Recovery from early cortical damage in rats, VII. Comparison of the behavioural and anatomical effects of medial prefrontal lesions at different ages of neural maturation

Kolb, Bryan; Petrie, Bruce F.; Cioe, Jan

doi:10.1016/0166-4328(95)00254-5

Cited by 77 publications

(39 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There may be peaks and valleys of vulnerability, similar to those shown for neuronal plasticity, related to cycles of cell growth, apoptosis, synaptic connectivity, and myelination. 10,12,27,28 For this reason, the three age groups were chosen to correspond to specific human developmental stages. During the first few weeks of life in piglets (infant stage), myelination and electroencephalographic patterns remain similar to those of the human newborn.…”

Section: Discussionmentioning

confidence: 99%

Maturation-dependent response of the piglet brain to scaled cortical impact

Duhaime¹,

Margulies²,

Durham³

et al. 2000

Journal of Neurosurgery

148

120

View full text Add to dashboard Cite

Object. The goal of this study was to investigate the relationship between maturational stage and the brain's response to mechanical trauma in a gyrencephalic model of focal brain injury. Age-dependent differences in injury response might explain certain unique clinical syndromes seen in infants and young children and would determine whether specific therapies might be particularly effective or even counterproductive at different ages.Methods. To deliver proportionally identical injury inputs to animals of different ages, the authors have developed a piglet model of focal contusion injury by using specific volumes of rapid cortical displacement that are precisely scaled to changes in size and dimensions of the growing brain. Using this model, the histological response to a scaled focal cortical impact was compared at 7 days after injury in piglets that were 5 days, 1 month, and 4 months of age at the time of trauma. Despite comparable injury inputs and stable physiological parameters, the percentage of hemisphere injured differed significantly among ages, with the youngest animals sustaining the smallest lesions (0.8%, 8.4%, and 21.5%, for 5-day-, 1-month-, and 4-month-old animals, respectively, p = 0.0018).Conclusions. These results demonstrate that, for this particular focal injury type and severity, vulnerability to mechanical trauma increases progressively during maturation. Because of its developmental and morphological similarity to the human brain, the piglet brain provides distinct advantages in modeling age-specific responses to mechanical trauma. Differences in pathways leading to cell death or repair may be relevant to designing therapies appropriate for patients of different ages.

show abstract

Section: Discussionmentioning

confidence: 99%

Maturation-dependent response of the piglet brain to scaled cortical impact

Duhaime¹,

Margulies²,

Durham³

et al. 2000

Journal of Neurosurgery

148

120

View full text Add to dashboard Cite

show abstract

“…Following bilateral motor cortex lesions, postnatal day 10 (P10)-lesioned rats showed better behavioral performance (Whishaw reaching task, beam walking) than adult or P1-lesioned animals, although anatomical measures (brain weight, cortical thickness) seemed to favor the adult-lesioned animals . Bilateral medial frontal lesions showed that the youngest rats (P3, P6) actually had worse ana-tomical and functional outcomes [Kolb et al, 1996]. Furthermore, bilateral medial frontal lesions in the perinatal period (P2) resulted in markedly reduced brain weight, dendritic arborization and spine density, leading to the conclusion that, in some settings, 'earlier may be worse' .…”

Section: Principles Of Plasticity and Development After Injurymentioning

confidence: 99%

Is Being Plastic Fantastic? Mechanisms of Altered Plasticity after Developmental Traumatic Brain Injury

Giza

Prins²

2006

Dev Neurosci

188

115

View full text Add to dashboard Cite

Traumatic brain injury (TBI) is predominantly a clinical problem of young persons, resulting in chronic cognitive and behavioral deficits. Specifically, the physiological response to a diffuse biomechanical injury in a maturing brain can clearly alter normal neuroplasticity. To properly evaluate and investigate developmental TBI requires an understanding of normal principles of cerebral maturation, as well as a consideration of experience-dependent changes. Changes in neuroplasticity may occur through many age-specific processes, and our understanding of these responses at a basic neuroscience level is only beginning. In this article, we will particularly discuss mechanisms of TBI-induced altered developmental plasticity such as altered neurotransmission, distinct molecular responses, cell death, perturbations in neuronal connectivity, experience-dependent ‘good plasticity’ enhancements and chronic ‘bad plasticity’ sequelae. From this summary, we can conclude that ‘young is not always better’ and that the developing brain manifests several crucial vulnerabilities to TBI.

show abstract

“…If such surgery is performed in adulthood, however, the patients become hemiplegic [1]. Similarly in rodents, adult animals receiving unilateral cortical lesions during the neonatal stage exhibit much more skilled motor function in the contralesional fore- and hindlimbs than the animals whose sensorimotor cortex (SMC) is lesioned in adulthood [2,3,4,5]. …”

Section: Introductionmentioning

confidence: 99%

A Retrograde Tracing Study of Compensatory Corticospinal Projections in Rats with Neonatal Hemidecortication

Yoshikawa

Atobe²,

Takeda³

et al. 2011

Dev Neurosci

View full text Add to dashboard Cite

To examine the compensatory mechanisms in rats that underwent left decortication at postnatal day 7 (P7), we injected the retrograde tracers fluorescein isothiocyanate-cholera toxin B subunit (FITC-CTB) and Fast Blue (FB) into the right and left upper cervical spinal cord, respectively, at postoperative weeks 2, 3, 4, and 5 and counted the number of retrogradely labeled corticospinal neurons in the right cerebral cortex compared with that in normally developed rats. Significantly more ipsilaterally projecting neurons were labeled with FITC-CTB in the decorticated rats compared with normal rats at all time points examined. The number of labeled neurons was similar to that at P7 in normal rats. There were also some FITC-CTB and FB double-labeled neurons in both decorticated and normal rats. The number of double-labeled neurons in the decorticated rats increased each week and was significantly greater than that in normal rats at postoperative weeks 4 and 5. The present results suggest that the elimination of ipsilaterally projecting axons observed in normal rats was prevented in the decorticated rats, so that the cerebral cortex neurons on the unlesioned side projected corticospinal tracts to the ipsilateral spinal cord. Furthermore, the collaterals of the corticospinal tracts originating from the cerebral cortex on the unlesioned side also project to the ipsilateral spinal cord. These compensatory mechanisms might underlie the acquisition of motor function in these animals.

show abstract

Recovery from early cortical damage in rats, VII. Comparison of the behavioural and anatomical effects of medial prefrontal lesions at different ages of neural maturation

Cited by 77 publications

References 34 publications

Maturation-dependent response of the piglet brain to scaled cortical impact

Maturation-dependent response of the piglet brain to scaled cortical impact

Is Being Plastic Fantastic? Mechanisms of Altered Plasticity after Developmental Traumatic Brain Injury

A Retrograde Tracing Study of Compensatory Corticospinal Projections in Rats with Neonatal Hemidecortication

Contact Info

Product

Resources

About