Right so let’s get it back on track.
Along with an apology, you are correct, I didn’t really notice, or read this paper where you first posted it, because frankly it’s irrelevant to that particular discussion.
Although you are correct, it still seems to me, this is about the systems and mechanics of the brain and the process of producing thoughts,
Bringing it back to the point about microtubules being an essential component (widget) of the process of thinking and consciousness -
but that to understand consciousness itself, especially higher levels of complex consciousness, that requires more than simply recognizing microtubules contribution within the outrageously complex system.
I’ve taken the liberty of moving the following post from the thread discussion, where it didn’t belong, over here, since this is really proper thread for this contribution to our debate.
Okay, I stand corrected in so far a this paper and its limited implications.
No, it doesn’t.
Alzheimer’s is symptomatic of microtubule catastrophe, not the other way around.
This is actually demonstrated by my quoted science .
Anesthetics bind to tubulin, causing microtubules to destabilize** [84,85]. They can also cause microtubule-based molecular motors, such as kinesin, to reversibly fall off the micro- tubule lattice and thus disrupt transport of vesicles, proteins, and organelles to synapses .Nov 18, 2019
In this case, the introduction of anesthetics is causal to microtubule malfunction, which leads to disruption of regular data processing and/or loss of consciousness.
[quote=“citizenschallengev4, post:5, topic:9661”]
Do we really?
Where are your papers on that - and please not another paper on microtubules and mitosis! When you’re supposedly to be discussing better understanding of our consciousness.
We don’t have clue about how consciousness is created! And you want to discuss our understanding of consciousness?
Are you accusing me of not having the answer to the “hard question”? Ask Chalmers if has the answer to the “hard question”. He is the one that posed it!
Here again I’ll bet you are elevating assumptions, and the usual PR driven hopes, to the level of certitude, when it’s no more than dreams at this point.
No, you are making unwarranted assumptions. I only post what IS known about the hard facts about the neural network and that most definitely includes the properties and functions of microtubles.
Obviously you do NOT read everything I post or you would not be asking such a fundamental question which I have already answered several times.
But I’m glad to provide proof of that claim.
CC, I have explained that Chalmers has asked for answers to the “hard question” but I agree with Tegmark that before we ask that, we should start with identifying “hard facts” which are all contained in the physical properties of the brain.
Tegmark’s argument that consciousness is an emergent property of physical processes is irrefutable unless you want to assign a magical agency that creates consciousness. But if even if there is such an agency that can act over and above the physical substrate, then that difference should be measurable and quantifiable as different from what the laws of physics predict what it should be.
Thus what you call is the limited approach is exactly the correct way of approaching the problem.
Asking a hard question without knowing what to ask is a useless waste of time.
All of this first requires knowledge of the physical processes, the “hard facts”, which due to the nano scales at which the information is being processed has been unattainable until the refinement of electron microscopy is beginning to allow us access and observation at the physical substrate level.
In the past 10 -15 years the research in neural networking and microtubule function within it has increased by hundredfold and the data is beginning to yield hard facts that will allow us to begin asking the hard question or even allow us to create an artificial conscious intelligence.
For his part, Baars writes (along with two colleagues) that there is no hard problem of explaining qualia over and above the problem of explaining causal functions, because qualia are entailed by neural activity and themselves causal. Dehaene, in his 2014 book Consciousness and the Brain, rejected the concept of qualia and argued that Chalmers’ “easy problems” of consciousness are actually the hard problems.
He further stated that the “hard problem” is based only upon ill-defined intuitions that are continually shifting as understanding evolves:
Once our intuitions are educated by cognitive neuroscience and computer simulations, Chalmers’ hard problem will evaporate. The hypothetical concept of qualia, pure mental experience, detached from any information-processing role, will be viewed as a peculiar idea of the prescientific era, much like vitalism… [Just as science dispatched vitalism] the science of consciousness will keep eating away at the hard problem of consciousness until it vanishes.
This is the limited area of investigation that I am addressing in this thread.
Which he has shrewdly constructed so no solution is possible. Seems to me his phraseology does more to create an intellectual straight jacket, then anything.
The framing of your question, limits the conclusions your answers can provide.
