Lesion-induced synaptic plasticity in the somatosensory cortex of prenatally stressed rats

2011 ◽  
Vol 33 (5) ◽  
pp. 548-557 ◽  
Author(s):  
Emel Ulupinar ◽  
Ferruh Yucel ◽  
Kevser Erol
2019 ◽  
Author(s):  
Nicolas Deperrois ◽  
Michael Graupner

AbstractSynaptic efficacy is subjected to activity-dependent changes on short- and long time scales. While short-term changes decay over minutes, long-term modifications last from hours up to a lifetime and are thought to constitute the basis of learning and memory. Both plasticity mechanisms have been studied extensively but how their interaction shapes synaptic dynamics is little known. To investigate how both short- and long-term plasticity together control the induction of synaptic depression and potentiation, we used numerical simulations and mathematical analysis of a calcium-based model, where pre- and postsynaptic activity induces calcium transients driving synaptic long-term plasticity. We found that the model implementing known synaptic short-term dynamics in the calcium transients can be successfully fitted to long-term plasticity data obtained in visual- and somatosensory cortex. Interestingly, the impact of spike-timing and firing rate changes on plasticity occurs in the prevalent firing rate range, which is different in both cortical areas considered here. Our findings suggest that short- and long-term plasticity are together tuned to adapt plasticity to area-specific activity statistics such as firing rates.Author summarySynaptic long-term plasticity, the long-lasting change in efficacy of connections between neurons, is believed to underlie learning and memory. Synapses furthermore change their efficacy reversibly in an activity-dependent manner on the subsecond time scale, referred to as short-term plasticity. It is not known how both synaptic plasticity mechanisms – long- and short-term – interact during activity epochs. To address this question, we used a biologically-inspired plasticity model in which calcium drives changes in synaptic efficacy. We applied the model to plasticity data from visual- and somatosensory cortex and found that synaptic changes occur in very different firing rate ranges, which correspond to the prevalent firing rates in both structures. Our results suggest that short- and long-term plasticity act in a well concerted fashion.


Author(s):  
Olena V. Isaeva ◽  
Olexander O. Lunko ◽  
Artur K. Romanov ◽  
Dmytro S. Isaev

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e74667 ◽  
Author(s):  
Nadine Crouzin ◽  
Kevin Baranger ◽  
Mélanie Cavalier ◽  
Yannick Marchalant ◽  
Catherine Cohen-Solal ◽  
...  

1994 ◽  
Vol 6 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Granger G. Sutton ◽  
James A. Reggia ◽  
Steven L. Armentrout ◽  
C. Lynne D'Autrechy

Past models of somatosensory cortex have successfully demonstrated map formation and subsequent map reorganization following localized repetitive stimuli or deafferentation. They provide an impressive demonstration that fairly simple assumptions about cortical connectivity and synaptic plasticity can account for several observations concerning cortical maps. However, past models have not successfully demonstrated spontaneous map reorganization following cortical lesions. Recently, an assumption universally used in these and other cortex models, that peristimulus inhibition is due solely to horizontal intracortical inhibitory connections, has been questioned and an additional mechanism, the competitive distribution of activity, has been proposed. We implemented a computational model of somatosensory cortex based on competitive distribution of activity. This model exhibits spontaneous map reorganization in response to a cortical lesion, going through a two-phase reorganization process. These results make a testable prediction that can be used to experimentally support or refute part of the competitive distribution hypothesis, and may lead to practically useful computational models of recovery following stroke.


2008 ◽  
Vol 364 (1515) ◽  
pp. 369-381 ◽  
Author(s):  
Kevin Fox

Functional rehabilitation of the cortex following peripheral or central nervous system damage is likely to be improved by a combination of behavioural training and natural or therapeutically enhanced synaptic plasticity mechanisms. Experience-dependent plasticity studies in the somatosensory cortex have begun to reveal those synaptic plasticity mechanisms that are driven by sensory experience and might therefore be active during behavioural training. In this review the anatomical pathways, synaptic plasticity mechanisms and structural plasticity substrates involved in cortical plasticity are explored, focusing on work in the somatosensory cortex and the barrel cortex in particular.


2015 ◽  
Vol 61 (6) ◽  
pp. 11-16 ◽  
Author(s):  
E.V. Isaevа ◽  
◽  
O.O. Lunko ◽  
А.К. Romanov ◽  
D.S. Isaev ◽  
...  

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