The Life & Mind Seminar Network

Seminar #47: Extending Autopoiesis to Incorporate Behavior

Posted in Seminars by Tom Froese on February 2, 2009

This week we will have a joint seminar between the Alergic and the Life and Mind seminar series, entitled:

Extending Autopoiesis to Incorporate Behavior

Matthew Egbert

4:30 p.m. Wednesday, 4th February – Arundel 401

“Bare” autopoiesis fails to fully address behavior and explains only direct self-maintenance (Di Paolo, 2005). As a case in point, up until recently, most computational models of autopoiesis fail to demonstrate any behavior beyond direct self-maintenance. One of the first models of autopoiesis to demonstrate behavior is that by Suzuki and Ikegami (2004,2006) which extends Varela, Maturana and Uribe’s original 1974 model with a few extra rules, resulting in a chemotactic autopoietic unity. The way that Suzuki and Ikegami extended the original model resulted in a highly entangled organization of behavior and autopoiesis — that is to say, the mechanism of behavior and of autopoiesis are one and the same. I will describe some limitations of this kind of organization and outline some alternative more “decoupled” organizations. I will then describe our new model of autopoiesis that incorporates decoupled behavioral mechanisms that we have developed to explore some of these ideas. Finally I will report on some ideas that have been clarified through our explorations of our model: “Dynamical Operational Closure” and “Autonomous Behavioral Mechanisms”.

All welcome!

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17 Responses

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  1. Ante Lauc said, on February 3, 2009 at 5:25 am

    can you send me more information because i do think that autopoiesis is the crucial concept to understand LIFE. It can not be explained without deeper understanding of LOVE and FREEDOM. If you do not agree with it forget my message.

  2. Tom Froese said, on February 5, 2009 at 12:00 pm

    Hi Matt,

    Thanks for your seminar yesterday – it’s good that we have another model in order to discuss things more concretely. Here some additional thoughts:

    1) Nobody picked up on this during the seminar, but I would suggest that you avoid talking in terms of more/less, better/worse autopoiesis. I agree with Di Paolo (2005) that, as it is traditionally defined, autopoiesis is a class theoretic notion that allows no gradation: Either a system is organized in an autopoietic way or it is not. Still, your model shows that we lack a concept for the varying precariousness of the autopoietic system. Perhaps it would be better to talk about the stability or rates of self-production or regeneration? Another question would be: do you think that these changes in viability are relative to our perspective, or do they form norms for the system itself? We need to be careful here.

    2) Anil and others commented about the advantage of looking at the relations within your model in hierarchical terms, and I agree. One of the most important insights of the autopoietic tradition is the distinction between the system as a network of component processes, and the system as a unity, which form two separate domains of discourse, though they do enable and constrain each other (cf. Di Paolo, in press).

    3) In fact, this distinction also enables us to clear up some of the confusion regarding the relationship between autopoiesis and behavior: autopoiesis is a concept that applies to the system as a network of processes, whereas behavior is a relational concept that applies to the system as a unity, namely the way that unity is coupled to its environment.

    4) More specifically, as Di Paolo (2005) argues, perhaps we should see behavior as the regulation of this structural coupling by the unity, since behavior is something done by the system rather than the environment (i.e. relational asymmetry). We need to be able to differentiate, for example, between the following situations: (i) when I push you, and you fall over from the force that I applied to your body, or (ii) you just happen to throw yourself to the floor. In both cases we are presented by the same movement, but isn’t only the latter what we might want to call behavior?

    Cheers,
    Tom

  3. Nathaniel Virgo said, on February 5, 2009 at 12:33 pm

    This is mostly in reply to Tom’s first point:

    Personally, I thought Matt did very well at avoiding talking about degrees of autopoiesis, even though his simulation clearly showed evidence for such a thing. It’s obvious that, especially in a system such as Matt’s whose underlying dynamics are stochastic, that the ability to survive (continue maintenance of an autopoietic organisation) in a given environment is (a) a matter of probability rather than an all-or-nothing absolute, and (b) heavily dependent on the details of that environment. Indeed, this seems to be what the word “precarious” must ultimately mean. Given all of this, might it not be better to discard the all-or-nothing dogma than to try to ignore the issue and pretend that degrees of autopoiesis are not there in the data, plain for everyone to see?

