurobiology & quantum mechanics - Hameroff 8.) The dendritic cytoskeleton Anaesthesia, consciousness and hydrophobic pockets Stuart Hameroff Studies made in recent decades indicate that anaesthetic gases act on hydrophobic regions of proteins. Studies include Wulf & Featherstone (1957), Franks and Lieb (1982-94) and Halsey (1989). The anaesthetic gases act on hydrophobic pockets with van der Waals forces providing solubility for the gases. The forces act between anaesthetic molecules and non-polar amino acids. The post-synaptic receptors for neurotransmitters, such as, GABA, serotonin and acetylcholine are the areas most susceptible to anaesthetics, and they allow both excitatory and inhibitory functions to be effected. However, anaesthetics appear to effect a wide range of proteins, including receptors, ion channels, second messengers, microtubules and other cytosleletal proteins. The mode of operation of anaesthetics is taken to be suggestive of the involvement of quantum activity in consciousness. Proposals for quantum consciousness include Beck & Eccles who suggested there could be probabilistic behaviour in neurotransmitter vesicles. Stapp links pre-synaptic calcium inflow to the possible collapse of the wave function. Protein function depends on its shape and conformation. Proteins are created out of chains of amino-acids. The folding of protein depends on the attractions and repulsions of amino-acid side groups. Computer simulation or prediction of the folding of protein has proved difficult, with the suggestion of the possible need for quantum computing, in order to deal with this type of problem. The main driving force in proteins are non-polar amino acids, repelled by water and attracted by van der Waals forces. They are non-polar but polarisable. Anaesthetics may prevent conformational switching in protein. They may inhibit electron mobility, which may be required for protein dynamics to function. Search for quantum & classical modes of information processing in microtubules Stuart Hameroff & Jack Tuszzynski Biochemical energy is provided to microtubules in several ways, including from tubulin bound GTP which is hydrolysed to GDP. The forces operating among amino acid side groups in protein include ions, and dipoles including van der Waals forces. Hameroff suggests that the tubulins could be the bits of a calculating system. Hameroff and Tuszynski say that by using the Protein Data Bank and the Tinker molecular dynamic package, they have demonstrated quite a high negative charge on tubulin at normal pH, with 40% of this concentrated in the tail-like ‘C’ terminal of the monomer. It is also indicated that mapping of electrostatic charges in the tubulin shows two wells of positive charge near the junction between the alpha and the Beta monomers, which mapping work suggests would result in quantum tunnelling. W. Bras (1) has demonstrated microtubules align parallel to magnetic fields, and this is also considered as likely to allow electron tunnelling. Work by Binhi et al (2) indicates the existence of unpaired electron spins for networks in protein interiors, which are shielded from the environment and lead to functional quantum interaction at physiological temperatures. The conclusion of the article is that work on microtubules and the component tubulins suggests several mechanisms for quantum information processing. Reply to Grush & Garland Roger Penrose & Stuart Hameroff Journal of Consciousness, 1995, 2 (2) pp. 99-112 One interesting thing about this reply is that exists at all. Commentators on quantum consciousness are apt to quote the Grush & Garland article as a comprehensive dismissal of the Penrose/Hameroff model, without even mentioning that there was a reply to it. Penrose and Hammeroff claim that Grush & Churchland’s (G&C) arguments are misleading, and that with respect to the physiological evidence of the brain they are factually incorrect. With respect to non-computability, their main argument hinges on the statement that mathematical thinking can contain errors. Penrose says that he does not deny this, but does not see it as invalidating the Gödel argument. Penrose also says that G&C claim that he said that in some and perhaps in all instance human thought was sound but non-algorithmic. He states that this is incorrect and that he never denied that human thought and even rigorous mathematical thinking could be in error. Penrose says that he wishes to restrict the argument to P1 sentences, which are sentences that assert that a particular computation does not halt. An example of a P1 sentence is the Goldbach conjecture, which states that ‘every even number greater than 2 is the sum of two prime numbers. It is an assertion that the computation does not halt, in the sense that it says that a programme looking for an even number that was not the sum of two primes would never find it and would therefore never come to a halt. Penrose says the issue is as to how accessible to human reason P1 sentences are. G&C also claimed that there was no evidence that non-computability was involved in quantum gravity. Penrose replied that there was some evidence. This relates to the work of Geroch and Hartle, which showed that there was no algorithm for certain problems related to the superposition of four dimensional space-time, which is in turn closely related to Penrose’s version of quantum gravity. Grush & Garland on Physiology The latter part of the reply is devoted to G&C’s criticisms relative to the physiology of the brain. They claimed that a drug, colchicine, which is used for the treatment of gout, acts by depolymerising microtubules, but does not result in the loss of consciousness. In reply, Hameroff says that this argument fails to take account of differences between microtubules in the body and microtubules in the brain. The brain microtubules are much more stable. In its medical use colchicine does not penetrate to the brain, but animal experiments