NERVOUS PLASTICITY

    Characteristics of critical periods. Intermodal plasticity from early sensory deprivation. Environmental enrichment. Cortical plasticity in the adult. Reorganization of cortical maps after injury and rehabilitation therapy. Increase cortical plasticity in adults to promote brain repair. Bibliography

The cerebral cortex is made up of modules formed by columns of neurons that are repeated throughout the cortical surface. Each cortical area comprises many of these modules, each of them responsible for analyzing a particular aspect of the function of this cortical area. Both in the cortical areas dedicated to the analysis of sensory stimuli and in the motor areas or areas dedicated to cognitive aspects, such as short-term memory (working memory), it is noted that the cortical representation forms an ordered map. For example, in the visual cortex the cortical columns close to each other analyze the visual information relating to points of the visual field close to each other, thus forming a real map. Cortical maps are created during development, thanks to mechanisms mediated by molecular factors encoded by specific gene expression programs. However, it has been observed that changes in experience can induce profound alterations in the organization of cortical maps during postnatal development. Cortical maps are therefore not rigid and immutable, but malleable structures that can be modified by experience. The mechanism underlying the action of experience appears to be synaptic plasticity, i.e. the property that the connections between neurons have to modify their strength as a function of their previous activation (Levelt, Hübener 2012). The action of experience on the formation of cortical circuits is greatest during denominated developmental time windows it has been observed that changes in experience can induce profound alterations in the organization of cortical maps during postnatal development. Cortical maps are therefore not rigid and immutable, but malleable structures that can be modified by experience. 

The mechanism underlying the action of experience seems to be synaptic plasticity, i.e. the property that the connections between neurons have to modify their strength as a function of their previous activation (Levelt, Hübener 2012). The action of experience on the formation of cortical circuits is greatest during denominated developmental time windows it has been observed that changes in experience can induce profound alterations in the organization of cortical maps during postnatal development. Cortical maps are therefore not rigid and immutable, but malleable structures that can be modified by experience. The mechanism underlying the action of experience seems to be synaptic plasticity, i.e. the property that the connections between neurons have to modify their strength as a function of their previous activation (Levelt, Hübener 2012). The action of experience on the formation of cortical circuits is greatest during denominated developmental time windows but structures that are malleable and modifiable by experience. The mechanism underlying the action of experience seems to be synaptic plasticity, i.e. the property that the connections between neurons have to modify their strength as a function of their previous activation (Levelt, Hübener 2012). The action of experience on the formation of cortical circuits is greatest during denominated developmental time windows but structures that are malleable and modifiable by experience. The mechanism underlying the action of experience appears to be synaptic plasticity, i.e. the property that the connections between neurons have to modify their strength as a function of their previous activation (Levelt, Hübener 2012). The action of experience on the formation of cortical circuits is greatest during denominated developmental time windowscritical periods(Berardi, Pizzorusso, Maffei 2000). The existence of critical periods for experience-dependent plasticity has been clearly demonstrated for the auditory cortex, for the somatosensory cortex and in particular for the visual cortex, which constitutes the structure on which most of the studies on critical periods of plasticity focus cortical. Starting in the 1960s, the studies of David H. Hubel and Torsten N. Wiesel, who used the developing visual cortex as an experimental model, introduced the concept of critical period. This concept comes from Konrad Lorenz's ethological studies of innate and learned behaviors. There are critical periods for many functions, eg, a song in birds and speech in humans. In the latter case,

Characteristics of critical periods.

 – Classical studies have shown that sensory deprivations (such as monocular deprivation or occlusion of one ear) or sensory impairments (e.g., caused by strabismus or rearing in an auditory depleted environment) cause functional deficits in the sensory system only affected when manipulating the input sensory is carried out in the critical period. Similar deprivations and alterations in mature animals are much less or not at all effective. The length of the critical periods depends on the function being analyzed and on the type of manipulation of experience being carried out. For example, the pain periods measured in terms of recovery from the effects of sensory deprivation are longer than the pain periods measured in terms of the induction of sensory deprivation effects. It should be noted that critical periods have also been observed for forms of sensory plasticity induced by increased sensory experience: in humans, musical training initiated in infancy leads to the increased auditory cortical representation of musical stimuli only if practice begins before age of nine.

The modification of the circuits determined by the plasticity of the critical periods seems to leave a trace that would remain even after the functional effects of the alteration of the experience have regressed with the restoration of a normal experience. Studies in animals have shown that a short period of monocular deprivation causes a decrease in cortical responses to the deprived eye, which may return to normal if the deprivation is quickly removed. However these animals, despite the return to normal from a functional point of view, remain more sensitive to the effects of monocular deprivation. In fact, a second period of monocular deprivation, which in control animals would have no effect because it is too short, becomes effective (Hofer, Mrsic-Flogel, Bonhoeffer et al. 2009).

Intermodal plasticity from early sensory deprivation. 

– The high levels of plasticity observable during development can cause the deprivation of a specific sensory modality to determine changes in the other sensory modalities as well (intermodal plasticity). For example, subjects who became blind early show a better ability to locate sound sources than sighted subjects, especially for peripheral sources. This improved capability could result from the expansion of neural inputs that carry auditory information to visual areas lacking stimulation. Similar phenomena were also observed for tactile inputs in early blind and congenitally deaf subjects, indicating that it is a general phenomenon and not related to the specificity of a sensory area or modality.

Environmental enrichment. – A quality of lifestyle marked by physical activity, cognitive activity, and social interactions is beneficial not only for muscles and social life but also for brain functionality. In animals, exposure to an environment characterized by voluntary physical exercise and exploratory activity with new objects (enriched environment, AA) has both structural effects, with an increase in cortical thickness and synapse density, and functional effects, as it improves learning (Sale, Berardi, Maffei 2014). Exposure to AA from birth produces an acceleration of visual development and prevention of adverse effects due to lack of visual experience. AA acts by influencing the expression of factors crucial for visual cortical plasticities, such as neurotrophic factors and inhibitory circuitry. Even in adults, AA produces effects on visual cortical plasticity, increasing it to the point of favoring recovery from the effects of a previous monocular deprivation. Furthermore, in a mouse model of Alzheimer's, it has been demonstrated that early exposure to AA prevents the onset of cognitive and anatomical deficits, while late exposure slows down their progression.