Neuroplastic Recovery During Development - Aspects of Neuroplasticity

The Adaptable Mind: What Neuroplasticity and Neural Reuse Tell Us about Language and Cognition - John Zerilli 2021

Neuroplastic Recovery During Development
Aspects of Neuroplasticity

While critical-period plasticity may under the right set of circumstances be “reopened” in later life, the potential for plastic recovery following injury is still very much a function of age. During development, so-called spontaneous changes to the brain resulting from injury are likely overall to reduce the plasticity of the region affected; “[i]n contrast, when the brain fails to change in response to injury there is considerable capacity for modification of cortical circuitry,” particularly through experience, and here the general rule seems to be that the earlier the injury and therapeutic intervention, the better the chance of functional recovery (Kolb et al. 2001, pp. 236—237, 239). This is ostensibly because earlier interventions influence spontaneous changes “in such a way as to maximize functional recovery.” On the whole, younger animals are more plastic than older ones, when it comes to both experience- or activity-dependent learning and spontaneous recovery from injury (Shaw & McEachern 2001, p. 430).

The developing brain is obviously different at different stages, so the character of spontaneous responses to injury can naturally be expected to differ with age. (Whether these responses are beneficial will also depend on age.) The best-studied case of mammalian plasticity is probably in the rat. Neurogenesis in the rat is essentially complete by birth and produces a cortex that is initially equipotential. Between seven and ten days of age, the process of cell migration in the cortex—a process that begins well before birth—comes to an end, at which point activity-independent cell differentiation begins. This process itself ends by about 15 days of age (i.e., at about the time of eye opening), although synaptogenesis continues for a further two to three weeks beyond this point. Compensation for injury suffered during neurogenesis can be quite extensive (Kolb et al. 2001, pp. 228—229). Even the killing of all cerebral neurons by X-radiation appears to provoke regeneration resulting in up to 50 percent of the cerebrum being rebuilt (Kolb et al. 2001, p. 229). Injuries occurring during the period of cell migration and differentiation, however, are functionally devastating, with effects even more pronounced than those caused by the same injuries in adult rats. Then again, during the period immediately following this—and therefore concurrent with a period of intense synaptogenesis—the brain’s capacity for recovery seems to be optimal (Kolb et al. 2001, p. 230).

Just why young neurons are more plastic than older ones is unclear, but a very plausible hypothesis attributes it to the impact of homeostatic mechanisms after the critical period (Shaw & McEachern 2001, pp. 443—444). The absence of homeostatic regulatory mechanisms (like lateral inhibition) during critical periods means that potentiation is ubiquitous and the central nervous system highly unstable. Later, however,

homeostatic regulation of receptors and synapses becomes paramount, and lateral inhibition becomes a dominant feature of neural circuits and the interaction between systems. Given such mechanisms of global homeostasis, the alterations that do occur in the adult CNS [central nervous system] only do so in response to the strongest stressors. (Shaw & McEachern 2001, pp. 443—444)

One upshot of this explanation is that, in one sense, the brain remains intrinsically as plastic as ever, its plastic potential merely suppressed by mechanisms that can themselves be reversed, as we now know they can, “under precisely defined and controlled conditions.”