Question
Asked 29th May, 2014
  • Rutgers University, Camden, NJ

What hypotheses are alternatives (or parallels) to synaptic plasticity as substrates for learning and consolidation of memory in the brain?

Aims Neuroscience is requesting paper submissions for our November issue. Manuscripts will need to be received by September 28, 2014, and decisions on acceptance will be completed by October 28. While research indicates synaptic plasticity is often correlated with acquisition and/or consolidation of new learning and that treatments that interfere with or enhance plasticity interfere with or enhance memory, similar conditions are met by other neural mechanisms not necessarily occurring at synapses, for example alteration of intrinsic excitability of neurons. Problems with synaptic plasticity mechanisms, including odd time courses of events or dissociation from behavioral outcomes, have been explained away via the notion of sparse coding, although experimental evidence for such hidden plasticity is inherently difficult to obtain. Is it time for our field to entertain alternate hypotheses, based upon available experimental data?

Most recent answer

I would like to remain modest. However, since we need to discover the mechanism, we have be very hard on the problem. I tried to look at the nervous system with the following thoughts.
1. Keep replication of the mechanism in an engineered system as the gold standard. This will put real pressure on oneself.
2. Now ask the question, “where should be memories be stored for the cue stimulus (stimulus 1) to retrieve it?”
3. For this, at the time of learning two stimuli (stimulus 1 and stimulus 2) should make certain changes. It is reasonable to take place at the location of their convergence.
4. Also accept the fact that memories are first-person internal sensations to which only the owner of the nervous system has access. Behavior of the animals are only surrogate markers for memory.
5. Because of the above challenge, we can only make hypotheses based on logical arguments about the location and mechanism of its storage. We can then go and search for the testable predictions made the hypotheses. This is a highly efficient method used in physics.
6. These led to the development of semblance hypothesis (www.semblancehypothesis.org). Continued searching by this method led to the finding that there should an interaction between the postsynaptic terminals (dendritic spines) that belong to different neurons as a default.
I hope that you will examine this work.

Popular answers (1)

14th Jun, 2014
Hazem Toutounji
University of Nottingham
Recently, Danko Nikolic suggested what he terms Practopoiesis theory. This might be the sort of an alternative hypothesis to the plasticity-centric view of neural adaptability. Nikolic' website states:
"our classical approach to organization of the brain — based on neural networks and the learning mechanisms for the connectivity of those networks — is not sufficient. One additional adaptive mechanism is needed and only then can we explain or mimic biological-like intelligence."
3 Recommendations

All Answers (8)

29th May, 2014
Cheryl Johnston
Self employed
Dear Joseph, I have been considering writing an article on the possible (theoretical) relationship between the combination of BDNF and IGF-I in repairing cognitive Deficits and impairments across disorders. For instance in Depression pharmacological agents that increase BDNF do not necessarily result in improvements in cognitive impairments and deficits, but do have an impact in many cases. On the other hand patients with TBI who do physical execrcise (thereby increasing BDNF expression) and receive exogenous GH (Expressing as IGF-I in the hippocampus) show in most cases a higher level of cognitive recovery than is seen in pharmacological treatments. The hypothesis I hold currently is that Cognitive impairments and deficits may be linked to neuroplasticity which in turn can alter genetic expression and levels of neurotransmitters. This is just my basic hypothesis, naturally many other factors are involved and isolating the effect of any specific element is dangeous ground. I would appreciate your opinion on this.
30th May, 2014
Riccardo Melani
New York University
Hi! There is increasing evidence that an interesting feature of several neural diseases is the GABA switch from hyperpolarizing to depolarizing, it seems to happen also in some kinds of environmental treatments. Homeostatic plasticity is becaming also an intriguing issue studying neural pathologies, and its role in learning and memory could be nice to study deeper.
1 Recommendation
6th Jun, 2014
Hossein Hassanpoor
Dade Pardazi Shenakht Mehvare Atynegar (DSA)
Dear friends
I'm working on a new idea. I believe to "infra synaptic plasticity" which is controlled by astrocytes. Furthermore BDNF which is secreted by astrocytes effect on the neural structure and lead to increasing the capacity of learning. Unfortunately all of my ideas are theoretical, because I don't have any setup for experimental testing and I have just use experimental papers and computational modeling methods.
14th Jun, 2014
Hazem Toutounji
University of Nottingham
Recently, Danko Nikolic suggested what he terms Practopoiesis theory. This might be the sort of an alternative hypothesis to the plasticity-centric view of neural adaptability. Nikolic' website states:
"our classical approach to organization of the brain — based on neural networks and the learning mechanisms for the connectivity of those networks — is not sufficient. One additional adaptive mechanism is needed and only then can we explain or mimic biological-like intelligence."
3 Recommendations
1st Nov, 2014
Danko Nikolić
(Ex) Max Planck Institute for Brain Research
I would like to state that what Hazem wrote above is correct. Practopoiesis is a theory of adaptive systems, from which then follows that synapses could not possibly be place for storing majority of our knowledge. If the system would rely on synapses for that kind of storage, the system would not have enough adaptability to behave intelligently.To be adaptive, the system must implement anapoiesis, which means that knowledge must be stored in a more general form than what can be done with synapses. Specific knowledge is then extracted "on-line" i.e., in real time. This continuous extraction of specific knowledge is the reason why we are conscious (and why machines are not).
1 Recommendation
I would like to remain modest. However, since we need to discover the mechanism, we have be very hard on the problem. I tried to look at the nervous system with the following thoughts.
1. Keep replication of the mechanism in an engineered system as the gold standard. This will put real pressure on oneself.
2. Now ask the question, “where should be memories be stored for the cue stimulus (stimulus 1) to retrieve it?”
3. For this, at the time of learning two stimuli (stimulus 1 and stimulus 2) should make certain changes. It is reasonable to take place at the location of their convergence.
4. Also accept the fact that memories are first-person internal sensations to which only the owner of the nervous system has access. Behavior of the animals are only surrogate markers for memory.
5. Because of the above challenge, we can only make hypotheses based on logical arguments about the location and mechanism of its storage. We can then go and search for the testable predictions made the hypotheses. This is a highly efficient method used in physics.
6. These led to the development of semblance hypothesis (www.semblancehypothesis.org). Continued searching by this method led to the finding that there should an interaction between the postsynaptic terminals (dendritic spines) that belong to different neurons as a default.
I hope that you will examine this work.

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