Multiscale Modeling and Synaptic Plasticity

Bhalla, Upinder S.

doi:10.1016/b978-0-12-397897-4.00012-7

Cited by 10 publications

(21 citation statements)

References 119 publications

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“…http://dx.doi.org/10.1101/203943 doi: bioRxiv preprint first posted online Oct. 16, 2017; Retrograde messengers are responsible for intimating the presynaptic terminal about postsynaptic calcium elevation. Illustration incorporates conclusions from previous studies (Bhalla, 2014;Bhalla and Iyengar, 1999;Kotaleski and Blackwell, 2010;Manninen et al, 2010;Regehr, 2012;Regehr et al, 2009). synaptic strength, and independent or concomitant long-term changes in any of these components would result in the expression synaptic plasticity.…”

Section: (B)mentioning

confidence: 91%

“…http://dx.doi.org/10.1101/203943 doi: bioRxiv preprint first posted online Oct. 16, 2017; pre-and post-synaptic sides, that are involved in the translation of induction to expression include several enzymes that mediate posttranslational modification of disparate protein substrates, protein synthesis regulators, retrograde messengers, protein trafficking regulators and mechanisms mediating structural plasticity of spines, dendrites and boutons (Ajay and Bhalla, 2006;Berridge, 2006;Bhalla, 2014;Bhalla and Iyengar, 1999;Derkach et al, 2007;Eungdamrong and Iyengar, 2004;Holtmaat and Svoboda, 2009;Kandel et al, 2014;Kennedy, 2000;Kennedy et al, 2005;Kholodenko, 2006;Korte and Schmitz, 2016;Lamprecht and LeDoux, 2004;Larkman and Jack, 1995;Malenka and Bear, 2004;Malinow and Malenka, 2002;Manninen et al, 2010;Mayford et al, 2012;Neves and Iyengar, 2009;Neves et al, 2008b;O'Dell et al, 1991;Parekh, 2008;Raymond, 2007;Regehr et al, 2009;Rizzuto and Pozzan, 2006;Shah et al, 2010;Soderling and Derkach, 2000;Weng et al, 1999;Wenthold et al, 2003;Wilson and Nicoll, 2002).…”

Section: Degeneracy In Signaling Cascades That Regulate Synaptic Plasmentioning

confidence: 99%

“…Future theoretical and experimental investigations into hippocampal plasticity should therefore account for the truly ubiquitous nature of plasticity in designing their experiments and addressing outstanding questions, rather than assuming that plasticity is confined to one single component or the other (Bhalla, 2014;Kim and Linden, 2007).…”

Section: Degeneracy In the Induction And Expression Of Non-synaptic Pmentioning

confidence: 99%

“…As is evident from this complexity and associated animal-to-animal and cell-to-cell variability, which involves the ensemble of mechanisms and interactions discussed above not just from within the hippocampus but also from other brain regions, demonstrating causality with reference to learning and memory and any one specific form of plasticity or cellular/molecular substrate, has proven extremely challenging (Andersen et al, 2006;Bennett and Hacker, 2003;Bhalla, 2014;Bhalla and Iyengar, 1999;Bliss and Collingridge, 1993;Collingridge and Bliss, 1987;Jazayeri and Afraz, 2017;Kandel, 2001;Kandel et al, 2014;Kim and Linden, 2007;Kotaleski and Blackwell, 2010;Krakauer et al, 2017;Lynch, 2004;Manninen et al, 2010;Martin et al, 2000;Martinez and Derrick, 1996;Mayford et al, 2012;Mozzachiodi and Byrne, 2010;Neves et al, 2008a;Zhang and Linden, 2003).…”

Section: Degeneracy In Learning and Memorymentioning

confidence: 99%

“…Blocking NMDAR would also induce a significant amount of metaplasticity in all forms of plasticity, thereby leaving several things altered apart from the intended response. Returning to our experimental plan on the role of component X, there could several other secondary and unintended effects of blocking plasticity in component X that spans the hippocampus and other brain regions (Bhalla, 2014;Jazayeri and Afraz, 2017;Kotaleski and Blackwell, 2010;Krakauer et al, 2017). Thus, it is prudent not to dismiss absence of measurements as absence of evidence for other components.…”

Section: Inevitable Flaws In An Experimental Plan To Establish Causalmentioning

confidence: 99%

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Degeneracy in hippocampal physiology and plasticity

Rathour

Narayanan

2017

Preprint

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Degeneracy, defined as the ability of structurally disparate elements to perform analogous function, has largely been assessed from the perspective of maintaining robustness of physiology or plasticity. How does the framework of degeneracy assimilate into an encoding system where the ability to change is an essential ingredient for storing new incoming information? Could degeneracy maintain the balance between the apparently contradictory goals of the need to change for encoding and the need to resist change towards maintaining homeostasis? In this review, we explore these fundamental questions with the mammalian hippocampus as an example encoding system. We systematically catalog lines of evidence, spanning multiple scales of analysis, that demonstrate the expression of degeneracy in hippocampal physiology and plasticity. We assess the potential of degeneracy as a framework to achieve encoding and homeostasis without cross-interferences, and postulate that multiscale parametric and interactional complexity could establish disparate routes towards accomplishing these conjoint goals. These disparate routes then provide several degrees of freedom to the encodinghomeostasis system in accomplishing its tasks in an input-and state-dependent manner. Finally, the expression of degeneracy spanning multiple scales offers an ideal reconciliation to several outstanding controversies, through the recognition that the seemingly contradictory disparate observations are merely alternate routes that the system might recruit towards accomplishment of its goals. Juxtaposed against the ubiquitous prevalence of degeneracy and its strong links to evolution, it is perhaps apt to add a corollary to Theodosius Dobzhansky's famous quote and state "nothing in physiology makes sense except in the light of degeneracy".peer-reviewed)

