Plasticity of nonneuronal brain tissue: Roles in developmental disorders

Abstract

Neuronal and nonneuronal plasticity are both affected by environmental and experiential factors. Remodeling of existing neurons induced by such factors has been observed throughout the brain, and includes alterations in dendritic field dimensions, synaptogenesis, and synaptic morphology. The brain loci affected by these plastic neuronal changes are dependent on the type of experience and learning. Increased neurogenesis in the hippocampal dentate gyrus is a well-documented response to environmental complexity ("enrichment") and learning. Exposure to challenging experiences and learning opportunities also alters existing glial cells (i.e., astrocytes and oligodendrocytes), and up-regulates gliogenesis, in the cerebral cortex and cerebellum. Such glial plasticity often parallels neuronal remodeling in both time and place, and this enhanced morphological synergism may be important for optimizing the functional interaction between glial cells and neurons. Aberrant structural plasticity of nonneuronal elements is a contributing factor, as is aberrant neuron plasticity, to neurological and developmental disorders such as epilepsy, autism, and mental retardation (i.e., fragile X syndrome). Some of these nonneuronal pathologies include abnormal cerebral and cerebellar white matter and myelin-related proteins in autism; abnormal myelin basic protein in fragile X syndrome (FXS); and abnormal astrocytes in autism, FXS, and epilepsy. A number of recent studies demonstrate the possibility of using environmental and experiential intervention to reduce or ameliorate some of the neuronal and nonneuronal abnormalities, as well as behavioral deficits, present in these neurological and developmental disorders.

Altered differentiation of neural stem cells in fragile X syndrome

“…This finding is in agreement with observations in imaging studies, which indicate that the gross morphology of the fmr1-KO mouse brain is normal (38). Structural brain abnormalities with different characteristics depending on the specific brain location, however, have been reported in MRI studies of fragile X patients (39,40). It is possible that such subtle abnormalities might result from alterations of NSC differentiation, a possibility that remains to be investigated.…”

Neuroanatomical Markers of Social Hierarchy Recognition in Humans: A Combined ERP/MRI Study

“…An important implication of this possible difference in cellular underpinnings is that some of the associations found are more prone to be explained by environmental effects, whereas others would be driven by genetic factors to a higher extent. More specifically, CT associations may be more sensitive to environmental pressures, given that CT-related microstructures such as glial and capillary support, as well as dendritic arborization (Thompson et al, 2007), dendritic and spine rearrangement and elimination (Petanjek et al, 2008), and gliogenesis (Dong and Greenough, 2004) are sensitive to learning and experience, whereas CSA-related results are likely to be under a higher genetic control, given that CSA is thought to depend on neurogenesis and neuronal migration and such processes are known to suffer little modifications after term gestation (Hill et al, 2010). Because most of the results at the cortical level of analysis were found for CSA, the question arises of to what extent is social status recognition under genetic control and whether appropriate training would allow modulating the effect of social hierarchy over other cognitive processes (Santamaría-García et al, 2014).…”

White Matter Plasticity and Enhanced Remyelination in the Maternal CNS

“…The process of myelination represents a major form of plasticity in the developing and adult CNS and is postulated to influence neuronal health, conductance velocity, and the synchronicity of spike time arrival, thus enhancing CNS function (Dong and Greenough, 2004;Fields, 2005). Furthermore, OPCs and newly generated oligodendrocytes are required for the intrinsic repair of myelin damage in the adult CNS (Polito and Reynolds, 2005).…”

“…Plasticity at the level of myelination has been well documented during brain development (Dong and Greenough, 2004), and, in part, myelination in the developing brain is an activity-dependent phenomenon (Szeligo and Leblond, 1977;Tauber et al, 1980;Sirevaag and Greenough, 1987;Demerens et al, 1996;Stevens et al, 2002). In the adult CNS, the total number of oligodendrocytes (Dawson et al, 2003;Peters and Sethares, 2004) and myelinated axons (Sturrock, 1980;Nunez et al, 2000) increases with age, suggesting that myelination continues throughout life.…”