Dynamic Brains and the Changing Rules of Neuroplasticity: Implications for Learning and Recovery

Abstract

A growing number of research publications have illustrated the remarkable ability of the brain to reorganize itself in response to various sensory experiences. A traditional view of this plastic nature of the brain is that it is predominantly limited to short epochs during early development. Although examples showing that neuroplasticity exists outside of these finite time-windows have existed for some time, it is only recently that we have started to develop a fuller understanding of the different regulators that modulate and underlie plasticity. In this article, we will provide several lines of evidence indicating that mechanisms of neuroplasticity are extremely variable across individuals and throughout the lifetime. This variability is attributable to several factors including inhibitory network function, neuromodulator systems, age, sex, brain disease, and psychological traits. We will also provide evidence of how neuroplasticity can be manipulated in both the healthy and diseased brain, including recent data in both young and aged rats demonstrating how plasticity within auditory cortex can be manipulated pharmacologically and by varying the quality of sensory inputs. We propose that a better understanding of the individual differences that exist within the various mechanisms that govern experience-dependent neuroplasticity will improve our ability to harness brain plasticity for the development of personalized translational strategies for learning and recovery following brain injury or disease.

Stability in the Face of Change: Lifelong Experience-Dependent Plasticity in the Sensory Cortex

“…Structural changes in inhibitory neurons seen in LPZ suggest that dynamic changes in inhibitory tone may represent a global rule for initiation of plasticity and adjustment of cortical activity following peripheral injury in adults (Keck et al, 2011;Resnik and Polley, 2017), but it is unclear if this plasticity can be modulated by top-down pathways. Identifying precise cellular mechanisms of plasticity after injury, as well as defining potential roles of attention in this process may prove to be crucial for development of novel translational approaches for treatment of brain injury (Voss et al, 2017).…”

Towards an understanding of women's brain aging: the immunology of pregnancy and menopause

“…While the brain may be able to adapt to perimenopausal changes in estrogen receptor networks [166], these processes may also give rise to neurological symptoms, such as cognitive dysfunction [37], particularly in women with lower capacity for neuroplastic adaptation [167].…”

“…E2 is a potent regulator of neuroplasticity in the female brain [59], and it has been suggested that neuroplasticity may play a vital part in understanding the borders between normal aging and early stages of AD [231]. Several of the neural symptoms observed in AD are also found in normal brain aging, including accumulation of amyloid protein and brain atrophy [231,232,233,234], and the levels of neuropathology that can be tolerated without neurological symptoms and cognitive decline varies substantially between individuals [167]. Interestingly, research indicates that intensity and duration of perimenopausal symptoms may represent warning signs for an increased risk of adverse health consequences later in life, particularly neurodegenerative diseases such as AD [37].…”

Brain (re)organization following visual loss

“…A well‐known feature of cortical plasticity is that it is primarily constrained within limited time epochs during early development (Hensch, ; Knudsen, )—although the cortex does retain some plasticity throughout the lifespan (de Villers‐Sidani et al, ; Mishra, de Villers‐Sidani, Merzenich, & Gazzaley, ; Voss, Thomas, Cisneros‐Franco, & de Villers‐Sidani, ). The same is true for visual deprivation, where the loss of sight early in life typically results in significantly more robust cross‐modal plastic changes than for adult‐onset loss of sight (Büchel et al, ; Burton, Snyder, Conturo, et al, ; Burton, Snyder, Diamond, & Raichle, ; Sadato, Okada, Honda, & Yonekura, ; Voss, Gougoux, Lassonde, Zatorre, & Lepore, ; Voss, Gougoux, Zatorre, Lassonde, & Lepore, ).…”