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Developmental plasticity

About: Developmental plasticity is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 103438 citations.


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TL;DR: The gross anatomy of Einstein’s brain was within normal limits, with the exception of his parietal lobes, which exhibited increased expansion of the inferior parietal region, which is not surprising.
Abstract: In their detailed necropsy case study recently published in The Lancet, Sandra Witelson et al. described the exceptional brain of Albert Einstein [1]. They found that the gross anatomy of Einstein’s brain was within normal limits, with the exception of his parietal lobes, which exhibited increased expansion of the inferior parietal region (Fig. 1). In view of the knowledge about the brain derived from the neurosciences, this finding is not surprising. In other scientists, too, including the mathematician Karl F. Gauss, an extensive development of the inferior parietal regions was noted [2] and could be described as a kind of brain plasticity. Interestingly, around the turn of the twentieth century, increasing attention was paid to anatomical correlates of intelligence through necropsy studies of the brains of outstanding persons. At that time, functional brain imaging techniques might have been helpful, possibly providing us with data on whether Einstein’s parietal lobes were mainly enlarged through use orthrough constitution; it would have been of most interest to find out which particular linkage of brain areas or systems contributed to his extraordinary creativity. The term “brain plasticity” is, however, usually used to denote the capacity of the brain to compensate the effects of lesions through structural functional changes [3]. Many pathological processes of the nervous system (including the spinal system, the cortico-spinal tracts, the cerebellum and the cortical regions affecting visual, language, motor and other systems) are potentially involved in neuronal plasticity. Neuronal plasticity can appear after suitable rehabilitation, but is also reported spontaneously. Although it is preponderantly seen early in life after prenatal, neonatal or childhood brain damage, reorganization and plastic functional brain changes can be observed in adulthood as well. Brain plasticity has been reported in many diseases and conditions: following a spinal cord injury, after amputation of a limb, after shunt surgery, in Alzheimer’s disease, after stroke, or after traumatic brain injuries. In addition to evaluation on the basis of the clinical findings, the plasticity of the brain can be assessed by electrophysiology, magnetic resonance imaging, positron emission tomography (PET), single-photon emission tomography (SPET), transcranial magnetic stimulation and, of course – especially in experimental studies –, by histology.

34 citations

Journal ArticleDOI
TL;DR: Cellular events which alter protein availability could relieve a constraint on synaptic competition and disturb synaptic clustering mechanisms, which may be detrimental to modifications in neural circuitry following activity.
Abstract: Connections between neurons can undergo long-lasting changes in synaptic strength correlating with changes in structure. These events require the synthesis of new proteins, the availability of which can lead to cooperative and competitive interactions between synapses for the expression of plasticity. These processes can occur over limited spatial distances and temporal periods, defining dendritic regions over which activity may be integrated and could lead to the physical rewiring of synapses into functional groups. Such clustering of inputs may increase the computational power of neurons by allowing information to be combined in a greater than additive manner. The availability of new proteins may be a key modulatory step towards activity-dependent, long-term growth or elimination of spines necessary for remodelling of connections. Thus, the aberrant growth or shrinkage of dendritic spines could occur if protein levels are misregulated. Indeed, such perturbations can be seen in several mental retardation disorders, wherein either too much or too little protein translation exists, matching an observed increase or decrease in spine density, respectively. Cellular events which alter protein availability could relieve a constraint on synaptic competition and disturb synaptic clustering mechanisms. These changes may be detrimental to modifications in neural circuitry following activity.

34 citations

Journal ArticleDOI
TL;DR: Evidence is presented that EE affects social plasticity, via both direct and indirect mechanisms, as well as under pathological conditions, which could inform therapeutic approaches to the many brain disorders involving social dysfunction, including schizophrenia and autism spectrum disorders.

34 citations

Journal ArticleDOI
TL;DR: A clarification of advantageous as well as of aberrant brain plasticity mechanisms in pathological conditions may help to improve the development of rehabilitation methods to better address and facilitate such processes.
Abstract: Brain plasticity can be considered the main result of brain communication with the 'external' and 'internal' environment. Learning new skills as well as endogenous brain function recovery following a lesion are based on neural plasticity, a dynamic phenomenon occurring in response to modification of conscious and pre- or sub-conscious experiences as they progressively stabilize at the synaptic and neural networks level. In spite of previously accepted theory, brain plasticity occurs throughout lifespan being an inner property of the system. Different models of brain plasticity are examined in relation with different modifications of the CNS: healthy brain ageing, neurodegenerative disorders, ischemic stroke and multiple sclerosis. A clarification of advantageous as well as of aberrant brain plasticity mechanisms in pathological conditions may help to improve the development of rehabilitation methods to better address and facilitate such processes.

34 citations

Posted Content
TL;DR: In this article, the authors summarize studies showing that the visual brain of sighted adults retains a type of developmental plasticity called homeostatic plasticity, and this property has been recently exploited successfully for adult amblyopia recover.
Abstract: Between 1 to 5 out of 100 people worldwide has never experienced normotypic vision due to a condition called amblyopia, and about 1 out of 4000 suffer from inherited retinal dystrophies that progressively lead them to blindness. While a wide range of technologies and therapies are being developed to restore vision, a fundamental question still remains unanswered: would the adult visual brain retain a sufficient plastic potential to learn how to see after a prolonged period of abnormal visual experience? In this review we summarize studies showing that the visual brain of sighted adults retains a type of developmental plasticity, called homeostatic plasticity, and this property has been recently exploited successfully for adult amblyopia recover. Next, we discuss how the brain circuits reorganizes when visual stimulation is partially restored by means of a bionic eye in late blinds with Retinitis Pigmentosa. The primary visual cortex in these patients slowly became activated by the artificial visual stimulation, indicating that sight restoration therapies can rely on a considerable degree of spared plasticity in adulthood.

34 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202316
202244
202172
202076
201953
201864