Quantum Processing by Microtubules and Neurocognition

It is tantalizing to pursue the idea of subneuronal information processing since information processing at the level of microtubules within each neuron would provide an enormous increase in the brain's computing power. The currently accepted scientific model suggests that consciousness arises as a result of computational complexity among the approximately 1011 neurons in the brain. There are on the order of 104 synapses per large neuron, which switch their states at a rate of some 103 switches per second, so that we arrive at a number of 1018 operations per second in the brain on average. While this is a truly huge number, it may pale by comparison with the yield given by the brain if neuronal microtubules were actively involved in computational processes. Consider that at the cytoskeletal level there are roughly 107 microtubule-tubulin dimers in each neuron that can switch their conformational states on the order of nanoseconds resulting in on the order of 1016

operations per second per neuron or 1027 operations per second in an entire brain instead of 1018 operations per second estimated for the coarse-grained approach where neurons are taken as the smallest computational units. Moreover, if each tubulin dimer does function as a qubit and not a classical bit processor, then the computational power becomes almost unimaginably vast. It has been claimed that as few as 300 qubits have the same computational power as a hypothetical classical computer comprised of as many processing units as there are particles in the universe.

Classical flow of information along the microtubule length putatively links tubulin qubits together. Indeed, some experimental evidence shows that mi-crotubules do propagate signals in cells, as will be discussed in this book. Moreover, several types of interactions between microtubules and membrane activities are clearly recognized. That computations are carried out by micro-tubule subunits may imply that one of the brain's fundamental units of information is tubulin's protein conformational state. Other processes involved in the functioning of the brain, such as ion channels opening and closing, enzymes catalyzing, motor proteins moving cargo inside cells, and the propagation of ionic waves along filaments, may be inextricably linked to, or even determined by, tubulin's conformational changes, as will be detailed later in this chapter and in various other chapters of this volume. Tubulin consumes a large amount of chemical and thermal energy in the process of microtubule assembly, and is only marginally stable. Consequently, tubulin's conformation must strike a balance in response to delicate countervailing forces. The nature of tubulin and of these complex and opposing forces may confer a functional advantage and lie at the core of microtubules being able to carry out computations by component units.

There is accumulated evidence that microtubules are computationally relevant to neurocognition. Early work by Cronly-Dillon and Perry [10] showed that neurons in the visual cortex produce massive amounts of tubulin during the critical period (from the day the eyes open to postnatal day 35). The critical period is the time during which synaptogenesis and visual learning occur at highest rates. Thus, tubulin is implicated in these developmental cognitive processes. Aging is often viewed as the counterpart of postnatal development. In this regard, Alzheimer's disease, which is accompanied by deficits in intellect, memory and consciousness, has been linked to mi-crotubule degradation [20]. Paired helical filaments are aberrant formations resulting from hyperphosphorylated microtubule-associated protein (MAP), tau. Axonal transport is compromised in Alzheimer's disease, not unexpectedly, given that microtubules are responsible for the transport of nutrients and other important substances from the cell body to the axon terminal [57]. Microtubules have been directly linked to consciousness because they provide a nonselective mechanism for general anesthesia. Anesthetics inhibit a number of neurotransmitter receptors, but differ from receptor inhibitors by having effects on the cytoskeleton, especially actin [7, 32]. Hameroff proposes that the most likely mechanism for general anesthetics acting upon micro-tubules is inhibition of electron movement within the hydrophobic pockets of tubulin dimers [23]. These oil-based hydrophobic pockets occupy approximately 1/30th to 1/250th the total volume of the protein, which works out to be less than one half of a cubic nanometer; nonetheless, these pockets control the overall protein conformation of tubulin. Moreover, the properties of these hydrophobic pockets create a suitable environment to support electron delocalization [26]. Electron motion or motility may well be the critical site of action for anesthetic gases. In the presence of an anesthetic gas, electron mobility that is required for protein conformation and quantum superposition is inhibited. Hence we should expect to see a loss of consciousness. Conversely, instead of inhibiting electron movement, hallucinogenic drugs such as LSD appear to be potent electron donors [59]. Thus, actions of both anesthetics and hallucinogens may involve alterations in electron states within hydropho-bic pockets, which in turn affect the state of human consciousness.

Hameroff further proposes that microtubules are the place where reductions of quantum states can take place in an effective way [25]. Microtubules are, in theory, capable of extending coherent superposition states to adjacent microtubules by way of MAP bridges and to neighboring neurons by way of gap junctions or electromagnetic fields. The question has been raised whether quantum states can survive long enough in the thermal environment of the brain to affect neurocognition [64]. Tegmark estimated that decoher-ence caused by the noisy environment typical of the brain is likely to disrupt tubulin superpositions in under 10"12 s. Microtubule protein functions take on the order of nanoseconds; moreover, neurophysiologycial events range in the order of milliseconds. Hence, it was Tegmark's contention that tubulin superpositions are much too short to significantly contribute to neurophysio-logical processes in the brain. Hagan et al. [21] argue that Tegmark's criticism is misplaced and that the calculations he did were on a reformulation of the Hameroff-Penrose model of his own making. After adjusting to account for that error made by Tegmark, revised calculations produce decoherence times between 10 and 100 |s, which can be extended up to the neurophysiologically relevant range of 10 to 100 ms given that the particular physical mechanisms discussed earlier come into play.

In addition to exploring the potential for quantum approaches to consciousness (including quantum field theories), this multiauthor collection of chapters will discuss alternative theories that are based on physical and mathematical principles. In particular, an entirely classical formulation of the evolution of living systems culminating in the development of awareness and self-awareness is based on the idea of emergence. Emergent phenomena abound in the natural sciences and they are characterized by a higher level of complexity resulting from an aggregation of units whose individual properties differ from those of the aggregate. It is argued that while an individual neuron may only participate in information transfer, their clusters may col lectively process information and clusters of neuronal clusters may achieve a yet higher level of complex behavior giving rise to the emergence of awareness eventually leading to consciousness. Indeed most accepted views within neuroscience see the brain as a nested hierarchy of information-processing subsystems. The firings of nerve cells and the transmissions between them via action potential propagation are at the bottom rung of the hierarchy - the fundamental units of information, analogous to bits in a digital computer. Unfortunately, these classical, deterministic activities, while explaining a number of neurophysiological phenomena, are unable to account for a number of key properties of conscious experience, most notably free-will, the unitary sense of self and many other enigmatic features of consciousness. Hence we may be again driven to delve more deeply inside the neuron, searching for a way to connect with the quantum level. However, most physicists would also argue that the rule of quantum effects ceases to exist in warm biological systems. Presumably that would make them unavailable to influence activities on the level of the neuron.

The challenge is to show how brain-cell firings and communication between cells may be influenced by weak and delicate, very small-scale quantum processes. To put it another way, we need to answer: At what level of organization are quantum effects required in order to explain biological phenomena? Can that level, in turn, influence activities at the neural level? The search for answers to these questions is, in a nutshell, the objective of this book. We have solicited contributions from a number of eminent scientists in the field, some very original thinkers, and several well-known science writers. We are hoping that this book will set the tone for future explorations in this field by new generations of scientists. It would be gratifying if this volume made many of its readers think about the concept of consciousness as a journey of scientific discovery.

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