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Section: (B)mentioning

confidence: 91%

Section: Degeneracy In Signaling Cascades That Regulate Synaptic Plasmentioning

confidence: 99%

Section: Degeneracy In the Induction And Expression Of Non-synaptic Pmentioning

confidence: 99%

Section: Degeneracy In Learning and Memorymentioning

confidence: 99%

Section: Inevitable Flaws In An Experimental Plan To Establish Causalmentioning

confidence: 99%

See 3 more Smart Citations

Degeneracy in hippocampal physiology and plasticity

Rathour

Narayanan

2017

Preprint

View full text Add to dashboard Cite

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Degeneracy in hippocampal physiology and plasticity

2019

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Degeneracy, defined as the ability of structurally disparate elements to perform analogous function, has largely been assessed from the perspective of maintaining robustness of physiology or plasticity. How does the framework of degeneracy assimilate into an encoding system where the ability to change is an essential ingredient for storing new incoming information? Could degeneracy maintain the balance between the apparently contradictory goals of the need to change for encoding and the need to resist change towards maintaining homeostasis? In this review, we explore these fundamental questions with the mammalian hippocampus as an example encoding system. We systematically catalog lines of evidence, spanning multiple scales of analysis that point to the expression of degeneracy in hippocampal physiology and plasticity. We assess the potential of degeneracy as a framework to achieve the conjoint goals of encoding and homeostasis without cross‐interferences. We postulate that biological complexity, involving interactions among the numerous parameters spanning different scales of analysis, could establish disparate routes towards accomplishing these conjoint goals. These disparate routes then provide several degrees of freedom to the encoding‐homeostasis system in accomplishing its tasks in an input‐ and state‐dependent manner. Finally, the expression of degeneracy spanning multiple scales offers an ideal reconciliation to several outstanding controversies, through the recognition that the seemingly contradictory disparate observations are merely alternate routes that the system might recruit towards accomplishment of its goals.

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Dominant role of adult neurogenesis‐induced structural heterogeneities in driving plasticity heterogeneity in dentate gyrus granule cells

2022

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Neurons and synapses manifest pronounced variability in the amount of plasticity induced by identical activity patterns. The mechanisms underlying such plasticity heterogeneity, which have been implicated in context-specific resource allocation during encoding, have remained unexplored. Here, we employed a systematic physiologically constrained parametric search to identify the cellular mechanisms behind plasticity heterogeneity in dentate gyrus granule cells. We used heterogeneous model populations to ensure that our conclusions were not biased by parametric choices in a single hand-tuned model. We found that each of intrinsic, synaptic, and structural heterogeneities independently yielded heterogeneities in synaptic plasticity profiles obtained with two different induction protocols. However, among the disparate forms of neural-circuit heterogeneities, our analyses demonstrated the dominance of neurogenesis-induced structural heterogeneities in driving plasticity heterogeneity in granule cells. We found that strong relationships between neuronal intrinsic excitability and plasticity emerged only when adult neurogenesis-induced heterogeneities in neural structure were accounted for. Importantly, our analyses showed that it was not imperative that the manifestation of neural-circuit heterogeneities must translate to heterogeneities in plasticity profiles. Specifically, despite the expression of heterogeneities in structural, synaptic, and intrinsic neuronal properties, similar plasticity profiles were attainable across all models through synergistic interactions among these heterogeneities. We assessed the parametric combinations required for the manifestation of such degeneracy in the expression of plasticity profiles. We found that immature cells showed physiological plasticity profiles despite receiving afferent inputs with weak synaptic strengths. Thus, the high intrinsic excitability of immature granule cells was sufficient to counterbalance their low excitatory drive in the expression of plasticity profile degeneracy. Together, our analyses demonstrate that disparate forms of neural-circuit heterogeneities could mechanistically drive plasticity heterogeneity, but also caution against treating neural-circuit heterogeneities as proxies for plasticity heterogeneity. Our study emphasizes the need for quantitatively characterizing the relationship between neural-circuit and plasticity heterogeneities across brain regions.Sameera Shridhar and Poonam Mishra contributed equally to this study.

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Multiscale Modeling and Synaptic Plasticity

Cited by 10 publications

References 119 publications

Degeneracy in hippocampal physiology and plasticity

Degeneracy in hippocampal physiology and plasticity

Degeneracy in hippocampal physiology and plasticity

Dominant role of adult neurogenesis‐induced structural heterogeneities in driving plasticity heterogeneity in dentate gyrus granule cells

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