Neurons versus Networks: The Interplay between Individual Neurons and Neural Networks in Cognitive Functions

Arshavsky, Yu. I.

doi:10.1177/1073858416670124

Cited by 24 publications

(19 citation statements)

References 114 publications

(138 reference statements)

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“…It is commonly accepted that memory formation is based on the changes in efficacy of synaptic connections among neurons leading to modifications of neural networks (the synaptic plasticity hypothesis, SPH) (Mansvelder and others 2019; Neves and others 2008; Squire and Kandel 2003). The SPH can be briefly formulated as follows: “fire together, wire together.” However, the SPH can hardly explain all known features of memory (Abraham and others 2019; Arshavsky 2006b, 2017; Peña de Ortiz and Arshavsky 2001; Queenan and others 2017; Trettenbrein 2016). One of the most fundamental characteristics of memory is its stability.…”

Section: Mechanism Of Memorymentioning

confidence: 98%

Alzheimer’s Disease: From Amyloid to Autoimmune Hypothesis

Arshavsky

2020

Neuroscientist

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Although Alzheimer’s disease (AD) was described over a century ago, there are no effective approaches to its prevention and treatment. Such a slow progress is explained, at least in part, by our incomplete understanding of the mechanisms underlying the pathogenesis of AD. Here, I champion a hypothesis whereby AD is initiated on a disruption of the blood-brain barrier (BBB) caused by either genetic or non-genetic risk factors. The BBB disruption leads to an autoimmune response against pyramidal neurons located in the allo- and neocortical structures involved in memory formation and storage. The response caused by the adaptive immune system is not strong enough to directly kill neurons but may be sufficient to make them selectively vulnerable to neurofibrillary pathology. This hypothesis is based on the recent data showing that memory formation is associated with epigenetic chromatin modifications and, therefore, may be accompanied by expression of memory-specific proteins recognized by the immune system as “non-self” antigens. The autoimmune hypothesis is testable, and I discuss potential ways for its experimental and clinical verification. If confirmed, this hypothesis can radically change therapeutic approaches to AD prevention and treatment.

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Section: Mechanism Of Memorymentioning

confidence: 98%

Alzheimer’s Disease: From Amyloid to Autoimmune Hypothesis

Arshavsky

2020

Neuroscientist

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“…Cognitive scientists attempting to describe "mentality" face near insurmountable difficulties [29]. There are no objective means for technically describing the subjective aspects of mentality.…”

Section: Limitationsmentioning

confidence: 99%

“…The neural net model first described by the histologist Cajal posited that memory resulted from the cumulative performance of sets of synaptically connected neurons [11]. Hebb, a later generation physiologist, suggested that memory was represented by the joint activation of (sparse) groups of synaptically connected neurons [12] reviewed by [28,29,30]. "Learning" and "memory" followed the strengthening (increased functionality) of synaptic connections, termed "synaptic plasticity (SP)" or "long term potentiation (LTP)".…”

Section: Introductionmentioning

confidence: 99%

Memory, Emotions, Language & Mind

2020

J Psychol Neurosci

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Is “mind” universal to all neural creatures or is it unique to homo sapien, whose talent for language greatly enlarges his/ her ability to recall and enunciate past experience. Philosophers have wrestled with the concept of “mind” but have not delineated whether it emanates from body or spirit. Physicists have called on quantum mechanics to provide an explanatory rationale for mental states. Unfortunately, one cannot employ the metrics of physics to formulate emotions. Computer scientists aspire to emulate the workings of the brain with binary coded algorithms. Though capable of programing a memory function in robots, they too have been hampered by an inability to encode emotions. Upon consideration, “emotions” and “memory” must be integral to the cognitive process implied by “mind”. We biochemists review two proposed processes for the formation and recall of memory. The popular neurological concept is based on “synaptic plasticity”, the ability of neurons to scupt their shape and thereby modulate their signaling functions. It suggests that morphologic and functional modifications of the synapse follow a learning experience, recalled as memory. An alternate biochemical tripartite mechanism is based on interactions of neurons with their surrounding extracellular matrix (nECM) and dopants (metal cations and neurotransmitters (NTs)). Such a chemodynamic process seems physiologically credible in that it involves materials available to the neuron. It invokes a chemical code comprising metalcentered complexes representing cognitive units of information (cuinfo); with emotive states elicited and encoded by neurotransmitters (NTs). The neural chemical code, which evolved from primitive signaling modes of bacteria and slime mold, retained the identical signaling molecules, though augmented with additional neuropeptides. The evolved neurons became organized into ever more complex neural nets instigated a new dimension (phase) of metabolic energy, a mental state characterized by emotive memory, manifest in homo sapien as language and “mind”.

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“…In addition to Trettenbrein’s ( 2016 ) critique, models of learning and memory based on non-synaptic plasticity have been proposed (Mozzachiodi and Byrne, 2010 ; Cacha et al, 2017 ), but these appear to involve neuromodulatory actions which alter the parameters of LTP and LTD, and thus the efficacy of synaptic plasticity. In addition, Arshavsky ( 2006 , 2017 ), Chen et al ( 2014 ) and Bèdècarrats et al ( 2018 ) have advocated a genomic rather than a synaptic theory of memory and argue that changes in individual neurons rather than interconnected neural networks form the basis of memory. Bèdècarrats et al ( 2018 ) demonstrated that the transfer of RNA from trained to naïve animals is sufficient to induce behavioral correlates of memory and that these changes are dependent on DNA methylation.…”

Section: Reconciliation Of the Differences Between Physiologists And mentioning

confidence: 99%

The Synaptic Theory of Memory: A Historical Survey and Reconciliation of Recent Opposition

Langille

Brown

2018

Front. Syst. Neurosci.

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Trettenbrein (2016) has argued that the concept of the synapse as the locus of memory is outdated and has made six critiques of this concept. In this article, we examine these six critiques and suggest that the current theories of the neurobiology of memory and the empirical data indicate that synaptic activation is the first step in a chain of cellular and biochemical events that lead to memories formed in cell assemblies and neural networks that rely on synaptic modification for their formation. These neural networks and their modified synaptic connections can account for the cognitive basis of learning and memory and for memory deterioration in neurological disorders. We first discuss Hebb’s (1949) theory that synaptic change and the formation of cell assemblies and phase sequences can link neurophysiology to cognitive processes. We then examine each of Trettenbrein’s (2016) critiques of the synaptic theory in light of Hebb’s theories and recent empirical data. We examine the biochemical basis of memory formation and the necessity of synaptic modification to form the neural networks underlying learning and memory. We then examine the use of Hebb’s theories of synaptic change and cell assemblies for integrating neurophysiological and cognitive conceptions of learning and memory. We conclude with an examination of the applications of the Hebb synapse and cell assembly theories to the study of the neuroscience of learning and memory, the development of computational models of memory and the construction of “intelligent” robots. We conclude that the synaptic theory of memory has not met its demise, but is essential to our understanding of the neural basis of memory, which has two components: synaptic plasticity and intrinsic plasticity.

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Neurons versus Networks: The Interplay between Individual Neurons and Neural Networks in Cognitive Functions

Cited by 24 publications

References 114 publications

Alzheimer’s Disease: From Amyloid to Autoimmune Hypothesis

Alzheimer’s Disease: From Amyloid to Autoimmune Hypothesis

Memory, Emotions, Language & Mind

The Synaptic Theory of Memory: A Historical Survey and Reconciliation of Recent Opposition

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