Though I’ve said it before, Chalmers is a wonderful example of getting lost within the human mindscape.
And I don’t have years to read up on all the rabbit holes that a closer look demands, I’ve spent the better part of the past couple hours doing some random reading to refresh my memory - this isn’t the first time I’ve heard of Chalmers - and find myself getting the same stuck in the same head spinning space that days worth of reading and trying to make sense out of him got me. Fortunately, must extract myself and get back to the real world of action and living.
“This would in effect be to say that any solution to the hard problem must be reductive realist in form; on this view, dualism/non-reductive realism and eliminativism are merely ways of claiming that the hard problem is unsolvable or illusory. …”
Chalmers is a philosopher creating intractable problems is his job. His “Hard Problem” is tailor made to be impossible.
Besides a solution is impossible especially when you keep it all within your mindscape and dismiss physical reality as optional. We don’t need meta-reality to get a handle on our own consciousness. Biology is making amazing head way, and that deserves more attention, but hey our daydreaming has always taken priority hasn’t it?
There’s a direct line from Chalmers to Donald Hoffman, so why should I be impressed?
Then before ya know it, you’re reading stuff like,
Then to discover, they are still struggling with the God question.
Since the time of Hume, or, more accurately, since the appearance of occasionalism as championed by the likes of al-Ghazali and Gabriel Biel in the Middle Ages and by Malebranche and Berkeley in a subsequent era, philosophers have been propounding what we might aptly call subjectivistic explications of natural necessity.1
The occasionalists located the source of this necessity in God’s free decision to bring about natural events in accordance with certain arbitrary but (barring only a few exceptions /216/ strictly adhered to rules, rules reflected in the empirical generalizations that scientists strive to discover and systematize. Modern thinkers, as is their wont, shift the focus from the divine mind to the human mind.
We people love talking, and love the stories our minds can create. Believe me I can relate.
If I had a life time to sit on my ass and do all the reading needed to really immersion myself into other’s people’s minds, I could probably offer a much more solid defense. But alas, I got actual living to contend with and real people to concern myself with.
Department of Psychology, University of Cape Town, Cape Town, South Africa
This article applies the free energy principle to the hard problem of consciousness. After clarifying some philosophical issues concerning functionalism, it identifies the elemental form of consciousness as affectand locates its physiological mechanism (an extended form of homeostasis) in the upper brainstem. This mechanism is then formalized in terms of free energy minimization (in unpredicted contexts) where decreases and increases in expected uncertainty are felt as pleasure and unpleasure, respectively. Emphasis is placed on the reasons why such existential imperatives feel like something to and for an organism.
I recently published a dense article on this topic (Solms and Friston, 2018)—a sort of preliminary communication—which I would like to expand upon here, in advance of a book-length treatment to be published under the title Consciousness Itself(Solms, in press). Since this is a psychoanalytic journal, I will supplement my argument with cross-references to Freud’s views on these themes. Readers with a mathematical background will benefit from a close reading of Solms and Friston (2018) in conjunction with this paper, which is aimed primarily at a psychologically educated readership.
My argument unfolds over four sections, of unequal length. …
Some critiques you’ll probably appreciate.
Anyway, Solms also sees Karl Friston’s free energy principle as a major part of his theory. He gives one of the best descriptions of that principle that I’ve seen. Unfortunately my understanding of it remains somewhat blurry, but my takeaway is that it’s about how self organizing systems arise and work. He identifies four principles of such systems:
They are ergodic, meaning they only permit themselves to be in a limited number of states.
They have a Markov blanket, a boundary between themselves and their environment.
They have active inference, that is, they make predictions about their own states and the environment from that environment’s effects on their Markov blanket.
They are self preservative, which means minimizing their internal entropy, maintaining homeostasis, etc. …
… Nevertheless, the book repays a close read. Even if, like me, you remain unconvinced by his vision for neuropsychoanalysis, his analysis of David Chalmers’ famous ‘hard problem of consciousness’, or his claim to have provided a blueprint for building a conscious machine (and what to do about it), there is plenty to provoke and fascinate along the way. And the book’s primary message – that the source of consciousness is deeply bound up with our nature as flesh-and-blood living creatures – stands up by itself. Solms is one of a small number of scientists making this important argument, and for this alone his book is a welcome contribution.