    This might seem radical, but to my mind it’s no more radical than discarding the idea that behaviour is an inherent part of the autopoietic organisation. It seems to me that if we do soften the dividing line between autopoietic and not-autopoietic then the relation between autopoiesis and behaviour becomes less problematic: a behaviour might not be necessary for autopoiesis, but it might improve the quality of autopoiesis, either by decreasing the probability of death or by extending the range of environments in which the organism can survive.

    Anyway, that’s just a random thought, but perhaps one that could inspire something interesting…

  4. Tom Froese said, on February 5, 2009 at 2:36 pm

    Nathaniel,

    Yes, I agree that there is clearly a need for us to be better able to talk about all the processes that go on in the currently muddled area between basic autopoiesis and full-fledged behavior. Nevertheless, I think we should also be careful: autopoiesis refers to a particular type of organization, and this organization can of course be structurally realized in different ways depending on the circumstances.

    It now turns out that there are different ways for an autopoietically organized system to structurally realize itself, and we want to be able to distinguish between some of these ways. But rather than bending the original concept of autopoiesis to fit our needs, I suggest that we come up with new organizational concepts, which can be seen as subclasses of autopoiesis. Then we could talk about the system being autopoietic, and also being something else, a more specific type of organization that picks out some relevant structural differences.

    Of course, Ezequiel proposed adaptivity as one such specialization, but the organization defined by that concept might be, as you suggested after the talk, too much like a sense-plan-act model to account for low-level differences in viability.

    Perhaps it is possible to conceive the notion of precariousness in some systemic manner in order to fill in the gap?

  5. Colin Reveley said, on February 6, 2009 at 2:02 am

    Hello. I was an easy student in 2004, with a considerable interest in autopoiesis. Currently I am doing a PhD supervised by Scott Kelso, looking at brain and behavior with EEG and fMRI, with our theoretical framework based on nonlinear dynamics and especially coupled non-linear oscillators. Your brain is composed of non-linear oscillators (neurons), and these form assemblies which can be regarded as oscillators themselves and so on. The key to understanding the cortex lies in the role of synchronization and desychronization at different levels (neuron, microcolumn, macrocolumn, pute cortical ‘region’ etc).

    Anyway, last year I had the great pleasure of entertaining Evan Thompson at my lab, and we had a good few hours of discussion, perhaps selfishly centered on my view of neuronal autopoiesis as the foundation for the phenomenological concept of ‘intentionality’.

    That is to say, first order, cellular autopoiesis; not second order organismic autopoiesis.

    He says this was a view that Varela (who by the way in his ‘day job’ practiced neuroscience in much the same way we do here until his death, which was really a loss to science since he was just getting somewhere – his final work was called ‘the brain web’ which I believe is in nature reviews neuroscience, and contains some of my bosses work. This is a highly recommended review paper; no specialist knowledge needed)

    I’m not up to speed on the no doubt highly sophisticated work you have all been doing on extending the concept of autopoiesis towards a proper explanation of agency in animals.

    But in my view, autopoiesis works well as an explanation of what makes a single cell a living thing, and an agent, but it is not very easily extended to multicellular organisms. Second order autopoiesis seems flimsy to me, and very possibly unnecessary

    To explain agency in animals, I don’t see the need to extend autopoiesis beyond the cell. The autopoiesis of neurons and other cells as independent organisms, coupled and cooperating as an organism towards a common goal of their mutual (ultimate) viability is enough to explain agency.

    what is needed is more work on short term homeostatic and metabolic changes in neurons, glia and other cells, which should start with short term synaptic plasticity. Based on a calcium economy, synaptic strengths can change in as little as 10ms.

    But not much work is being done on this, and none from the perspective we are presently discussing.

    Evan and I agreed that neuronal autopoiesis playing the central role in agency or intentionality is tremendously hard to prove (mostly due to technological limitations of the devices we sue to measure brain activity, and a lack of interest in the scientific community). But He said it was basically what Varela himself thought, unless I misunderstood Evan.

