Here is my short talk from the Models of Consciousness 6 conference of the Association for Mathematical Consciousness Science. I think the microtubule-centered quantum consciousness (MCQC) discourse has often blurred the line between science and mysticism and has made it harder for life sciences professionals to give serious consideration to quantum effects in biological systems. Some leading proponents of MCQC were reportedly invited to the conference but did not attend; I would have welcomed a direct scientific exchange. https://t.co/dcY7GGWTcX
In particular, (1) below found that vinblastine inhibited the stimulation-induced release of norepinephrine and dopamine-β-hydroxylase from sympathetic nerve terminals by disrupting microtubule-dependent exocytosis, suggesting that microtubule destabilization can impair vesicular neurotransmitter release more broadly. If a similar mechanism applies to central dopaminergic neurons, this could be relevant because (2) found that activation of D1 receptors by chloro-APB decreases time to emergence from isoflurane anesthesia, which implies that inhibiting dopaminergic tone would increase sensitivity to isoflurane. A single dose of epothilone might improve resistance by stabilizing microtubules and preserving their function as anesthetic targets, whereas daily dosing for several weeks could have other systemic effects that account for the observation that it increased sensitivity, such as (3) by attenuating microglial activation and shifting microglia from a pro-inflammatory to a less-active phenotype, which could in turn alter the neuroinflammatory milieu supporting dopaminergic neuron function.
1. Thoa, Nguyen B., et al. "Inhibition of release of dopamine-β-hydroxylase and norepinephrine from sympathetic nerves by colchicine, vinblastine, or cytochalasin-B." Proceedings of the National Academy of Sciences 69.2 (1972): 520–522.
2. Taylor, Norman E., et al. "Activation of D1 dopamine receptors induces emergence from isoflurane general anesthesia."Anesthesiology 118.1 (2013): 30–39.
3. Yu, Zhongyuan, et al. "Epothilone B benefits nigral dopaminergic neurons by attenuating microglia activation in the 6-hydroxydopamine lesion mouse model of Parkinson's disease." Frontiers in Cellular Neuroscience 12 (2018): 324.
This study is flawed because it does not consider the classical neuroscience explanations. Quantum mechanics is only needed if classical science explanations don't work.
In particular, (1) below found that vinblastine inhibited the stimulation-induced release of norepinephrine and dopamine-β-hydroxylase from sympathetic nerve terminals by disrupting microtubule-dependent exocytosis, suggesting that microtubule destabilization can impair vesicular neurotransmitter release more broadly. If a similar mechanism applies to central dopaminergic neurons, this could be relevant because (2) found that activation of D1 receptors by chloro-APB decreases time to emergence from isoflurane anesthesia, which implies that inhibiting dopaminergic tone would increase sensitivity to isoflurane. A single dose of epothilone might improve resistance by stabilizing microtubules and preserving their function as anesthetic targets, whereas daily dosing for several weeks could have other systemic effects that account for the observation that it increased sensitivity, such as (3) by attenuating microglial activation and shifting microglia from a pro-inflammatory to a less-active phenotype, which could in turn alter the neuroinflammatory milieu supporting dopaminergic neuron function.
1. Thoa, Nguyen B., et al. "Inhibition of release of dopamine-β-hydroxylase and norepinephrine from sympathetic nerves by colchicine, vinblastine, or cytochalasin-B." Proceedings of the National Academy of Sciences 69.2 (1972): 520–522.
2. Taylor, Norman E., et al. "Activation of D1 dopamine receptors induces emergence from isoflurane general anesthesia."Anesthesiology 118.1 (2013): 30–39.
3. Yu, Zhongyuan, et al. "Epothilone B benefits nigral dopaminergic neurons by attenuating microglia activation in the 6-hydroxydopamine lesion mouse model of Parkinson's disease." Frontiers in Cellular Neuroscience 12 (2018): 324.
Our new paper ‘Home-administered unfocused ultrasound in subjective cognitive decline and dementia: An open-labeled, uncontrolled feasibility pilot study’ will be published soon in Frontiers in Aging. Here’s a preprint;
https://t.co/zEbdw01ItK
@leafs_s No, this must be wrong, the quantum woo folks are adamant that it is quantum collapse of some wavefunction or other in microtubules, not "cartoon neurons." 🤣🤣🤣
Glad to see someone is looking at the basal ganglia w.r.t. consciousness - "The basal ganglia, a key component of the cortico-basal ganglia-thalamo-cortical loop, are known to play a crucial role in mediating consciousness and behavioural responsiveness to the environment." Mapping basal ganglia circuitry in altered states of consciousness: from pathology to pharmacology - https://t.co/EZnvH8zmRl #ScholarAlerts
Many scientists reject quantum biology because of Hameroff and Penrose and they ignore it. They probably aren't staying in their lane as much as making an assessment based on perceived "leaders" in a field. That is unfortunate, because there are quantum effects in biological systems that are not understood yet, like chiral induced spin selectivity. In case it is of any interest, I debunked the farcical use of some of the microtubule studies that Hameroff uses to prop up Orch-OR, see https://t.co/LF77qIxHZE.