where it has been administered to the brain show that brain microtubules do not depolymerise. The differences between brain and body microtubules also appear to account for the fact that consciousness does not arise in the other parts of the body. G&C and other commentators have seen the restriction of consciousness to the brain as an argument against the microtubule theory. In general, brain microtubules are more stable and exist in denser networks than those in other parts of the body. G&C also queried how microtubules communicated with the cell membrane and in particular with the synapses, since microtubules, which extend most of the length of the axon stop some way short of the synapses. Hameroff answers that the connections are made by smaller cytoskeletal proteins and some incoming communication is via second messengers. They also question how microtubules encode information. Hameroff agues for the suitability of the cyclical lattice for information processing, although more complex arguments for amino acid structures and quantum tunnelling appear in later papers. He also quotes Vassilev (1985) for evidence of signal transmission. Here again, there seems to have been some more recent data for signalling since the Penrose/Hameroff reply was published. G&C suggested that sodium, calcium and magnesium ions would cause decoherence in cytoplasm, but the reply denies this on the grounds that the ions are smaller than the surrounding water molecules. More neural than thou (Reply to Patricia Churchland's 'Brainshy') Stuart Hameroff from: 1996 Tucson discussion and debates Patricia Churchland is an exponent of the mainstream neural theory of consciousness, where consciousness arises from the firing patterns of neurons driven by axonal synapses. Hameroff principally criticises the neural theory for what it leaves out, notably the failure to take account of what is going on inside the neuron, particularly in respect of probabilistic firing of synapses, the role of the cytoskeleton and dendritic processing. The discussion stresses that there is no consensus regarding the anatomical sites of anaesthetic effect. The anaesthetic molecules are widely distributed in the brain. Frank & Lieb (1) and Halsey (2) have shown the anaesthetics act directly on proteins, rather than on membrane lipids, which was the older theory. The anaesthetics work on hydrophobic pockets in proteins, including hydrophobic pockets in microtubule tubulins. GABA is particularly important for anaesthetics and this receptor is regulated by cytoskeletal microtubules. A Neural Mechanism that Randomnises Behaviour R.H.S. Carpenter Physiology Laboratory, University of Cambridge Journal of Consciousness Studies, vol. 6, No. 1, 1999, pp. 13-22 The paper starts by stating that the time taken to react voluntarily to stimulus is far longer than can be accounted for by known nervous system processing. The strength of response is shown to rise in proportion to the incoming sensory data, until a critical level, at which point action is taken. However, the rate of rise fluctuates randomly from trial to trial. This claim is based on studies of neurons in the frontal eye field and the time taken between presenting a visual stimulus and making a saccade (an eye movement). The saccade itself is very quick, lasting only 20-30ms. The average gap between presentation of the stimulus and the saccade is 200ms. Normal processing in the nervous system is claimed to account for at most one third of this time. The shortest route from the retinal receptors to the eye muscles passes through the superior colliculus and should take only 60ms. However, the colliculus receives input that comes ultimately from parietal cortex and the frontal eye fields. The control is inhibitory, otherwise the eyes would be constantly darting towards each and every stimulus. The blanket of inhibition has to be lifted for a saccade to be made. The colliculus lacks the information to make useful decisions, because it registers only where things are in space, but not what they are. The biggest problem is seen to be that over a series of trials the response time varies over a surprisingly large range. While the average saccadic latency is 200ms, on some 5% of trials the latency is either less than 150ms or more than 300ms. In the first stage of the latency period neurons distinguish between a target stimulus and distractors. This takes about the same period of time, about 70ms, whether the eventual latency period is short or long, so the whole of the variability is concentrated in the latter part of the latency period. The paper suggests that this means that the variability is not due to noise in the sensory pathways, but to something actually introduced by the brain. The randomness of the reaction times is seen as a function of deliberate randomisation by neural processes in the brain. Carpenter does says that the underlying process is obscure, although he mentions that its is consistent with the Penrose/Hameroff model, and that the delay periods involved are similar to those seen in Libet’s experiments. Microtubules in the Cerebral Cortex: Role in Memory & Consciousness Nancy Woolf Behavioural Neuroscience, Dept. of Psychology, UCLA In: Tuszynski, J. ED. The Emerging Physics of Consciousness Springer ISBN-13 978-3-540-23890-4 The author starts by querying whether the standard model of synaptic connections in the cerebral cortex adequately accounts for cognition. Neurotransmitters are indicated to act on microtubules, as well as membrane receptors. It is argued that this action on microtubules is related to the physical basis of memory and consciousness. It is suggested that learning alters microtubules, and that this forms the basis of long-term memory storage. The storage microtubules determine the synapse strength by directing actin filaments and transport of synaptic proteins. Neurons are filled with microtubules, actin filaments and neurofilaments. The