    I don’t want to speak for Evan, but I think that is definitely the way to go. Playing with the relatively clearly defined concept of cellular autopoiesis so that it applies to things other than cells, may prove destructive to the simplicity of the concept – and also may not even be the right explanation of agency/directedness/concernfullness.

    But, you guys do this for a living not me. I’m just presenting a view – specifically the view that the concept of autopoiesis is best left as simple as possible, and that the coupling between first order autopoietic entities be examined, preferably experimentally, as a candidate explanation for organismic agency.

    best,

    Colin

  6. Colin Reveley said, on February 6, 2009 at 2:14 am

    Sorry – a quick addendum.

    Autopoiesis has never really been a scientific concept. It proposes nothing testable (so far), and makes no predictions that are specifically to do with autopoiesis. Rather, it is a description of a kind of organization.

    It seems to me that as this concept is complexified more and more, it moves further and further away from making predictions and being testable, and more towards being a purely philosophical concept. Which I think is bad. But I’ve been trained for the last 4 years by a kind of scientific drill sergeant to respect nothing that is not amenable to strict scientific method. I would not, for example, regard artifical life as science, but as rigorous hypothesis formulation – something the community tacitly acknowledges when it speaks of ‘existence proofs’

  7. Colin Reveley said, on February 7, 2009 at 3:15 am

    actually – one further addendum. I don’t see the original formulation of first order autopoiesis lacking a mechanism for behavior as a problem, basically for the reasons I describe above. The requirement that autopoeitic systems maintain viability (directly by interacting with the environment, or by interacting with other cells) implies behavior of a certain stripe (which ion channels to open when, which protein networks need to be modified and so on.)

    where spatial, motile behavior comes in (and indeed the philosophical notion of agency) is at the organismic level. And this, I have argued, can be understood as a product of *coupled* first order autopoetic systems.

    where that argument falls down is that single celled organisms are often motile, and often behave. But tinkering with a clear concept with the potential for testability in order to accommodate a wider and wider range of phenomena seems perhaps the wrong approach. The behavior of amoebas may be due to processes linked to their autopoietic structure, and contingent upon, it nonetheless distinct from autopoiesis itself.

  8. matthewegbert said, on February 13, 2009 at 2:13 pm

    Hello Everyone,

    Thanks for the interesting comments. I will try to reply to a few of them now. First though, I just want to point out that I have uploaded an mp3 and slides of the talk (plus the video of the model) to the audio/video portion of the life and mind blog.

    https://lifeandmind.wordpress.com/audio-video/

    Responses:

    1) More/less/better/worse autopoiesis.

    Just to be clear, I think this discussion is happening at two levels.

    level i) Degrees of contribution to autopoiesis
    During my talk, I mentioned how the agent in Suzuki and Ikegami’s model (and my L/-/- lesioned agent) have regions which are contributing more to the maintenance of the membrane than others. In this sense there are different areas of the agent that have different `degrees of contribution’ to the autopoiesis. This particular fact however contributes nothing to the idea of partial/more/less/better autopoiesis, as it is the agent in its entirety (not a subsection of the agent) that is classified as `autopoietic’ or `not autopoietic’.

    level ii) “the ability to survive” is not all or nothing concept..

    This largely comes out of Nathaniels’ comment, which I’ll quote here:

    It’s obvious that, especially in a system such as Matt’s whose underlying dynamics are stochastic, that the ability to survive (continue maintenance of an autopoietic organization) in a given environment is (a) a matter of probability rather than an all-or-nothing absolute, and (b) heavily dependent on the details of that environment.

    My response to this is that autopoiesis is not a measurement of success surviving — but a measurement of contribution to survival. Whether or not an agent survives is indeed a matter of probability, but whether or not an organization contributes to its own survival is not a matter of probability. So an autopoietic system is a system that contributes to the likelihood of its own existence regardless as to whether or not it succeeds in continuing to exist.

    I admit that this is debatable…in fact, I’d like to debate it…but perhaps it is a debate that would be easier in person!