And here is where I look for the actual mechanism that processes the energy and experiences the effect of “differential equations” and the microtubule is a perfect candidate due to its dipolar properties.
The microtubule is in fact a biological potentiometer and I believe that is an important link in the emergence of cognitive differential equations.
This is particularly useful in the processing of optics and sound.
Differential Binding Regulation of Microtubule-associated Proteins MAP1A, MAP1B, and MAP2 by Tubulin Polyglutamylation*
The major neuronal post-translational modification of tubulin, polyglutamylation, can act as a molecular potentiometer to modulate microtubule-associated proteins (MAPs) binding as a function of the polyglutamyl chain length.
The relative affinity of Tau, MAP2, and kinesin has been shown to be optimal for tubulin modified by ∼3 glutamyl units. Using blot overlay assays, we have tested the ability of polyglutamylation to modulate the interaction of two other structural MAPs, MAP1A and MAP1B, with tubulin. MAP1A and MAP2 display distinct behavior in terms of tubulin binding; they do not compete with each other, even when the polyglutamyl chains of tubulin are removed, indicating that they have distinct binding sites on tubulin.
Binding of MAP1A and MAP1B to tubulin is also controlled by polyglutamylation and, although the modulation of MAP1B binding resembles that of MAP2, we found that polyglutamylation can exert a different mode of regulation toward MAP1A. Interestingly, although the affinity of the other MAPs tested so far decreases sharply for tubulins carrying long polyglutamyl chains, the affinity of MAP1A for these tubulins is maintained at a significant level. This differential regulation exerted by polyglutamylation toward different MAPs might facilitate their selective recruitment into distinct microtubule populations, hence modulating their functional properties.
Among the multiple post-translational modifications of tubulin, polyglutamylation was the first oligomeric modification discovered (11). Functionally, and in a close parallel with its oligomeric structure, polyglutamylation was further shown to behave as a molecular potentiometer that modulates the binding of MAPs as a function of the polyglutamyl chain length (12, 13). For instance, Tau, MAP2, and kinesin motors have been shown to undergo the same mode of binding regulation by polyglutamylation: The relative affinity of these proteins first increases progressively for tubulin modified by 1 to 3 glutamyl units then progressively decreases when the chain lengthens further, up to 6 units. This effect is likely to be achieved by conformational changes of the C-terminal domain of tubulin, driven by the growth of the polyglutamyl chain (12, 13).
Thus, polyglutamylation could control the targeted binding of a particular MAP to MTs at a given level of glutamylation, without altering the binding of other MAPs. However, if polyglutamylation acts as a general regulator of MAP binding, it is difficult to imagine the manner in which it could distinguish between the different MAPs. Consequently, we have sought to determine the binding behavior of other MAPs, namely MAP1A and MAP1B, toward glutamylated tubulin and compared it to that of another high molecular weight MAP, MAP2.
We report that polyglutamylation regulates the binding of MAP1A and MAP1B in a chain length-dependent manner, MAP1B behaving like MAP2. On the other hand, we found that the binding of MAP1A was differentially regulated by polyglutamylation. In contrast to the other MAPs tested so far, which all display an optimal affinity for tubulins modified by around 3 glutamyl units, MAP1A has the selective property to maintain a high affinity for highly glutamylated α- and β-tubulins. A model for a transition between MAPs along axonal processes is presented.
Figure 8. Model for a Tau-MAP1A transition on axonal microtubules driven by tubulin polyglutamylation. Schematic representation of a neuronal cell showing part of the cell body and the beginning of the axon. After synthesis of tubulin heterodimers (step 1) and their assembly with Tau proteins (step 2), MTs are conveyed into the axon. Because MTs are formed and as they move down the axon, assembled tubulins are substrates to the enzyme tubulin-polyglutamylase that gradually lengthens the glutamyl chains (En) (steps 3 and 4). When the length of the glutamyl chains increases beyond 3 units, and up to 6 or 7 units (step 4), the relative affinity of Tau for these MTs decreases drastically and Tau can but detach from them.
