The Penrose-Hameroff ('Orch OR') model of quantum computation in brain microtubules has been criticized as regards the issue of environmental decoherence. A recent report by Tegmark finds that microtubules can maintain quantum coherence for only 10 −13 s, far too short to be neurophysiologically relevant. Here, we critically examine the assumptions behind Tegmark's calculation and find that: 1) Tegmark's commentary is not aimed at an existing model in the literature but rather at a hybrid that replaces the superposed protein conformations of the 'Orch OR' theory with a soliton in superposition along the microtubule, 2) Tegmark predicts decreasing decoherence times at lower temperature, in direct contradiction of the observed behavior of quantum states, 3) recalculation after correcting Tegmark's equation for differences between his model and the 'Orch OR' model (superposition separation, charge vs. dipole, dielectric constant) lengthens the decoherence time to 10 −5 − 10 −4 s and invalidates a critical assumption of Tegmark's derivation, 4) incoherent metabolic energy supplied to the collective dynamics ordering water in the vicinity of microtubules at a rate exceeding that of decoherence can counter decoherence effects (in the same way that lasers avoid decoherence at room temperature), and 5) phases of actin gelation may enhance the ordering of water around microtubule bundles, further increasing the decoherence-free zone by an order of magnitude and the decoherence time to 10 −2 − 10 −1 s. These revisions bring microtubule decoherence into a regime in which quantum gravity can interact with neurophysiology.

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Insulin signaling in the central nervous system (CNS) regulates energy balance and peripheral glucose homeostasis. Rictor is a key regulatory/structural subunit of the mTORC2 complex and is required for hydrophobic motif site phosphorylation of Akt at serine 473. To examine the contribution of neuronal Rictor/mTORC2 signaling to CNS regulation of energy and glucose homeostasis, we utilized Cre-LoxP technology to generate mice lacking Rictor in all neurons, or in either POMC or AgRP expressing neurons. Rictor deletion in all neurons led to increased fat mass and adiposity, glucose intolerance and behavioral leptin resistance. Disrupting Rictor in POMC neurons also caused obesity and hyperphagia, fasting hyperglycemia and pronounced glucose intolerance. AgRP neuron specific deletion did not impact energy balance but led to mild glucose intolerance. Collectively, we show that Rictor/mTORC2 signaling, especially in POMC-expressing neurons, is important for central regulation of energy and glucose homeostasis.

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