    2) Evaluating these systems with regards to Hierarchy

    I am not exactly how hierarchy fits into these systems. The one hierarchy I have observed in these systems is the (rather tautological):

    If we say that only autopoietic entities are capable of intrinsic behavior, then mechanisms of behavior ALWAYS depend upon a mechanism of autopoiesis, for without the autopoietic mechanism, there is no agent to behave. In this way, the autopoietic system (as I called it in my talk, “the core autopoietic system” is more fundamental than the behavioral system).

    Beyond this, what kind of hierarchies should we look at? I’m not sure I understand.

    3) Autopoiesis getting increasingly complicated?

    I agree that the idea of autopoiesis should not be made more complicated. I also agree with Colin’s comment that:

    It seems to me that as this concept is complexified more and more, it
    moves further and further away from making predictions and being testable, and more towards being a purely philosophical concept. Which
    I think is bad.

    …and in this vein, my hope with my research is to focus upon the more tractable, scientific aspects of the theory surrounding autopoiesis.

    I think that perhaps the title of my talk is misleading. I don’t want to extend autopoiesis _theory_ to incorporate behavior — I want to understand how mechanisms of behavior in an autopoietic entity can be related to its mechanisms of autopoiesis. One possibility is that mechanisms of behavior are completely unrelated to behavior! As Colin wrote,

    The behavior of amoebas may be due to processes linked to their autopoietic structure, and contingent upon, [but?] nonetheless distinct from autopoiesis itself.

    This relationship of contingent upon but distinct is exactly what I am interested in exploring. How does this idea fit with the idea of operational closure which also uses the idea of “contingent upon”. A better understanding of this relationship may allow us to argue convincingly that a truly cognitive agent must (or needn’t !) be autopoietic.

    As for Colin’s comments regarding “1st/2nd order” autopoiesis, I find this issue interesting, but I don’t have much to contribute to it at this stage. The model we developed is more similar to a single celled organism than a multicellular organism – so at this stage, I make no claims about multi-cellular behavior or agency.

    Thanks again for the interesting comments!

    Cheers,

    Matthew

  9. Colin Reveley said, on February 13, 2009 at 7:50 pm

    Hi Matthew –

    I’m gratified that you found my points pertinent – I was a bit worried that I was so out of the game that it would be just naive blathering.

    I would take strong issue with one statement you make:

    “My response to this is that autopoiesis is not a measurement of success surviving — but a measurement of contribution to survival.”

    I remain to be convinced that autopoiesis in living, biological cells can be measured as things stand. I would insist, on the basis of my own limited knowledge, that at present it is a *description* – that cannot be measured, and cannot make testable predictions, except in silica, which I’m afraid does not really count to a biologist.

    I tend to see the primary obstacle to autopoietic theory moving forwards into serious scientifc, rather than a purely descriptive/theoretical concept hinges deeply on this issue of whether it can be measured.

    I have some ideas on that. I will, in the next year or two be in a postdoctral position. (with any luck, but in general it looks good – the funding situation in the US is very positive right now, and according to my contacts (a faculty member of the center where I work currently serves at NSF) at NSF, further increases are planned for 2010 – unless of course the economy enters into a helpless state of depression. In the stimulus package NSF got an extra 50% funding beyond the bush years, and this represents only 0.186% of the entire stimulus package, yet fundamentally changes the situation for us basic scientists. So, we really do not need much in the grand scheme of things. Maybe 10 billion a year (in total, not increase) nationally accross all funding agencies for most high quality basic science (‘non-translational’ – i.e no money directly to be made as a result of the research, which Bush shortsightly insisted upon – and which it seems the UK government is moving towards according to the BBC) grants to get funded.

    My postdoctoral position will be in the area of theoretical (not in the wider sense, but in the sense of ‘theoretical phyiscs’ – i.e. quatitative theory that makes testable predictions, using dynamical systems theory) descriptions of cortical activity that are predicitive, neuroimaging experiments to confirm the theory (or suggest new ones), and of course advanced signal processing to analyse the data. That’s what I’ve been trained in, and I’m happy with it.

