Recovery from medial prefrontal cortex injury during adolescence: Implications for age-dependent plasticity

Nemati, Farshad; Kolb, Bryan

doi:10.1016/j.bbr.2012.01.002

Cited by 24 publications

(13 citation statements)

References 42 publications

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“…Gray matter volumes and functional connectivity have been shown to vary as a function of age, 40,46,47 and age at injury interacts with functional recovery in animal models. 48 However, a review of raw data confirmed that the reduction in cortical thickness occurred for the pmTBI cohort only over the four month study interval and was not due to an increase for the controls. Similarly, in adult mTBI, atrophy has been reported to progress over time, possibly due to neuronal or neuropil loss later in the course of mTBI.…”

Section: Discussionmentioning

confidence: 92%

Gray Matter Abnormalities in Pediatric Mild Traumatic Brain Injury

MayerAndrew

HanlonFaith

LingJosef

2015

Journal of Neurotrauma

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Pediatric mild traumatic brain injury (pmTBI) is the most prevalent neurological insult in children and is associated with both acute and chronic neuropsychiatric sequelae. However, little is known about underlying pathophysiology changes in gray matter diffusion and atrophy from a prospective stand-point. Fifteen semi-acute pmTBI patients and 15 well-matched healthy controls were evaluated with a clinical and neuroimaging battery, with a subset of participants returning for a second visit. Clinical measures included tests of attention, processing speed, executive function, working memory, memory, and self-reported post-concussive symptoms. Measures of diffusion (fractional anisotropy [FA]) and atrophy were also obtained for cortical and subcortical gray matter structures to characterize effects of injury as a function of time. Patients exhibited decreased scores in the domains of attention and processing speed relative to controls during the semi-acute injury stage, in conjunction with increased anisotropic diffusion in the left superior temporal gyrus and right thalamus. Evidence of increased diffusion in these regions was also present at four months post-injury, with performance on cognitive tests partially normalizing. In contrast, signs of cortical atrophy in bilateral frontal areas and other left-hemisphere cortical areas only emerged at four months post-injury for patients. Current results suggest potentially differential time-courses of recovery for neurobehavioral markers, anisotropic diffusion and atrophy following pmTBI. Importantly, these data suggest that relying on patient self-report or standard clinical assessments may underestimate the time for true injury recovery.

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Section: Discussionmentioning

confidence: 92%

Gray Matter Abnormalities in Pediatric Mild Traumatic Brain Injury

MayerAndrew

HanlonFaith

LingJosef

2015

Journal of Neurotrauma

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“…The results of the present study suggest that, at least in terms of neuron number, there is a brief period of rapid change coinciding withpuberty in females. Further evidence that the female mPFC is highly plastic during the pubertal period comes from Nemati and Kolb (2012) where female rats with induced damage to the PFC during early adolescence (P35), compared to late adolescence (P55), displayed greater dendritic reorganization and more prominent behavioral resilience in adulthood. Additionally, MRI analysis of human peripubertal adolescents indicates that the increase of estrogen at puberty is correlated with decreases in gray matter in females while no changes were found in the peripubescent males (Peper et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

The timing of neuronal loss across adolescence in the medial prefrontal cortex of male and female rats

