Motor cortex injury has different behavioral and anatomical effects in early and late adolescence.

Nemati, Farshad; Kolb, Bryan

doi:10.1037/a0020911

Cited by 16 publications

(7 citation statements)

References 58 publications

(72 reference statements)

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“…One such technique is the Sunflower Seed Test (Gonzalez & Kolb, 2003; Nemati & Kolb, 2010; Whishaw & Coles, 1996; Whishaw, Sarna, & Pellis, 1998). Rats typically manipulate a sunflower seed with their forelimbs, bite a corner of the seed, split it longitudinally (into two pieces), and then eat the seed (Whishaw et al, 1998).…”

Section: Methods Preliminary Results and Discussionmentioning

confidence: 99%

Assessing the role of dopamine in limb and cranial-oromotor control in a rat model of Parkinson's disease

Kane

Ciucci

Jacobs

et al. 2011

Journal of Communication Disorders

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Parkinson’s disease (PD) is a neurodegenerative disorder primarily characterized by sensorimotor dysfunction. The neuropathology of PD includes a loss of dopamine (DA) neurons of the nigrostriatal pathway. Classic signs of the disease include rigidity, bradykinesia, and postural instability. However, as many as 90% of patients also experience significant deficits in speech, swallowing (including mastication), and respiratory control. Oromotor deficits such as these are underappreciated, frequently emerging during the early, often hemi-Parkinson, stage of the disease. In this paper, we review tests commonly used in our labs to model early and hemi-Parkinson deficits in rodents. We have recently expanded our tests to include sensitive models of oromotor deficits. This paper discusses the most commonly used tests in our lab to model both limb and oromotor deficits, including tests of forelimb-use asymmetry, postural instability, vibrissae-evoked forelimb placing, single limb akinesia, dry pasta handling, sunflower seed shelling, and acoustic analyses of ultrasonic vocalizations and pasta biting strength. In particular, we lay new groundwork for developing methods for measuring abnormalities in the acoustic patterns during eating that indicate decreased biting strength and irregular intervals between bites in the hemi-Parkinson rat. Similar to limb motor deficits, oromotor deficits, at least to some degree, appear to be modulated by nigrostriatal DA. Finally, we briefly review the literature on targeted motor rehabilitation effects in PD models. Learning outcomes Readers will: (a) understand how a unilateral lesion to the nigrostriatal pathway affects limb use, (b) understand how a unilateral lesion to the nigrostriatal pathway affects oromotor function, and (c) gain an understanding of how limb motor deficits and oromotor deficits appear to involve dopamine and are modulated by training.

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Section: Methods Preliminary Results and Discussionmentioning

confidence: 99%

Assessing the role of dopamine in limb and cranial-oromotor control in a rat model of Parkinson's disease

Kane

Ciucci

Jacobs

et al. 2011

Journal of Communication Disorders

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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%

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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“…2). 13–15 This tissue does not appear normal in lamination but it does have functional connections with the spinal cord and the cells have fairly normal patterns of spontaneous discharge. Removing the regenerated tissue produces immediate loss of the recovered functions.…”

Section: Modulating Recovery From Early Injurymentioning

confidence: 99%

“…Table II summarizes a range of factors that modulate recovery from early brain injury. [9][10][11][12][13][14][15][16][17][18] We will consider these factors in three general categories: behavioural therapies, neurotrophic factor therapies, and drug therapies.…”

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confidence: 99%

Brain plasticity and recovery from early cortical injury

Kolb

Mychasiuk

Williams

et al. 2011

Develop Med Child Neuro

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FGF2 Fibroblast growth factor 2Neocortical development represents more than a simple unfolding of a genetic blueprint: rather, it represents a complex dance of genetic and environmental events that interact to adapt the brain to fit a particular environmental context. Most cortical regions are sensitive to a wide range of experiential factors during development and later in life, but the injured cortex appears to be unusually sensitive to perinatal experiences. This paper reviews the factors that influence how normal and injured brains (both focal and ischemic injuries) develop and adapt into adulthood. Such factors include prenatal experiences in utero as well as postnatal experiences throughout life. Examples include the effects of sensory and motor stimulation, psychoactive drugs (including illicit and prescription drugs), maternal and postnatal stress, neurotrophic factors, and pre-and postnatal diet. All these factors influence cerebral development and influence recovery from brain injury during development.Over the past 25 years we have developed a model of early cortical injury in the rodent cortex.1 The underlying assumption of our experiments has been that there are critical periods during development in which the brain is more able to reorganize, and others where it is less able to reorganize, to allow restoration of function after neocortical injury. The critical periods are constrained by the ongoing developmental processes that are occurring at the time of injury. For example, when there is proliferation of neurons (such as on embryonic day 18 in rats) or astrocytes (such as on postnatal day 8), the brain can recruit these proliferative processes to facilitate processes leading to functional recovery. In contrast, if neurons are migrating or the brain is shedding synapses or neurons, injury may lead to a disruption (or enhancement) of this process, which may exacerbate the effects of injury. The challenge is to identify pre-and postnatal treatments that will shift the critical periods to make it possible partly to stimulate functional restoration at times when it would not normally occur.We began by searching for factors that can influence development in the normal brain of laboratory animals. It is now possible to identify a wide range of pre-and postnatal experiences that can produce significant changes in both brain and behavioural development (Table I).2-8 Several principles emerged from these studies. First, both pre-and postnatal factors could influence brain and behavioural development. Second, early experiences led to changes in the organization of adult neural networks throughout the cerebral cortex. Third, one clear mechanism of the brain and behavioural changes was epigenetic. Thus, early experiences could chronically alter gene expression, which in turn was presumably responsible, at least in part, for the altered development. Consider one example. When pregnant rats were given a moderate stressor (10 min sitting on a small platform in an open room) twice daily during the second week of ...

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Motor cortex injury has different behavioral and anatomical effects in early and late adolescence.

Cited by 16 publications

References 58 publications

Assessing the role of dopamine in limb and cranial-oromotor control in a rat model of Parkinson's disease

Assessing the role of dopamine in limb and cranial-oromotor control in a rat model of Parkinson's disease

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

Brain plasticity and recovery from early cortical injury

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