microtubules comprise alpha and beta tubulin dimers, and have plus and minus ends. The plus ends undergo polymerisation/depolymerisation cycles to a much greater extent than the minus ends. The tubulin that comprises the microtubules accounts for up to a quarter of the soluble protein in the brain. Microtubule asociated proteins (MAPs) are found in high concentration in neurons. MAP2 is particularly abundant in dendrites. Areas possessing many pyramidal cells associated with higher cognition, are ofen rich in MAP2 , suggesting a connection between this protein and cells involved in higher cognition. MAP2 expression is also altered by the recent experience of learning. The connection between microtubules and synapses is indirect. The region of the dendrites where microtubules are concentrated is called the sub-synaptic zone. The microtubules are connected with the dendritic spines by actin filaments. The proteins MAP2 and MAP1B provide the link between actin and microtubules ( 1 Dehmelt & Halpain). Protein kinases regulate the binding process. It has been suggested elsewhere that there is no connection between microtubules and dendritic spines, but the author here appears to describe a full mechanism. MAP2 has been identified as a signal transduction molecule and it also anchors other signal transduction molecules. Signal transduction by MAP 2 stems from synaptic inputs. MAP2 is also indentified as a gelation factor, a process that rigidifies microtubules, and in the Penrose/Hameroff model this is suggested to screen microtubule quantum activity from decoherence. Ionic currents from receptors penetrate the sub-synaptic area of the microtubules. AMPA receptors can also affect microtubules via the actin filaments. Proteins link the synaptic density with the actin filaments, and the actins in turn link to microtubules ( 2. Qualman, Ladrech). Glutamate also binds to the NMDA receptors. Activation of the NMDA receptor results in an influx of calcium ions. These have the capability to penetrate deep ito the neuron, so it is likley that they come into contact with microtubules. Recent studies have shown that the shape of dendrite spines is altered by learning and experience ( 3. Yuste & Bonhoeffer ). Synapse and dendrite spine densities are also altered by learning ( 4. Leuner ). On the basis of various studies, the author thinks that neither dendrite spines nor actin near spines is sufficiently stable to act as permanent memory store. This suggests the hypothesis that the permanent memory store is in the sub-synaptic zone of the dendrites. High concentrations of ATPase in the subsynaptic zone suggests a high metabolic rate, which would be requirement of laying down memories. Microtubules are also more stable than actin spines, partly due to their connection with associated proteins. Plus end binding proteins help to stabilise the plus end of the microtubules. The initial segments of neurites are exceptionally stable, and the means available for stabilising microtubules makes them good candidates to act as memory stores. Polymerisation/depolymerisation cycles are used to update the microtubule network. Plus ends of microtubules near the sub-synaptic zone are affected by glutamate synaptic activation and with the additional presence of a neuromodulator, there will be widespread effects along the dendrite shaft. Woolf quotes initial experimental evidence that changes in dendrite spines may depend on microtubules. The alkaloid, vinpocetine, increases spine changes, because of its effects on microtubules ( 5. Lendvai ). It is suggested that microtubules could initiate or maintain potentiation of synaptic acivity. The dependence of long term potentiation (LTP) on the transport of AMPA receptors along the microtubules is suggested as evidence for this. Studies demonstrate the importance of MAP2. Mice bred with a knockout of MAP2 show a reduction in microtubule density and dendritic length. Microtubule transport is seen as important for learning. Brain reorganisation following learning leads to increased receptors in the post synaptic density and decreases further transport to the synapse. There is usually an inverse relationship between microtubule transport activity and stability, and the reduction in transport here suggests increased microtubule stability. Experiments with learning involving MAP2 and kinesin suggest that microtubules are central to learning and memory. The author asks how it is that stored memory is able to influence neural processing. The ways in which microtubules could do this include effect on the size and position of synapses, and transport rates of protein and RNA. Microtubules regulate or effect some ion channels, an example being cytoskeletal proteins regulating the GABAa channel ( 6. Whatley ). Microtubules self-initiate activity such as polymerisation/depolymerisation, so they are good candidates for self-iniating memory effects. If microtubules do not initiate these changes another candidate needs to be changed. The author looks for something that can initiate the direction of attention, and suggests that the polymerisation/depolymerisation of microtubules could allow then to search for and activate particular sub-synaptic areas, including those connected with attention and consciousness. Sleep The paper also looks at sleeping and waking in relation to the general question of consciousness. The waking brain is a complex mix of alpha, beta and gamma waves, while in dreamless sleep there are fewer theta waves and more delta waves. In REM sleep the wave patterns are more akin to waking. Neurotransmitter levels change over the sleep/wakefulness cycle. Acetylcholine, noradrenalin and serotonin levels are high duting wakefulness but low during non-REM sleep. During REM sleep acetylcholine levels are high, but noradrenalin and serotonin levels are low. This suggests that noradrenalin and serotonin are important for dealing with incoming stimuli. The