    But I would like, somehow, to add a solid understanding of experimental microbiology to my range of expertise. This may take the form of courses taken at a university during my postdoc, or possibly a one year taught course in England on that subject (there are no such things in th US) when the postoc concludes.

    Armed with this knowledge, I would like to frame biological experiments to confirm that a cell must have an autopoietic organization in order simply to remain viable in the easiest of circustnaces (e.g. a readily available energy supply that does not require motile behavior to obtain – but elemnets in its environment that are detrimental to it if it cannot maintain itself)

    An example of such an experiment might be manipulating protien networks genetically, so that they are different from those in the the orignal cell, yet are organizationally autopoietic. A tall order, but I’m sufficiently interested to give it a try. A pipe dream perhaps.

    With repsect to cognitio and agentcy, next would be experiments to see if very short term plasticity (10-100ms) has direct, swift metabolic consequences in the cell (and hence it’s autopoiesis), and influences synaptic death and formation on a somewhat longer timescale of days or weeks.

    Eve Marders work (upon which Ezequiel based his homeostatic ctrnn nodes and evolutionary robotic repeat of the kohler vision inversion experimment) is great, but it does not really link neuronal homeostasis (she speaks not of autopoiesis of course) to cognition because the timescales are very far apart – it takes weeks for vision to right itself through prims glasses. I want cogntive/perceptual loop events to be shown to have direct effects on cells at the time scale of cognition (100ms more or less), short term connectivity (through short term plascticity) and ultimately more permanent connectivty changes through the formation and death of synapses.

    I think Marder’s work is very relevant, but a cell rapidly altering the emmission of calcium ions (reponsible for short term plasticity) being linked to cognitive processes would be something to see. Technology is lacking however, and experiments would be in vitro with patch clamps and such, or *maybe* in a live rat according to some lectures I’ve attended recently (by the head of the munich max planck no less)

    re: second order autopoiesis – As Even tells me Varela was never happy with the concept. It was a stop gap. As I understand it, his vision, at least as far as the brain is concerned is that our philosophical notions of intentionality, agency, and so on arise from the coupled actions of our billions of neurons competing with other for survival. Neurons are maintained partly by their own metabolic activity, which in turns hinges on how much they fire.

    That is, blood flows to active nerons, not inactive (*if* we are to believe the thoery behind the fMRI which is the blood oxygen dependant response (BOLD) response, which is much more contentious than it seems; use caution in assessing those pretty fMRI pictures. They represent tiny increases in blood flow above or below a very large baseline of brain wide blood flow, and the jury is out on whether or not increases blood flow necessarily follow from cell assembly activation) and this is contingent on their connectivity/activation.

    Additionally, they are supported by glial cells (which outnumber neurons 10 to one) which are traditionally thought to have the role of feeding and maintaininng the neurons, but recent research suggests they may have a role in cognitive activity more directly. Glial cells ignore neurons with little connectivity, and they die. And of course, they are dynamic, autopoietic entities in thier own right.

    The whole thing meshes wonderfully with Gerald Edelamn’s theory of neuronal goup selection (neural darwinsim). There is a 1988 book by edelman, and ,many papers on this subject. And of course, your own Anil Seth is expert on this topic. Edelman is talking mostly about synaptic selection, but it still seems entirely compatible to me.

    I think these issues are worth trying to predicate a career on, and I intend to do so if I can. So I am not dismissing autopoiesis as doomed forever to be a descriptive concept – rather I’m trying to think of ways to make it testable for cells, and then link it to neural activity, and large scale cognition.

    best,

    Colin

  10. Colin Reveley said, on February 13, 2009 at 8:09 pm

    One last thing:

    It seems to be the the modern evolutionary/genetic synthesis sees an “organism” like a person as a unity in its own right, because all it’s cells share the same genes.

    I’ve nothing against the ‘selfish gene idea’ – it was designed to explain things like suicidal altruism in termites, and so it did.

    So, it is true as far as it explains the phenomena it sought to address.