Willing¹,

Juraska²

2015

Neuroscience

140

111

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Adolescence is a critical period for brain maturation characterized by the reorganization of interacting neural networks. In particular the prefrontal cortex, a region involved in executive function, undergoes synaptic and neuronal pruning during this time in both humans and rats. Our laboratory has previously shown that rats lose neurons in the medial prefrontal cortex (mPFC) and there is an increase in white matter under the frontal cortex between adolescence and adulthood. Female rats lose more neurons during this period, and ovarian hormones may play a role as ovariectomy before adolescence prevents neuronal loss. However, little is known regarding the timing of neuroanatomical changes that occur between early adolescence and adulthood. In the present study, we quantified the number of neurons and glia in the male and female mPFC at multiple time points from preadolescence through adulthood (postnatal days 25, 35, 45, 60 and 90). Females, but not males, lost a significant number of neurons in the mPFC between days 35 and 45, coinciding with the onset of puberty. Counts of GABA immunoreactive cell bodies indicated that the neurons lost were not primarily GABAergic. These results suggest that in females, pubertal hormones may exert temporally specific changes in PFC anatomy. As expected, both males and females gained white matter under the prefrontal cortex throughout adolescence, though these gains in females were diminished after day 35, but not in males. The differences in cell loss in males and females may lead to differential vulnerability to external influences and dysfunctions of the prefrontal cortex that manifest in adolescence.

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“…Age clearly affects prospects for recovery of executive function after focal injury in rat models; rats recover poorly from lesions made in the first week of life, but lesions made during the second week of life—roughly analogous to the first year of life in humans (Kolb and Cioe, 2000)—often results in full recovery of executive function in adulthood (Kolb, 1987; Kolb and Gibb, 1990; Kolb et al, 1998; Nonneman and Corwin, 1981; Prins and Hovda, 1998). The data are more sparse during the late juvenile to peripubertal period (~P35-P40), but prepubertal rats recover better from lesions than postpubertal rats (Nemati and Kolb, 2010; Nemati and Kolb, 2012). Still, recovery potential from late juvenile lesions is lower than P7–14 rats (Kolb and Nonneman, 1978; Nemati and Kolb, 2012; Prins and Hovda, 1998).…”

Section: How Does the Function Of Associative Neocortex Change Durmentioning

confidence: 99%

“…The data are more sparse during the late juvenile to peripubertal period (~P35-P40), but prepubertal rats recover better from lesions than postpubertal rats (Nemati and Kolb, 2010; Nemati and Kolb, 2012). Still, recovery potential from late juvenile lesions is lower than P7–14 rats (Kolb and Nonneman, 1978; Nemati and Kolb, 2012; Prins and Hovda, 1998). These data suggest that recovery capacity peaks during the second week of life before gradually declining across the juvenile period.…”

Section: How Does the Function Of Associative Neocortex Change Durmentioning

confidence: 99%

Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex?

et al. 2017

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Postnatal brain development is studded with sensitive periods during which experience dependent plasticity is enhanced. This enables rapid learning from environmental inputs and reorganization of cortical circuits that matches behavior with environmental contingencies. Significant headway has been achieved in characterizing and understanding sensitive period biology in primary sensory cortices, but relatively little is known about sensitive period biology in associative neocortex. One possible mediator is the onset of puberty, which marks the transition to adolescence, when animals shift their behavior toward gaining independence and exploring their social world. Puberty onset correlates with reduced behavioral plasticity in some domains and enhanced plasticity in others, and therefore may drive the transition from juvenile to adolescent brain function. Pubertal onset is also occurring earlier in developed nations, particularly in unserved populations, and earlier puberty is associated with vulnerability for substance use, depression and anxiety. In the present article we review the evidence that supports a causal role for puberty in developmental changes in the function and neurobiology of the associative neocortex. We also propose a model for how pubertal hormones may regulate sensitive period plasticity in associative neocortex. We conclude that the evidence suggests puberty onset may play a causal role in some aspects of associative neocortical development, but that further research that manipulates puberty and measures gonadal hormones is required. We argue that further work of this kind is urgently needed to determine how earlier puberty may negatively impact human health and learning potential.

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Recovery from medial prefrontal cortex injury during adolescence: Implications for age-dependent plasticity

Cited by 24 publications

References 42 publications

Gray Matter Abnormalities in Pediatric Mild Traumatic Brain Injury

Gray Matter Abnormalities in Pediatric Mild Traumatic Brain Injury

The timing of neuronal loss across adolescence in the medial prefrontal cortex of male and female rats

Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex?

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