author considers it likely that the microtubule network organises the release of neurotransmitters. Further to this, the author searches for what it is that provides the motive force to drive movement and thought. Microtubules are suggested as good candidates, because the polymerisation/depolymerisation cycle microtubles are capable of influencing membrane potentials. The paper proposes that long-term memory storage is concentrated in the sub-synaptic zones beneath the dendritic spines. This differs from the mainstream view of memory storage that pinpoints changes in the actual synapse, the post-synaptic membrane, dendrite spines and receptor density. It is suggested that there is a mechanism keeping receptors and spines within certain parameters, which would appear to limit usefulness in terms of memory storage. On the other hand, changes in dendrite structure that occur with learning indicate probable long-term changes in the underlying microtubules. Binding Problem The brain is not that heavily interconnected, and a part of the 'binding problem' is that brain areas that are unified in perception are not necessarily communicating. Thus the left and right visual fields may not be in communication, but are still unified. The author suggests that the sub-synaptic areas in dendrites are connected by microtubules and that quantum entanglement in the microtubules deals with the binding problem. The paper points out that the tubulin structure of the microtubules allows dimer/dimer interactions to be felt for a long way along the microtubule. The author rejects the idea that coherence cannot persist in brain tissues pointing to an opposing calculation ( 8. Hagan). MAP2 interactions would suggest that if entanglement does exist in microtubules, it could exist between different microtubules in the same neuron. The third stage would involve entanglements between microtubules in different neurons. This is suggested to be possible via the action of gap junctions. Changes in MAP2 that are uniform within cortical modules could suggest entanglement ( 9. Woolf & Hameroff ). Other studies ( 10. Ghosh et al and Veral ) calculate that a very small amount of entanglement can produce significant effects in the macroscopic world. All the history of a synapse could be stored in the microtubules in the sub-synaptic zone. Consciousness, Neurobiology & Quantum Mechanics: The Case for Connection Stuart Hameroff In: The Emerging Physics of Consciousness, Ed. J. Tuszynski Springer, 2006 ISBN-13 978-3-540-23890-4 In this chapter in 'The Emerging Physics of Consciousness', Hameroff classifies all the mainstream approaches to consciousness as 'classical functoionalism'. Functionalism takes no account of what the brain is made of or of anything finer grained than the level of neuron-to-neuron connections. It beleives that these connections could be copied in another material such as silicon, and that the resulting construct would be conscious. However, Hameroff argues that although axonal spikes and synaptic connections clearly play a key role in information processing in the brain, they may not be the main currency of consciousness. He considers that quantum processing in microtubules within the dendrites and gap junctions between dendrites are the main currency of consciousness. The main case against quantum processing in the brain has always been the view that any quantum coherence in the brain would decohere faster than the time taken for any useful biological process. Hameroff accepts that this is in principle a valid argument. However, he claims that a gelatinous non-liquid ordered state can arise in the neuronal interior, and provide screening for microtubules against the rest of the environment. A further objection to quantum processing was that even if it arose in one neuron, it would be difficult for it to communicate across the brain. This is countered by the suggestion that there could be quantum tunneling at gap junctions between neurons. In recent years, gap junctions have been discovered to be more widespread in the brain than was previously thought. They are also related to the 40 Hz gamma synchrony. This oscillation was at one time promoted by Crick and Koch as the most promising correlate of consciousness. However, the idea fell from favour, when it was discovered that the gamma synchrony correlated with dendritic activity rather than axonal spiking. In general, Hameroff argues that the emerging evidence of neurobiology has moved in favour of the ORCH OR model over the last decade, not withstanding the continued unpopularity of the theory. Hameroff summarises his proposals in the early part of the chapter. He thinks that consciousness arises in the dendrites of neurons that are connected by gap junctions to form 'hyperneurons', and that these are related to the gamma synchrony. Axonal spikes and synapses are seen as making inputs to and receiving outputs from the microtubular process as part of an interactive systems. Backward Referral in Time The recent evidence of neurobiology suggests periodicity in perception and reaction times, notably the gamma synchrony and the alpha and theta waves. The former has sometimes been promoted as a correlate of consciousness, and the latter related to visual activity. Hameroff also touches on the famous Libet experiment that demonstrated a 500ms timelag between a stimulus and the perception of it entering consciousness. The subject is not aware of this time lag, as a result of so-called backward referral of the perceived timing of the event. Hameroff thinks that the backward referral in time should be taken seriously, and Penrose thinks that quantum processing could be involved in the backward referral effect. This is not as far fetched as it sounds, since the laws of physics, as embodied in the Maxwell and Schrodinger equations, do not preclude backward travel in time. It is just that we do not experience objects or even rays of light