    But it’s not incompatible with a ‘cell first view’. If we can agree that ‘life=cell’ and ‘complex organism=coupled cells’ then although genetic preservation concerns may be important (especially if all the cells share the same genome, as in the vast majority of organisms, except some some very weird creatures that have changed little since the pre-cambrian, and sort of operate as individual cells, but form collectives sometimes too), autopoietic/metabolic CELL FIRST ideas can be equally important, and indeed explananda for different aspects of biological phenomena.

    And anyway, since a whole human has the same genome in every cell, why would the selfish genes care which particular neurons live or die? That would seem to be their own concern.

    So, I don’t even see a point of disagreement between even so heavily dogmatic a person as Richard Dawkins and views like mine specifically, or ours generally in this group.

  11. Colin Reveley said, on February 13, 2009 at 9:33 pm

    and one more thing – I think the in silica work, that is artificial life studies of autopoiesis, are of tremendous value. The average (unenlightened?) experimental biologist is likely to be dismissive though and that it a sad fact, which may change in the future. Artificial life practitioners with more traditional biological training might be helpful, such as Chris Fernando whose work on the origin of life via protocells is both biologically and biochemically informed (through his medical training) and theoretically rigorous.

    I described artificial life as rigorous (quantitative) hypothesis generation, rather than ‘real’ experimental science that can answer questions about the real world, and such it is.

    but the development of autopoietic theory through computer experiments is a great way to come up with hypothesis that might one day be tested in vitro.

    Varela was a proponent of artificial life, and practiced it in producing the first (I think) computational model of autopoiesis. Maybe he saw it as a way of generating hypotheses too? I cannot say, and sadly he is dead so I cannot ask. I would have applied to work with him in a microsecond :) Perhaps his lab continues this work, you never know.

  12. Colin Reveley said, on February 13, 2009 at 9:47 pm

    final final thing – sorry to write such long responses. Understand that I do not have a forum for discussion on these issues where I work; I’ve maintained my enthusiasm on these ideas on my own for four years, so the opportunity to interact with others about them makes me over excited!

    Colin

  13. Nathaniel Virgo said, on February 17, 2009 at 5:41 pm

    To Matt (and Tom and others):

    I have various thoughts about all this, so at some point I’ll probably drop by the main lab for a chat, but for now I’d just like to respond to this bit:

    “My response to this is that autopoiesis is not a measurement of success surviving — but a measurement of contribution to survival. Whether or not an agent survives is indeed a matter of probability, but whether or not an organization contributes to its own survival is not a matter of probability. So an autopoietic system is a system that contributes to the likelihood of its own existence regardless as to whether or not it succeeds in continuing to exist.

    I admit that this is debatable…in fact, I’d like to debate it…but perhaps it is a debate that would be easier in person!”

    You’ll get no major debate out of me I’m afraid – this seems right. When I wrote about degrees of autopoiesis I was obviously not making an adequate distinction between an autopoietic system (which has degrees of probability of survival) and an autopoietic organisation, which does not.

    However, it occurs to me that, if we ever had proper mathematical definitions of these things then we might be able to talk about how much an organisation contributes to its own survival – something along the lines of how much it affects its own probability of continuing to be instantiated over time. Then we could say “an organisation is autopoietic if it has an autopoietivity greater than 0 (i.e. if it increases rather than decreases its own chances of survival in a given class of environments).” This would admit the possibility of talking about degrees of autopoiesis without diluting the organisational concept. Organisations which decrease their own likelihood of survival over time (negative autopoietivity) would be very unlikely ever to be observed in any type of system.

    Why do I think this might be a useful concept in the concept of your (Matt’s) work? Because it seems clear (to me at least) that [organism PLUS behaviour] is an organisation which contributes to its own survival, no matter how decoupled the behaviour generating mechanism is from the rest of the system. This seems to be true even if the behaviour itself is detrimental to the system’s survival, as long as it isn’t so detrimental that it causes instantaneous death. So [human PLUS tobacco smoking behaviour] is still an organisation which contributes to its own survival{*}.

    The organisation [human MINUS smoking behaviour] also contributes to its own survival. Perhaps this could point to a fritful way to look at the relationship between behaviour and autopoiesis in which we say that behaviour is part of autopoiesis, but it can be an optional part.

