scholarly journals Drifting Assemblies for Persistent Memory

Author(s):  
Yaroslav Felipe Kalle Kossio ◽  
Sven Goedeke ◽  
Christian Klos ◽  
Raoul-Martin Memmesheimer

Change is ubiquitous in living beings. In particular, the connectome and neural representations can change. Nevertheless behaviors and memories often persist over long times. In a standard model, memories are represented by assemblies of strongly interconnected neurons. For faithful storage these assemblies are assumed to consist of the same neurons over time. Here we propose a contrasting memory model with complete temporal remodeling of assemblies, based on experimentally observed changes of connections and neural representations. The assemblies drift freely as spontaneous synaptic turnover or random activity induce neuron exchange. The gradual exchange allows activity dependent and homeostatic plasticity to conserve the representational structure and keep inputs, outputs and assemblies consistent. This leads to persistent memory. Our findings explain recent experimental results on the temporal evolution of fear memory representations and suggest that memory systems need to be understood in their completeness as individual parts may constantly change.

2021 ◽  
Vol 118 (46) ◽  
pp. e2023832118
Author(s):  
Yaroslav Felipe Kalle Kossio ◽  
Sven Goedeke ◽  
Christian Klos ◽  
Raoul-Martin Memmesheimer

Change is ubiquitous in living beings. In particular, the connectome and neural representations can change. Nevertheless, behaviors and memories often persist over long times. In a standard model, associative memories are represented by assemblies of strongly interconnected neurons. For faithful storage these assemblies are assumed to consist of the same neurons over time. Here we propose a contrasting memory model with complete temporal remodeling of assemblies, based on experimentally observed changes of synapses and neural representations. The assemblies drift freely as noisy autonomous network activity and spontaneous synaptic turnover induce neuron exchange. The gradual exchange allows activity-dependent and homeostatic plasticity to conserve the representational structure and keep inputs, outputs, and assemblies consistent. This leads to persistent memory. Our findings explain recent experimental results on temporal evolution of fear memory representations and suggest that memory systems need to be understood in their completeness as individual parts may constantly change.


2013 ◽  
Vol 10 (78) ◽  
pp. 20120558 ◽  
Author(s):  
Felix Droste ◽  
Anne-Ly Do ◽  
Thilo Gross

Dynamical criticality has been shown to enhance information processing in dynamical systems, and there is evidence for self-organized criticality in neural networks. A plausible mechanism for such self-organization is activity-dependent synaptic plasticity. Here, we model neurons as discrete-state nodes on an adaptive network following stochastic dynamics. At a threshold connectivity, this system undergoes a dynamical phase transition at which persistent activity sets in. In a low-dimensional representation of the macroscopic dynamics, this corresponds to a transcritical bifurcation. We show analytically that adding activity-dependent rewiring rules, inspired by homeostatic plasticity, leads to the emergence of an attractive steady state at criticality and present numerical evidence for the system's evolution to such a state.


2019 ◽  
Vol 116 (47) ◽  
pp. 23783-23789 ◽  
Author(s):  
Igor Delvendahl ◽  
Katarzyna Kita ◽  
Martin Müller

Animal behavior is remarkably robust despite constant changes in neural activity. Homeostatic plasticity stabilizes central nervous system (CNS) function on time scales of hours to days. If and how CNS function is stabilized on more rapid time scales remains unknown. Here, we discovered that mossy fiber synapses in the mouse cerebellum homeostatically control synaptic efficacy within minutes after pharmacological glutamate receptor impairment. This rapid form of homeostatic plasticity is expressed presynaptically. We show that modulations of readily releasable vesicle pool size and release probability normalize synaptic strength in a hierarchical fashion upon acute pharmacological and prolonged genetic receptor perturbation. Presynaptic membrane capacitance measurements directly demonstrate regulation of vesicle pool size upon receptor impairment. Moreover, presynaptic voltage-clamp analysis revealed increased Ca2+-current density under specific experimental conditions. Thus, homeostatic modulation of presynaptic exocytosis through specific mechanisms stabilizes synaptic transmission in a CNS circuit on time scales ranging from minutes to months. Rapid presynaptic homeostatic plasticity may ensure stable neural circuit function in light of rapid activity-dependent plasticity.