arriving from the future, and there is a further argument in the form of the 'grandfather paradox' by which we could travel into the past and kill our own grandfather. However, this is an argument against macroscopic objects travelling a significant time into the past, it does not appear to preclude a 500ms adjustment within the brain. Hameroff points out that some physcists think that backward referral in time is the best way to account for non-local correlations or EPR effects by which a measurement on one particle instantaneosly effects another distant particle. Hameroff suggests that consciousness could be referred back to the original unconscious evoked potential (EP) in the brain. Particular mental states are normally associated with the action of assemblies of neurons. Hameroff asks why such brain assemblies should have the quality of consciousness. Daniel Dennett and Susan Greenfield both argue that brain activity accompanying consciousness is the same kind as unconscious brain activity. The conscious activity is simply the most powerful or successful bit of brain activity and therefore enters consciousness. Baars introduced the idea of the global workspace, a layer of neurons in between sensory inputs and executive functions, but this seems to only propose are architecture for where consciousness could occur in the brain, rather than an explanation of how it could arise from neurons in the first place. Hameroff points out that changes in dendrites can lead to increased synaptic activity. This is basic to ideas about learning, memory and neural correlates of consciousness. The changes in dendrites involve the number and arrangement of receptors, dendritic spines and dendrite to dendrite connections. Axon potentials or spikes have been assumed to be the main basis of consciousness, but Hammerof suggests that there could be other candidates. Electrodes placed on the scalp detect mostly dendritic activity in pyramidal cells. The main function of dendrites is seen to be the handling of input signals into the neuron which may eventually result in an axon spike. However, this is not the whole story, since many cortical neurons have dendrites but no axons. Here dendrites interact with other dendrites. The evidence suggests that there are complex logic functions in the dendrites, and these may oscillate over a wide area, while remaining below the axon spiking threshold. Gamma Synchrony Gamma synchronies, in the 30-70Hz range, have aroused interest as possible correlates of consciousness. Gray and Singer (1) found coherent gamma oscillations in the brain that were dependent on visual stimulation. It was suggested that this synchrony could solve the binding problem, which is the problem of how the different inputs into the brain are bound together into a single conscious experience. It was suggested that the synchrony reflected the activity of a relevant assembly of neurons. Varela (2) noted that synchrony operated whenever the processing of spatially separated parts of the brain were brought together in consciousness. Gamma synchrony has been demonstrated across cortical areas, hemispheres and the sensory/motor modalities. The synchrony is involved in a range of brain activities including perception of sound, REM dream sleep, attention, working memory, face recognition and somatic perception. Also gamma decreases during general anesthesia and returns on waking from this. Hameroff regards gamma synchrony as the best overall correlate of consciousness. He further addresses the question of how the gamma synchrony is mediated. There is coherence over large areas of the brain, sometimes including multiple cortical areas and both hemispheres of the brain, with zero or near zero phase lag. If the synchrony was based on the axon/synapse system a considerable lag would be expected. Hameroff proposes gap junctions as an alternative to synapses for connections between neurons. Neurons that are connected by gap junctions depolarise synchronously. Gap junctions play a more important role in the adult brain than was previously supposed. Numerous studies (3) show that gap junctions mediate the gamma synchrony. A neuron may have many gap junction connections, but not all of them are necessarily open at the same time. The opening and closing of the junctions may be regulated by the microtubules. Hameroff suggests that cells connected by gap junctions may in fact constitute a cell assembly, with the added advantage of snchronous excitation. Cortical inhibitory neurons are heavily studded with gap junctions, possibly connecting each cell to 20 to 50 others (4). The axons of these neurons tend to form inhibitory GABA chemical synapses on the dendrites of other interneurons. Cytoskeleton Hameroff moves on to discuss the role of the cytoskeleton, which is seen to determine the structure, growth and function of neurons. Actin is the main constituent of dendritic spines, and is present throughout the neuronal interior. Actin can depolymerise into a dense network, and when this happens the interior of the cell is converted from an aqueous solution into a gelatinous state. The whole of the cytoskeleton then forms a negatively charged matrix around which water molecules are bound into an ordered state (5). It is particularly remarked that the neurotransmitter glutamate binding to NMDA and AMPA receptors cause gel states in actin spines (6). The cytoskeleton of the dendrites is distinctive from both non-neuronal cells and the axons of neuronal cells. The microtubules are short, and have mixed polarity. This appears a sub-optimal arrangement from a structural point of view, and it is suggested that in conjunction with microtubule associated proteins (MAPs) this arrangement may be optimal for information processing. These microtubule/MAP arrangements are connected to synaptic receptors on the dendrite membrane by a variety of calcium and sodium influxes, actin and other inputs (7). Alterations