At the same time Tau is destabilized, and given the affinity of MAP1A for highly glutamylated tubulins, MAP1A can bind and/or stay efficiently bound to these axonal MTs to maintain their stability and confer new structural, functional, and interacting properties. According to the role of polyglutamylation as a differential regulator of MAP interactions, this post-translational modification could drive automatic MAP transitions (Tau-MAP1A in axons, MAP2-MAP1A in dendrites, MAP1B-MAP1A during development, etc.) and, more generally, could possibly control the recruitment of specific MAPs or motor proteins onto specialized subsets of MTs such as axonemes or mitotic spindles in non-neuronal cells.
They are not the key to human consciousness, they are the proto stage to evolving stages of refinement and differentiation of sensory data from simple kinetic pressure to sensory processing and physical responses to EM and sound waves.
Why do people cry when seeing color for the first time?
Colorblind people cry upon seeing color for the first time because the sight of colors is beyond what words can describe
A perfect example can be found in the original chemical light-sensitive patch that eventually evolved into the eagle’s eye that is some 6 times stronger than the human eye and can spot a rabbit 3+ km away.
The eagle eye is among the sharpest in the animal kingdom, with an eyesight estimated at 4 to 8 times stronger than that of the average human.
A bloodhound’s sense of smell is hundreds of times stronger than humans.
Researchers have estimated that a bloodhound’s nose consists of approximately 230 million olfactory cells, or “scent receptors” — 40 times the number in humans.Jun 9, 2008
This is the ultimate strength of “evolution via natural selection”, where nature favors increased sensitivity and interpretation that helps an individual survive to breed and add its improved genes to the species’ gene pool.
In humans it is not so much the extraordinary sensory abilities as the increased brain power and ability to process the information and make decisions based on “experiential memory”.
The human senses are but average as compared to many animals in the wild, but our strength lies in the level of intelligent interpretation of data.
But our extraordinary intelligence does not in any case minimize the natural intelligence at all levels of sentience, from single celled organisms, to insect hive minds, to an octopus’ ability to shapeshift its entire body at will.
The one single “common” information processor that all Eukaryotic organisms possess in overwhelming numbers regardless of neural networks, is the microtubule.
It is the microtubule network in cellular cytoplasm, cytoskeleton, and neural cells that are responsible for informing the entire system of changes (differential equations) that trigger physical responses and are the foundation for sentient behaviors. The rest is just a matter of increased complexity (growth) and sophistication in “understanding” the sensory data.
I found this statement on a science forum in regard to the chemical mechanism that responds to stimulus by producing neural “action potentials” that trigger response behaviors.
“They can only follow a very complex, yet technically predictable formula through sets of chemical reactions.”
What are human emotions?
Perhaps human emotions are triggered by a feed-back loop that in self-aware humans becomes an conscious emotional experience.
There is a clinical condition named Pseudobulbar Affect (BPA) that occurs when this feedback loop is constant instead of a single event.
What is pseudobulbar affect (PBA)?
Pseudobulbar affect (PBA) is a neurological condition that causes outbursts of uncontrolled or inappropriate laughing or crying. It is also known by other names including emotional lability, pathological laughing and crying, involuntary emotional expression disorder, compulsive laughing or weeping, or emotional incontinence. PBA is sometimes incorrectly diagnosed as a mood disorder – especially depression or bipolar disorder.
What causes pseudobulbar affect (PBA)?
It is not completely known why pseudobulbar affect (PBA) occurs, but it is essentially always associated with neurological disorders or diseases that cause brain damage or injury. Disorders, diseases, or injuries that are associated with PBA include:
Wilson disease (a disorder in which copper builds up in the brain, liver and other organs)
PBA occurs when there is a lack or loss of voluntary control over emotional responses. Various brain regions along a cerebro-ponto-cerebellar pathway are likely responsible for a loss of inhibitory or regulatory control on expression of emotions. Part of this pathway includes the cerebellum, which plays a key role in modulating or monitoring emotional responses and ensures they are appropriate to the social situation. Disruption of the neural (nerve) pathways from certain areas of the brain to the cerebellum may lead to a loss or lack of control over emotional expression.
Neurotransmitters, such as serotonin, norepinephrine, dopamine, and glutamate, are also thought to play a role in PBA.