The Functional Consequences of Cortical Plasticity in Adult Humans

1998 ◽  
Vol 95 (s39) ◽  
pp. 17P-17P
Author(s):  
Ceg Moore ◽  
W Schady
Keyword(s):  
Cortical Plasticity ◽  
Adult Humans ◽  
Functional Consequences

scholarly journals Somatosensory cortical plasticity in adult humans revealed by magnetoencephalography.

1993 ◽  
Vol 90 (8) ◽  
pp. 3593-3597 ◽  
Author(s):  
A. Mogilner ◽  
J. A. Grossman ◽  
U. Ribary ◽  
M. Joliot ◽  
J. Volkmann ◽  
...  
Keyword(s):  
Cortical Plasticity ◽  
Adult Humans

scholarly journals Sleep Slow Oscillations and Spindles encode ocular dominance plasticity and promote its consolidation in adult humans

2021 ◽  
Author(s):  
Danilo Menicucci ◽  
Claudia Lunghi ◽  
Andrea Zaccaro ◽  
Maria Concetta Morrone ◽  
Angelo Gemignani
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Ocular Dominance Plasticity ◽  
Slow Oscillations ◽  
Adult Humans ◽  
The Individual ◽  
Visual Cortical

Sleep and plasticity are highly interrelated, as sleep slow oscillations and sleep spindles are associated with consolidation of Hebbian-based processes. However, in adult humans, visual cortical plasticity is mainly sustained by homeostatic mechanisms, for which the role of sleep is still largely unknown. Here we demonstrate that non-REM sleep stabilizes homeostatic plasticity of ocular dominance in adult humans. We found that the effect of short-term monocular deprivation (boost of the deprived eye) was preserved at the morning awakening (>6 hours after deprivation). Subjects exhibiting stronger consolidation had increased sleep spindle density in frontopolar electrodes, suggesting distributed consolidation processes. Crucially, the individual susceptibility to visual homeostatic plasticity was encoded by changes in sleep slow oscillation rate and shape and spindle power in occipital sites, consistent with an early visual cortical site of ocular dominance homeostatic plasticity.

scholarly journals Functional Consequences of the Disturbances in the GABA-Mediated Inhibition Induced by Injuriesin the Cerebral Cortex

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Barbara Imbrosci ◽  
Thomas Mittmann
Keyword(s):  
Cortical Plasticity ◽  
Epileptiform Activity ◽  
Mammalian Brain ◽  
Negative Events ◽  
Plastic Properties ◽  
Beneficial Effects ◽  
Promising Strategy ◽  
Functional Consequences ◽  
Gathering Data ◽  
Cortical Injuries

Cortical injuries are often reported to induce a suppression of the intracortical GABAergic inhibition in the surviving, neighbouring neuronal networks. Since GABAergic transmission provides the main source of inhibition in the mammalian brain, this condition may lead to hyperexcitability and epileptiform activity of cortical networks. However, inhibition plays also a crucial role in limiting the plastic properties of neuronal circuits, and as a consequence, interventions aiming to reestablish a normal level of inhibition might constrain the plastic capacity of the cortical tissue. A promising strategy to minimize the deleterious consequences of a modified inhibitory transmission without preventing the potential beneficial effects on cortical plasticity may be to unravel distinct GABAergic signaling pathways separately mediating these positive and negative events. Here, gathering data from several recent studies, we provide new insights to better face with this “double coin” condition in the attempt to optimize the functional recovery of patients.

Adaptive and Maladaptive Neural Plasticity Due to Facial Nerve Palsy

2016 ◽  
Vol 224 (2) ◽  
pp. 102-111 ◽  
Author(s):  
Carsten M. Klingner ◽  
Stefan Brodoehl ◽  
Gerd F. Volk ◽  
Orlando Guntinas-Lichius ◽  
Otto W. Witte
Keyword(s):  
Facial Nerve ◽  
Neural Plasticity ◽  
Cortical Plasticity ◽  
Brain Plasticity ◽  
Motor Nerve ◽  
Predictive Coding ◽  
Theoretical Framework ◽  
Cortical Reorganization ◽  
Nerve Lesion ◽  
Peripheral Facial Palsy

Abstract. This paper reviews adaptive and maladaptive mechanisms of cortical plasticity in patients suffering from peripheral facial palsy. As the peripheral facial nerve is a pure motor nerve, a facial nerve lesion is causing an exclusive deefferentation without deafferentation. We focus on the question of how the investigation of pure deefferentation adds to our current understanding of brain plasticity which derives from studies on learning and studies on brain lesions. The importance of efference and afference as drivers for cortical plasticity is discussed in addition to the crossmodal influence of different competitive sensory inputs. We make the attempt to integrate the experimental findings of the effects of pure deefferentation within the theoretical framework of cortical responses and predictive coding. We show that the available experimental data can be explained within this theoretical framework which also clarifies the necessity for maladaptive plasticity. Finally, we propose rehabilitation approaches for directing cortical reorganization in the appropriate direction and highlight some challenging questions that are yet unexplored in the field.

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