in the microtubule/MAPs network in the dendrites correlate with the arrangement of dendrite synapatic receptors (8). Some studies (9) demonstrate that the cytoskeleton is also involved in signal transmission. It is suggested that the microtubule lattice could be more than just convenient wiring. The lattice is well designed to represent and process nformation. The microtubule is comprised of pieces of tubulin capable of representing bits of information. Tubulin switches between two conformations. It is suggested that tubulin conformational states could interact with with neighbouring tubulin by means of dipole interactions. The dipole-coupled conformation for each tubulin could be determined by the six surrounding tubulins. Hameroff describes protein conformation as a delicate balance between contervailing forces. Proteins are chains of amino acids that fold into three dimensional conformations. Folding is driven by van der Waals forces between hydrophobic amino acid groups. These groups can form hydrophobic pockets in some proteins. These pockets are critcal to the folding and regulation of protein. Amino acid side groups in these pockets interact by van der Waals forces. Non-polar atoms and molecules can have instantaneous dipoles. Anesthesia Hameroff discusses the process of anesthesia which erases consciousness, but leaves many non-conscious functions intact. Anesthetic gas molecules are soluble in a lipid-like hydrophobic environment. Such areas are present in the brain in the lipid regions of cell membranes and in hydrophobic pockets within proteins. It is suggested that anesthetic gas molecules interact with amino acid groups via London forces, altering the normal action of London forces on the conformation of protein. Hameroff further looks at quantum information processing. Quantum superpositions where the quantum waves represent multiple possibilities for the state of a particle, are known to persist until quanta are either measured or naturally interact with the rest of the environment. He takes the view that the original mainstream interpretation, Copenhagen Interpretation, puts not only consciousness but the concept of reality itself outside physics. Alternatives to this include the multiple worlds view, where there is no collapse, but the superpositions continue in multiple worlds and David Bohm's idea in which the quanta are guided by active information. Penrose suggests that the wave function collapse is a real event. He sees superposition as a separation in the underlying spacetime geometry. Each quanta is embedded in a bit of space, and as superpositions grow a blister or separation appears in spacetime. The separation collapses to one of the possible states seen in the superposition. If the separation between superpositions grows to more than the Planck length collapse occurs. The normal quantum wave collapse is seen as an entirely random choice of the state of a quantum particle, from amongst the various superpositions of states. However, these collapses involve interaction with the environment. Penrose suggests that a quanta, which does not interact with the environment will undergo objective reduction (OR), when the separation between superpositions begins to exceed the Planck length. He also suggests that while the normal collapse is totally random, OR is not totally random, but involves a non-computable process. This is suggested because Penrose thinks that the brain manifests a non-computational aspect, and that the wave function collapse is the only place in the universe where such a thing can exist. Penrose also proposes that OR based quantum computation occurs in the brain. It is important to stress that quantum computing as such is not expected to generate consciousness. In quantum computers, collapse will occur as a result of measurement or interaction with the environment. It is only in the event of OR that non-computability and consciousness could be brought into play. Hameroff suggests that quantum compuations take place in microtubules, orchestrated by the inputs of synapse via MAPs. Hence the theory is often known as ORCH OR for orchestrated objective reduction. The computations are suggested to persist for 25ms, which would link them to the 40Hz gamma synchrony, viewed as a correlate of consciousness. The computations are terminated by objective reduction. It is proposed that in dendrites, the tubulin sub-units of the microtubules interact by dipole coupling so as process information. The tubulin conformation is governed by quantum London forces, so that the tubulins can exist as quantum superpositions of different conformations. In superposition the tubulins would be qbits in a quantum computer, computing by means of non-local entanglement with other tubulin qbits. This entanglement would not just be with tubulins in the same microtubule, but other microtubules in the same dendrite, and in other dendrites connected by gap junctions. It should be remembered that neurons connected by gap junctions can be viewed as a single hyperneuron and the hyperneuron can be seen as a conventional neuron assembly. The dendritic interiors alternate between two states as a result of the polymerisation of actin. In the depolymerised form, the interior of the neuron is aqueous and microtubules signal and process information classically. There are synaptic inputs to the microtubules during this phase. When actin polymerises the interior of the dendrite becomes quasi-solid of gelatinous, and water near to the proteins beomes ordered as a result of the actin gelation. Debye layers of counterions may also shield the microtubules, due to the charged C-termini tails on the tubulins. This is suggested to make the microtubules sufficiently isolated from the environment for quantum superposition to occur in the tubulins. Coherent pumping of energy and quantum error correction may also help to prevent decoherence. Quantum error correction involves a