    But [human PLUS smoking behaviour] contributes to its own survival a little less than [human MINUS smoking behaviour]. This could give us a nice operational way of saying that the behaviour is detrimental.

    I think I’ll stop here and wait to see what other people think. But perhaps this way of thinking could lead us to some interesting new ideas without weakening Maturana and Varela’s original concept.

    To Colin:

    It’s great to have a new voice in this forum. I hope some time to respond to some of the things you’ve said. I tend to think that autopoiesis is a useful concept to apply to multicellular organisms, so it could lead to some interesting discussion. We’ll have to wait until my thoughts coalesce sufficiently though.

    {*} I’m deliberately holding off saying this means it’s autopoietic in order to avoid debates about whether something else is also required, particularly because I’ve chosen a multicellular example. I believe strongly that autopoiesis has the potential to be a useful concept but that the definitions in Maturana and Varela’s work are not sufficient to really tie it down. In my opinion work needs to be done to produce a better definition — but that’s a subject for another post.

  14. Colin Reveley said, on February 18, 2009 at 12:51 am

    Nat – I’m both old and new; It’s just we haven’t met. Ezequiel was my (Msc) supervisor and I know (Dr?) Mike Beaton well. I’m a very close friend of Dan Sayers from undergrad days (he’s new part time easy), and also people like Jim Dyke who I did easy with, if you’ve ever met him (i.e. if he’s actually ever turned up on campus ;). Lots of others too. Dan has a first in mathematics from Oxford. I think someone should persuade him to work on formalizing autopoiesis. But I think he’s more interested in evolution, so probably that’s that.

    in your third line you say: “You’ll get no major debate out of me I’m afraid”

    I understand that you are responding to what you see as the substance of Matt’s comments. w.r.t that, I do not comment. But w.r.t. the comment itself I insist that the notion that autopoiesis is a measurement is simply incorrect. What you cannot quantify (in a real living thing, not a model), you cannot measure.

    But in your comments you raise an interesting point: It is not even established what autopoiesis is in quantitative terms

    Contrast this to, for example, Fernando’s work on the chemoton where coupled differential equations where used successfully to model the self-maintenance of a proposed chemical organization of a protocell, and where indeed I myself tried (and failed) to produce a 2D spatial artificial chemistry that worked like a chemoton. I failed like I say, but I think with more time it could have worked.

    If there were a quantitative definition of autopoiesis complete with changing variables and parameters to twiddle, and if that model could be mapped in a predictive way to cells *generally* (i.e. all cells, regardless of wildly differing biochemistries – prokayotes, euchariotes etc). Then job done. Not that I’m being glib – it could take 500 years work to do that.

    But it would be worth it. the concept of AP has so much more potential than the chemoton. That system proposed specific chemical networks.

    Autopoiesis, on the other hand, is more abstract, and conceivably neutral or at least very flexible w.r.t substrate. That is it’s fascination, just as surely as it’s attribute of defining a ‘concernful’ entity is. It’s interest is its generality.

    If that could be formalized, well, wow. But I suspect even with 500 years it would have to be formalized in conjunction with biological experimentalists, just as theoretical and experimental physicists work together.

    re: 2nd order autopoiesis. I said it was a “stop gap” I think I got that from Dr. Thompson, but also I think it may be voiced in “the tree of knowledge”

    that it is a stop gap does not mean its bullshit. A human has a boundary, and a metabolism.

    I’m just pushing my own theory that 2nd order is not (directly) relevant to cognition/phenomenological experience/intentionality/perception or whatever we choose to call these related phenomena.

    2nd order certainly, and at least, has the relevance that single neurons are ultimately dependent on the large scale metabolism of the organism for their own maintainance. But here again, the timescale is wrong I feel. In the brain, there is arguably a ‘privileged’ timescale, of something like 100-200ms. It is at this timescale that cognitive and experiential effects/changes occur (remember Varela’s view that experience was snapshots, like an animation).

