Harnessing the power of neuroplasticity for intervention

Abstract

A fundamental property of the brain is its capacity to change with a wide variety of experiences, including injury. Although there are spontaneous reparative changes following injury, these changes are rarely sufficient to support significant functional recovery. Research on the basic principles of brain plasticity is leading to new approaches to treating the injured brain. We review factors that affect synaptic organization in the normal brain, evidence of spontaneous neuroplasticity after injury, and the evidence that factors including postinjury experience, pharmacotherapy, and cell-based therapies, can form the basis of rehabilitation strategies after brain injuries early in life and in adulthood.

Keywords: brain plasticity; neurorehabilitation; recovery of function.

Figure 1

Camera lucida drawings of representative segments from medium spiny neurons in the core (top) and shell (bottom) subregions of the nucleus of saline- or amphetamine-treated rats. The drawings to the right of the segments illustrate multiple heading spines, which show a very large drug-induced increase (After Robinson and Kolb, 1997). ^*p < 0.01.

Figure 2

Top: Illustration of location of, and cell morphology, for the analysis of the effects of amphetamine on neuronal structure. Bottom: Summary of the contrasting effects of amphetamine on the medial frontal and orbital frontal cortex. Abbreviations: UNTR, untrained; SUC, trained to bar press for sucrose; AMPH, trained to bar press for amphetamine (After Crombag et al., 2005). ^*Differs from control, p < 0.05; ^†differs from sucrose, p < 0.05.

Figure 3

Effect of tactile stimulation (stroking with a fine brush) on spine density in control, day 3 frontal injury, and day 3 parietal injury in rats (After Kolb and Gibb, 2010).

Figure 4

(A) Extent of ischemic injury across 8 planes of measurement. (C) Illustrate representative camera lucida drawings of layer V pyramidal neurons in anterior cingulate cortex (Cg3) ipsilateral to the lesion (B), or forelimb area (FL) in the contralesional hemisphere (C) from animals treated either with saline or nicotine. Increased dendritic length in the nicotine-treated animals was correlated with improved functional outcome (After Gonzalez et al., 2006).

Figure 5

Both dendritic length and spine density (shown here) in the contralateral forelimb cortex is enhanced by antibodies to NoGo-A (After Papadopoulos et al., 2006).

Figure 6

Inosine combined with NoGo-A receptor blocker (NEP1-40) restores performance with the impaired paw to preoperative levels. Similar results were found with a combination of inosine and complex housing (after Zai et al., 2011). ^* and ^** different from saline-treated controls significant at p < 0.05 and p < 0.01 respectively. ^† and ^†† different from rats treated animals with NEP1-40 at p < 0.05 and p < 0.01 respectively.