code that can detect and correct decoheence in a quantum system. The geometry of a quantum computer lattice could be formed so as to be resistant to decoherence. Microtubules are suggested to have a structure which is particularly suitable for error correction. When the superpositions in the microtubules are reduced, the result can be used to regulate axon firing and changes in synapses. Hameroff claims to refute Tegmark's attempt to disprove the Penrose/Hameroff model. This is significant as Tegmark's criticism of ORCH OR has been widely accepted as a completely satisfactory dismissal of the theory, and responses to Tegmark are habituaaly ignored. Tegmark calculated microtubule decoherence time as being 10^-13 seconds, which would certainly be much too short for any neural activity. However, he worked on the basis of his own model for quantum activity in microtubules, which was never proposed by Hameroff or anyone else. For some reason he did not choose to address the Penrose/Hameroff model. This invalidates his particular approach, whatever the truth is about decoherence. Tegmark based his calculation on a 24nm separation of solitons from themselves along the microtubules, whereas ORCH OR proposes a superposition separation distance six orders of magnitude smaller. Capability of Tested or Falsified The ability of a theory to be falsified is the acid test of a scientific theory. The Orch Or model is claimed to stand up well in this respect. In 1998, 20 testable predictions of Orch OR were published. Four of these have actually been validated over the last decade, being, signalling along microtubules (9), correlation of synaptic function and cytoskeleton (10), action of psychoactive drugs on microtubules (11) and gap junction mediation of gamma synchrony (12). Others are currently being tested. The 16 untested predictions are:- 1) Microtubule stabilising drugs could treat brain diseases (13). 2) Laser spectroscopy could demonstrate coherent oscillation in microtubules (14). 3) Correlation of vibrational states of microtubule networks with cell activity. 4) Correlation of cytoskeletal networks with memory and neural behaviour 5) Preponderance of 'A lattice' microtubules in dendrites, as these are more suited to information processing. 6) Demonstration of non-local correlations between tubulins on same and different microtubules. 7) Superconducting devices could detect quantum coherence in microtubules. 8) Coherent photons will be detected from microtubules. 9) Dendritic microtubules surrounded by cross linked actin gels. 10) Cycles of gelation linked to gamma synchrony. 11) Gelation cycles regulated by calcium ions associated with microtubules. 12) Quantum tunnelling across gap junctions. 13) Non-local correlation between tubulins in different neurons. 14) Neural mass involved in cognitive tasks is inversely proportional to preconscious time, as in E=hbar/t. 15) Gap junction connections with retinal glial cells. 16) Testing of objective reduction (OR). Will test if isolated quantum superpositions self-collapse according to E=hbar/t (15). The theory is 'fundamentalist' in assuming that consciousness has to be a fundamental property of the universe that is accessed by the brain. Penrose's OR relates to the fundamental level of the universe, where at 10^-35 m. the continuity of spacetime breaks down and becomes quantised. This is proposed as the level where non-computable processes and possibly qualia are embedded. The rarity of consciousness in the universe is because only in a structure like the brain is it possible to isolate relatively large superpositions, such as nanograms of tubulin. The Dendritic Cytoskeleton as a Computational Device: An Hypothesis Avner Priel, Jack Tuszynski & Horacion Cantiello Dept. of Physics, University of Alberta & Harvard Medical School In: Tuszynski, J. Ed. The Emerging Physics of Consciousness Springer ISBN-13 978-3-540-23890-4 The hypothesis in this paper is that microtubules (MTS) and actin in the dendritic cytoskeleton are active in neural computation. These proteins are suggested to interact with ion channels, microtubule associated proteins (MAPs) and kinesin. Particular importance is attached to the C-termini of the tubilin, which are suggested to exist in several conformational states and to be reponsible for the dynamic properties of the neuroskeleton. The authors contend that ionic wave propagation along the cytoskeleton affects channel function, and thence the behaviour of the dendritic tree and brain function as a whole. Dendrites are the main site of excitatory inputs, but relatively little is still known about their functions. The activity of the particular dendritic trees, which vary greatly in shape and size, are suggested to be related to these differences. The size and complexity of dendritic trees increases with development and this is assumed to be related to the complexity of the animal environment and memory ( 1. Kaech, Johnston, Matus ). Inputs come in at dendrite spines, which are more numerous in pyramidal neurons and less so in interneurons. The number os spines and the number of excitatory inputs is clearly correlated. The authors contends that the dynamics of the cytoskeletal structure process and deliver information to the synapse. The actin cytoskeleton is known to be related to the stability of dendritic spines ( 2. Fickova, Fischer, Landis ), ( 3. Crick, Dunaevsky ). The actin part of the cytoskeleton has a key role in the formation and maintenance of synapses, and is itself remodelled by synapses. Pruning of synapses is also associated with actin ( 4. Collicos, O' Leary, Sanes, Scott, Weimann, Zhang). The authors argue that the extent of dendritic change in terms of growing new branches or developing new spines argues against the rather fixed quality of the traditional Hebbian model of neuronal asseblies. Recent experiments also suggest that synaptic strength is less stable than the Hebbian model