Pre- and postnatal FGF-2 both facilitate recovery and alter cortical morphology following early medial prefrontal cortical injury

Comeau, Wendy; Hastings, Erica; Kolb, Bryan

doi:10.1016/j.bbr.2007.02.026

Cited by 37 publications

(14 citation statements)

References 42 publications

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“…We have shown elsewhere that administration of bFGF either prenatally or postinjury facilitates recovery from medial frontal injury on postnatal day 2/3 (Comeau et al, 2006;Gibb & Kolb, 2005). The current study is consistent with these findings.…”

Section: Bfgf Acts To Facilitate Functional Recovery After Perinatal-supporting

confidence: 95%

“…It is known, for example, that adult rats placed in enriched environments show an increased expression of bFGF and that psychomotor stimulants increase bFGF production (Flores & Stewart, 2000), an increase that also is correlated with increased synaptogenesis (Robinson & Kolb, 2004) and recovery from cortical injury (e.g., Feeney & Hovda, 1985). Furthermore, we have shown elsewhere that administration of bFGF after perinatal cortical lesions can enhance functional outcome (e.g., Comeau, Hastings, & Kolb, 2007), a result that again suggests that bFGF may play a role in enhancing synaptic reorganization. It is not known, however, whether enriched housing might further enhance functional recovery in animals with postlesion treatment with bFGF.…”

Section: Introductionmentioning

confidence: 93%

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Therapeutic effects of complex rearing or bFGF after perinatal frontal lesions

Comeau

Gibb

Hastings

et al. 2008

Developmental Psychobiology

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We investigated the effects of an enriched environment and/or basic fibroblast growth factor (bFGF) on recovery from neonatal frontal injury in rats. Rats received medial frontal lesions, or sham surgery, on postnatal day (P) 2/3. In the first set of experiments (Experiments 1 and 2), rats were housed in enriched environments that consisted of a large enclosure with multiple objects (or standard housing) for 90 days beginning at weaning (P22) or in adulthood (P110). In Experiment 3, the rats either received 7 days of subcutaneous bFGF beginning on the day after surgery or bFGF plus enriched housing beginning at weaning. After the 90-day housing period, the animals were tested on a spatial navigation task and a skilled reaching task. Early lesions of the medial frontal cortex caused severe impairments in spatial learning but this deficit was markedly reduced with enriched housing, bFGF, or a combination of both, with the latter being most effective. The housing effects varied with age, however: the earlier the experience began, the better the outcome. Enriched housing increased dendritic length in cortical pyramidal neurons, an effect that was greater in the lesion than the control animals, and enriched housing reversed the lesion-induced decrease in spine density. Enriched environment increased the thickness of the cortical mantle in both lesion and controls whereas bFGF had no effect. Experience thus can affect functional and anatomical outcome after early brain injury but the effects vary with age at experience and may be facilitated by treatment with bFGF.

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Section: Bfgf Acts To Facilitate Functional Recovery After Perinatal-supporting

confidence: 95%

Section: Introductionmentioning

confidence: 93%

Therapeutic effects of complex rearing or bFGF after perinatal frontal lesions

Comeau

Gibb

Hastings

et al. 2008

Developmental Psychobiology

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“…Moreover, forced use of one forelimb by constraining the other forelimb upregulates the expression of FGF-2 [31]. FGF-2 is also a potent chemotactic factor for endothelial cells [32], and it plays a role in modulating recovery from cerebral injury [33], [34]. FGF-2 was found to improve sensorimotor deficits and to reduce infarct size following cerebral ischemia in adult rats [35], and neutralizing antibodies to FGF-2 blocks recovery from motor cortex lesions [36].…”

Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor-2 Induced by Enriched Environment Enhances Angiogenesis and Motor Function in Chronic Hypoxic-Ischemic Brain Injury