2019 ◽  
Vol 42 (10) ◽  
pp. 680-692 ◽  
Author(s):  
Natalie C. Tronson ◽  
Ashley A. Keiser

2005 ◽  
Vol 93 (3) ◽  
pp. 1498-1509 ◽  
Author(s):  
Christina Schmitz ◽  
Per Jenmalm ◽  
H. Henrik Ehrsson ◽  
Hans Forssberg

When humans repetitively lift the same object, the fingertip forces are targeted to the weight of the object. The anticipatory programming of the forces depends on sensorimotor memory representations that provide information on the object weight. In the present study, we investigate the neural substrates of these sensorimotor memory systems by recording the neural activity during predictable or unpredictable changes in the weight of an object in a lifting task. An unpredictable change in weight leads to erroneous programming of the fingertip forces. This triggers corrective mechanisms and an update of the sensorimotor memories. In the present fMRI study, healthy right-handed subjects repetitively lifted an object between right index finger and thumb. In the constant condition, which served as a control, the weight of the object remained constant (either 230 or 830 g). The weight alternated between 230 and 830 g during the regular condition and was irregularly changed between the two weights during the irregular condition. When we contrasted regular minus constant and irregular minus constant, we found activations in the right inferior frontal gyrus pars opercularis (area 44), the left parietal operculum and the right supramarginal gyrus. Furthermore, irregular was associated with stronger activation in the right inferior frontal cortex as compared with regular. Taken together, these results suggest that the updating of sensorimotor memory representations and the corrective reactions that occur when we manipulate different objects correspond to changes in synaptic activity in these fronto-parietal circuits.


2016 ◽  
Vol 115 (6) ◽  
pp. 2989-2996 ◽  
Author(s):  
J. Huupponen ◽  
T. Atanasova ◽  
T. Taira ◽  
S. E. Lauri

Development of the neuronal circuitry involves both Hebbian and homeostatic plasticity mechanisms that orchestrate activity-dependent refinement of the synaptic connectivity. AMPA receptor subunit GluA4 is expressed in hippocampal pyramidal neurons during early postnatal period and is critical for neonatal long-term potentiation; however, its role in homeostatic plasticity is unknown. Here we show that GluA4-dependent plasticity mechanisms allow immature synapses to promptly respond to alterations in network activity. In the neonatal CA3, the threshold for homeostatic plasticity is low, and a 15-h activity blockage with tetrodotoxin triggers homeostatic upregulation of glutamatergic transmission. On the other hand, attenuation of the correlated high-frequency bursting in the CA3-CA1 circuitry leads to weakening of AMPA transmission in CA1, thus reflecting a critical role for Hebbian synapse induction in the developing CA3-CA1. Both of these developmentally restricted forms of plasticity were absent in GluA4 −/− mice. These data suggest that GluA4 enables efficient homeostatic upscaling and responsiveness to temporal activity patterns during the critical period of activity-dependent refinement of the circuitry.


2012 ◽  
Vol 55 (3) ◽  
pp. 903-918 ◽  
Author(s):  
Mathias Scharinger ◽  
Philip J. Monahan ◽  
William J. Idsardi

Purpose Speech perception can be described as the transformation of continuous acoustic information into discrete memory representations. Therefore, research on neural representations of speech sounds is particularly important for a better understanding of this transformation. Speech perception models make specific assumptions regarding the representation of mid vowels (e.g., [ɛ]) that are articulated with a neutral position in regard to height. One hypothesis is that their representation is less specific than the representation of vowels with a more specific position (e.g., [æ]). Method In a magnetoencephalography study, we tested the underspecification of mid vowel in American English. Using a mismatch negativity (MMN) paradigm, mid and low lax vowels ([ɛ]/[æ]), and high and low lax vowels ([ i ]/[æ]), were opposed, and M100/N1 dipole source parameters as well as MMN latency and amplitude were examined. Results Larger MMNs occurred when the mid vowel [ɛ] was a deviant to the standard [æ], a result consistent with less specific representations for mid vowels. MMNs of equal magnitude were elicited in the high–low comparison, consistent with more specific representations for both high and low vowels. M100 dipole locations support early vowel categorization on the basis of linguistically relevant acoustic–phonetic features. Conclusion We take our results to reflect an abstract long-term representation of vowels that do not include redundant specifications at very early stages of processing the speech signal. Moreover, the dipole locations indicate extraction of distinctive features and their mapping onto representationally faithful cortical locations (i.e., a feature map).


2017 ◽  
Vol 372 (1715) ◽  
pp. 20160157 ◽  
Author(s):  
Melanie A. Gainey ◽  
Daniel E. Feldman

We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.


Sign in / Sign up

Export Citation Format

Share Document