    And those phenomena are caused by the interaction of nerve cells, not large scale metabolism. So naturally, I seek to link autopoiesis of nerve cells at that timescale to those phenomena I am interested in: perception, experience, intentionality, etc – not that I necessarily accept those concepts as descriptors of experience.

    Actually, I’m not even trying to do that; I’m trying to link those phenemena to nerve cell metabolism because autopoiesis is as yet too ill-defined.

    Ultimately: I want to link the *mental* to the *autopietic/metabolic* *directly* – and that means the same timescale.

    why? Well, because the brain is a battle-ground between neurons. they compete with each other for connectivity, although not in a trivially simple way.

    I’ve spoken already at too much length about my views on that, so I wont repeat myslef.

    However, in 2006 I wrote quite an extensive paper on the subject. It’s not good enough to send round, and its too long, and anyway, it contains other irrelevant material.

    I moved house this weekend. I discovered a cache of papers that were far more directly relevant to these issues than I remembered.

    Armed with these papers, and whatever has hapenned between 2006 and 2009, I’d like to take another stab at a paper, this time about this and only this.

    My PhD is getting pretty hot now as it draws to a close, but nonetheless researching and writing this paper might be more fun than TV, If I can keep up the energy for tough thought for my whole wakeful day.

    It might happen. If It does, and it feels right (rigorous) to me, maybe some of you would be interested. It will be largely about the relation of short term calcium based plasticity in synapses to neuronal metabolism – but it will contain much more about nerve cell metabolism and it’s relation to network change at many timescales, neuronal homeostasis at many timescales, and all relevant stuff I can find. It’s important to find the short term plasticity link to metabolism, but a range of timescales are still important.

    I can promise it would not be dry. The plan is a hypothesis driven review (so, inevitably biased) of the literature to get my own thoughts in order, in case it becomes relevant in post-doc interviews, a miracle occurs, and I can work on this (at least partly) for a living. That might not happen quite yet ;) But one day..who knows

    What happens in Varela’s old lab nowadays? Is it still there? His own webpage is frozen at 2001 last I looked.

    cheers,

    C

  15. Tom Froese said, on February 18, 2009 at 11:20 am

    Colin,

    The relationship between timescales and agency has actually been a focus of discussion for many of us for quite some time. As far as I know, nobody has tied this debate closely to the biological literature on things such as neural metabolic rates, so I think it could be a worthwhile project to investigate.

    As for Varela’s old lab in Paris, it’s still carrying on the agenda, mainly in terms of neuro-phenomenology.

    Cheers,
    Tom

  16. Colin Reveley said, on February 18, 2009 at 7:01 pm

    Tom – that is great to know. I will probably apply. I think I’d be a pretty good candidate, looking at the body of varela’s neuroscience work in the literature, it is quite close to ours. Plus I am familiar with the rest of varela’s thought. I might be in with a chance, if something is going over there.

    • Colin Reveley said, on June 10, 2009 at 5:00 pm

      Upon discssion with a number of researchers, I’ve come to the following conclusion: autopoiesis is indeed an ummeasurable property. But the metabolism of a cell is essentially an instance of autopoiesis, and that is well defined.

      I therefore propose to examine the role of the metabolism of nerve cells to their function. A good place to do this is in the organism drosophila. Manipulating the genome and gene expression in drosophila is an established mehod, and there are several examples in the literature of people doing just what I suggest (altering the metabolism of drosophila nerve cells and examining the effect on function.

      But the best thing of all is that one could then rapidly grow a batch of adult flies with the genetic alterations and examine their behavior.

      Drosophila has a simple nervous system in relative terms. But it is complex enough that groups of neurons are important (in contrast to something like aplasia) and it also exhibits behavior hat suggests memory, and recognition of environmental properties with respect to those memories. These seem to me minimal requirements for phenomenological intentionality (what is it like to be a fly? Maybe nothing, but this is about intentionality, concernfulness and agency – not consciousness)

      So I propose to use those mehods to test whether the autopoiesis of nerve cells is related to intentionality, concernfullness, agency in a multicellular organism with a complex nervous system. Metabolism will have to do, but I think that is a good start.


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