Seo

Suh

et al. 2013

PLoS ONE

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This study aimed to investigate the effects of enriched environment (EE) on promoting angiogenesis and neurobehavioral function in an animal model of chronic hypoxic-ischemic (HI) brain injury. HI brain damage was induced in seven day-old CD-1® mice by unilateral carotid artery ligation and exposure to hypoxia (8% O2 for 90 min). At six weeks of age, the mice were randomly assigned to either EE or standard cages (SC) for two months. Rotarod, forelimb-use asymmetry, and grip strength tests were performed to evaluate neurobehavioral function. In order to identify angiogenic growth factors regulated by EE, an array-based multiplex ELISA assay was used to measure the expression in frontal cortex, striatum, and cerebellum. Among the growth factors, the expression of fibroblast growth factor-2 (FGF-2) was confirmed using western blotting. Platelet endothelial cell adhesion molecule-1 (PECAM-1) and α-smooth muscle actin (α-SMA) were also evaluated using immunohistochemistry. As a result, mice exposed to EE showed significant improvements in rotarod and ladder walking performances compared to SC controls. The level of FGF-2 was significantly higher in the frontal cortex of EE mice at 8 weeks after treatment in multiplex ELISA and western blot. On the other hand, FGF-2 in the striatum significantly increased at 2 weeks after exposure to EE earlier than in the frontal cortex. Expression of activin A was similarly upregulated as FGF-2 expression pattern. Particularly, all animals treated with FGF-2 neutralizing antibody abolished the beneficial effect of EE on motor performance relative to mice not given anti-FGF-2. Immunohistochemistry showed that densities of α-SMA+ and PECAM-1+ cells in frontal cortex, striatum, and hippocampus were significantly increased following EE, suggesting the histological findings exhibit a similar pattern to the upregulation of FGF-2 in the brain. In conclusion, EE enhances endogenous angiogenesis and neurobehavioral functions mediated by upregulation of FGF-2 in chronic hypoxic-ischemic brain injury.

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“…Cell-based therapies have been little used in development, the exception being Fibroblast Growth Factor-2 (FGF-2), a protein implicated in brain development and wound healing. FGF-2 stimulates functional improvement and synaptic changes after cortical injury in the first week of life but has much less impressive effects in adulthood (Comeau et al, 2007). Curiously, whereas FGF-2 induces synaptic change after perinatal injury, it mobilizes stem cells to generate and migrate to the site of injury in the second week of life (Monfils et al, 2008).…”

Section: Modulating Functional Recovery At Different Agesmentioning

confidence: 99%

Recovery of Function: Dependency on Age

Kolb¹

2015

International Encyclopedia of the Social &Amp; Behavioral Sciences

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When the brain is injured there is a cascade of cellular events that can both seriously compromise the functioning of the brain and stimulate reparative processes that underlie eventual functional improvement. The likelihood and intensity of these cellular changes vary with the age of the individual. In particular, there are times during brain development, which begins in utero and continues well into the third decade of life, when brain injury may lead to strikingly different outcomes. These critical periods are related to the varying maturational events occurring at different stages of brain development.Brain damage results in lost functions that do not completely return after injury. The brain is capable of compensatory change, however, thus allowing at least partial restitution of function, the extent of recovery varying with the precise developmental state of the brain at the time of injury. Thus, although some compensatory change is possible in the brain at any age the best outcome from cerebral injury occurs after damage during the period of maximal synaptogenesis, which is in the first two years of life in humans. The formation of new synapses provides a mechanism to modify the remaining cerebral circuitry, which in turn allows each neuron to increase its processing capacity. Although it is uncommon, in certain restricted cases the brain also may generate new neurons that can be integrated into the remaining brain and support functional recovery. Treatments that increase synaptogenesis or cell generation will enhance functional recovery and events that reduce synaptic formation will retard recovery.When the brain is injured in adulthood there is a loss of function followed by a prolonged period during which there is partial recovery of some types of cognitive and motor functions. The extent of functional recovery varies with age and although injury to the infant brain can have less severe consequences than similar injury in adulthood, there are times during development when injury is especially devastating. These differences are related to the details of anatomical changes at different stages of brain development. The difference in functional outcome after injury at different ages is related to the injury-induced changes in neuronal structure, changes that are referred to as plastic changes. These plastic changes are similar to the neural and glial changes that are associated with learning in the normal brain. Various factors, such as experience, hormones, and drugs modulate these plastic changes. Even these factors cannot completely restore lost functions because there are limits to brain plasticity.

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Pre- and postnatal FGF-2 both facilitate recovery and alter cortical morphology following early medial prefrontal cortical injury

Cited by 37 publications

References 42 publications

Therapeutic effects of complex rearing or bFGF after perinatal frontal lesions

Therapeutic effects of complex rearing or bFGF after perinatal frontal lesions

Fibroblast Growth Factor-2 Induced by Enriched Environment Enhances Angiogenesis and Motor Function in Chronic Hypoxic-Ischemic Brain Injury

Recovery of Function: Dependency on Age

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