suggests. Conventionally, actin and microtubule networks have been seen as performing separate roles, with actin involved in cell movement and microtubules in transport of organelles. However more recent studies suggest the both systems have a role in what were the traditional functions of the other system ( 5. Dehmelt, Letourneau ). Microtubules often grow along actin bundles. Microtubules and actin are both involved in the growth cones of cells. The authors suggest that the actin and microtubular cytoskeletons may be central to the functioning of cells. The interactions between these two cytoskeletal structures have only recently become apparent. The actin-microtubule relation might also be important for axonal path finding. Neurites have proteins capable of interacting with both microtubule's and axons and proteins that allow signalling between the two cytoskeletal systems. A potentially important role for the C-termini on tubulins is envisaged. It is apparent the neurons utilise MTs in some forms of cognitive processing, with both MAP2 and kinesin involved in learning and memory ( 6. Khuchua, Wong, Woolf ). It is considered likley that the transport of particular proteins and mRNA, important for synaptic development along MTs to the postsynaptic densities is important for learning. Each tubulin dimer has two C-termini either extending outward from the service or binding it to one of a few possible configurations. The C-terminii are negatively charged. According to the authors model the C-termini interact with the surface of the dimer, the neighboring C-termini or adjacent MAPs. It is thought that the orientation of the C-terminii can be altered by ionic waves. Actin Experiments show that there is a possibility of ionic wave generation along actin filaments, with large changes in the density of ions ( 7. Cantiello, Lin ). The electrical conditions are such that it is argued that most of the ions might be tightly bound in a 8nm round the actin filament. This sheath of ions around the filament could mean that the filament acts like an electric wire. These filaments could transmit localised waves or solitons. This actin structure has effects on the surrounding water. The water molecules reorientate themselves towards the ions and at the same time break the hydrogen bond network with neighbouring water molecules. There is a hydration cell with water molecules orientated around an ion. An experiment has shown that actin filaments are capable support ionic waves as axial non-linear currents. Another experiment with actin filaments produced solitary waves very similar to those in non-linear transmission lines ( 8. Kolosick, Longren, Noguchi ). Actin filaments are abundant in dendrites and axons and this means that the experimental findings about transmissions in actin filaments has implications for signalling and ionic transport within cells. There is extensive new information showing that actin filaments are linked to ion channels ( 9. Chasan, Janmey ). Actin filaments can change their configuration and it is speculated that ionic waves may be involved in this process. In neurons actin is mainly concentrated in the synaptic areas, and it is considered feasible that electrical signals through actin may help to trigger neurotransmitter release, and that in the dendrites it may be involved in the post-synaptic response. Kaech et al ( 1. ) showed that anesthetics inhibited the actin response in dendrites. The authors expect ionic waves along actin filaments to be shown to have a broad range of effects. They say that the core of their theory is the propagation of ionic waves along actin filaments, MAPs that interact with them and C-termini on tubulins. The interaction between these and membrane components such as ion channels could produce previously undetected modulatory effects to synaptic connections. Microtubules and actin filaments are interconnected and actin filaments are connected to ion channels. Actin bundles bind to post-synaptic densities in dendrites and dendrite spines. At the other end the actin binds to microtubules. Actin also binds to ion channels. It is envisaged that the electrical reponsiveness of the neuron may be regulated via the cytoskeletal connection to the ion channels. In this model, microtubules in dendrites receive signals from synapses via ion waves propagated along actin filaments that are connected to microtubules by MAP2. The inputs influence the evolution of an existing system. The microtubules develop the inputs by means of the changing conformation of the C-termini, with some operations recurrent where MAPs connected adjacent MTs. Finally, the MTs produce a read out to ion channels often via wave propagation along actin filaments, and are suggested to regulate voltage sensitive ion channels. This in turn regulates the axon hillock and the output of axons potentials by changing the distribution of open and closed ion channels. The information processing in dendrites is assisted by their special lay out with short microtubules of mixed polarity connected by MAP2. It is considered possible that there could be a Hebbian-type system in which frequent activity in parts of the microtubule could produce a higher or lower actin filament density, which would constitute memory/learning. Johnson and Byerly ( 9. ) showed that agents that modified the cytoskeleton also alter calcium ion activity in some neurons. Potassium channels have been shown to be controlled by disuption of actin filaments ( 10. Maguire ). These studies refer to exceptional conditions, but it is thought that they might indicate a more general system. Cytosketal control may deliver ion units to particular positions. At the close of the chapter, the authors stress their key finding, which is that MTs, MAPs and actin filaments support ionic waves, and their hypothesis that these ionic waves may have a role in neural function. |
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