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ULTIMATE COMPUTING - Quantum Consciousness Studies

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Anesthesia: Another Side of <strong>Consciousness</strong> 153<br />

we were when President Kennedy was shot. Similarly, threatening or derrogatory<br />

remarks are more likely to be heard and consolidated to long-term memory and<br />

recall in partially anesthetized patients (Bitnar, 1983). Amnesia (lack of recall)<br />

results from prevention of memory consolidation at any point from input to longterm<br />

memory storage. Anesthetic drugs can act at various stages of this process:<br />

narcotic painkillers prevent noxious input, amnestic tranquilizers block<br />

consolidation to long term memory, the general anesthetics inhibit these and all<br />

other cognitive functions. The consolidation process appears to occur in the<br />

brain’s hippocampal region but memory storage and awareness are more diffusely<br />

distributed.<br />

7.3 Mechanisms of Anesthesia<br />

A variety of quite different molecular structures have anesthetic activity.<br />

Other molecules, quite similar in structure to anesthetics, may have opposite<br />

effects and cause convulsions. Despite these paradoxes, imaginative attempts<br />

have been presented to unify a single mechanism for anesthesia and represent<br />

clues to the mechanism of consciousness.<br />

Figure 7.5: Anesthesia results from prevention of protein switching between two<br />

or more different conformational states induced by binding of ligand, calcium ion,<br />

or voltage change. Anesthetic gas molecules bind by Van der Waals forces within<br />

hydrophobic pockets within which electron dipole oscillations may be a trigger, or<br />

switching mechanism for protein conformation.<br />

Several neural functions and structures are inhibited by anesthetics, although<br />

some are inhibited at concentrations higher than that required for anesthesia.<br />

Propagation of action potentials resulting in nerve conduction as well as<br />

microtubule dependent axoplasmic transport are blocked by anesthetics such as<br />

halothane, which also causes depolymerization of MT. However, the measurable<br />

neural function which is sensitive to anesthetics at concentrations barely sufficient<br />

to erase consciousness is synaptic transmission. Neurotransmitter release and/or<br />

neurotransmitter receptor activation thus appear to be the specific actions whose<br />

inhibition results in anesthesia. Inhibition of collective communicative activities<br />

within the cytoskeleton and attached membrane proteins related to synaptic<br />

transmission are presently undetectable with current technologies and their<br />

inhibition may still account for anesthesia. Anatomical localization of sites of<br />

anesthetic action has focused on regions with many synapses. Accordingly, the<br />

reticular activating system which is involved with regulation of wakefulness and<br />

attention and is “polysynaptic” was originally viewed as a major site of anesthetic

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