Factors influencing cerebral plasticity in the normal and injured brain - PubMed (original) (raw)

Factors influencing cerebral plasticity in the normal and injured brain

Bryan Kolb et al. Front Hum Neurosci. 2010.

Abstract

An important development in behavioral neuroscience in the past 20 years has been the demonstration that it is possible to stimulate functional recovery after cerebral injury in laboratory animals. Rodent models of cerebral injury provide an important tool for developing such rehabilitation programs. The models include analysis at different levels including detailed behavioral paradigms, electrophysiology, neuronal morphology, protein chemistry, and epigenetics. A significant challenge for the next 20 years will be the translation of this work to improve the outcome from brain injury and disease in humans. Our goal in the article will be to synthesize the multidisciplinary laboratory work on brain plasticity and behavior in the injured brain to inform the development of rehabilitation programs.

Keywords: brain plasticity; cerebral cortex; recovery of function.

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Figures

Figure 1

Figure 1

Effects of amphetamine and complex housing on dendritic branches (A,C) and spines (B,D) on both apical (A,B) and basilar (C,D) of layer III pyramidal cells in parietal cortex. Branching: complex housing (C) increased the number of both apical and basilar branches, but amphetamine (A) had no effect. Prior amphetamine completely blocked the effect of housing in the complex environment. Spines: complex housing increased the number of spines and amphetamine decreased density. Spine density remained lower in the amphetamine group (A/C) than in the control group (S/C) (after Kolb et al., 2003a).

Figure 2

Figure 2

A schematic illustration of synaptic change in response to complex housing in rats. Pyramidal neurons in prefrontal cortex shows acute changes that revert by baseline in about 10 days. In contrast pyramidal neurons in sensory and motor regions show a slower change that remains months after treatment.

Figure 3

Figure 3

Reaching accuracy expressed as a percent of preoperative performance level. Complex housing improved performance in all groups. Reaching training was effective only in combination with infusion of basic fibroblast growth factor (bFGF) (from Witt-Lajeunesse et al., 2010).

Figure 4

Figure 4

Schematic illustration of the stroke and major cortical efferent pathways. (A) The sensorimotor cortex and other right hemisphere structures were damaged unilaterally by occluding the right middle cerebral artery. The pathways originating from the intact left hemisphere that were traced include the corticorubral (green) and corticospinal (blue) tracts. (B) Coronal section through the forebrain showing the extent of injury (black) and the cells of origin of the intact corticospinal (blue) and corticorubral (green) tracts. (C) Projections from the sensorimotor cortex to the ipsilateral red nucleus. Compensatory growth to the denervated (right) red nucleus is shown in red. (D) Corticospinal tract projections from the intact hemisphere decussate in the caudal medulla, course in the contralateral dorsal funiculus, and synapse primarily on layer 4–6 interneruons in the cervical and lumbar enlargements of the spinal cord. Inosine-induced collateral projections to the denervated side are shown in red (after Chen et al., 2002).

Figure 5

Figure 5

Epidermal growth factor + EPO infusions led to tissue regeneration in the motor cortex after focal stroke. (A,B) Experimental paradigm. Devascularizing lesion on day 0 was followed by EGF and/or EPO infusion via an intraventricular cannula in the contralateral hemisphere beginning on day 7 poststroke. EGF was infused for 7 days followed by EPO for 7 days. (C,D) Dorsal photographs of lesions brains (42 days after stroke), infused with either CSF + CSF (C) or EGF + EPO (D). The stroke produced a chronic cavity whereas treatment with EGF + EPO led to the development of newly generated cortical tissue. (E–H) Coronal cresyl violet-stained sections showing the lesion cavity in a CSF + CSF lesion brain (E) and an EGF + EPO lesion brain (F). The lesion cavity is filled with tissue in the latter brain. The intact hemisphere of the EGF + EPO brain has clear lamination characteristic of motor cortex (G) but there is no obvious organization in the newly generated cortical tissue and a complete absence of a layer I (H) (modified from Kolb et al., 2007).

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