Skilled reaching impairments from the lateral frontal cortex component of middle cerebral artery stroke: a qualitative and quantitative comparison to focal motor cortex lesions in rats

Gharbawie, Omar A.; Gonzalez, Claudia L. R.; Whishaw, Ian Q.

doi:10.1016/j.bbr.2004.05.015

Cited by 79 publications

(52 citation statements)

References 67 publications

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“…By Day 32, rats had returned to pre-lesion reaching success levels with the contralesional forelimb. However, analysis using Whishaw's rating scale of reaching movements revealed movement abnormalities compared to the shamoperated group at this time point, also consistent with previous findings [16,55,57]. Anesthetization of the ipsilesional/non-preferred forelimb at this stage partially normalized movements in the other limb on this rating scale in both groups of rats.…”

Section: Discussionsupporting

confidence: 90%

Abnormalities in skilled reaching movements are improved by peripheral anesthetization of the less-affected forelimb after sensorimotor cortical infarcts in rats

O'Bryant¹,

Bernier²,

Jones³

2007

Behavioural Brain Research

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Unilateral damage to sensorimotor cortical (SMC) regions can profoundly impair skilled reaching function in the contralesional forelimb. Such damage also results in impairments and compensatory changes in the less-affected/ipsilesional forelimb, but these effects remain poorly understood. Furthermore, anesthetization of the ipsilesional hand in humans with cerebral infarcts has been reported to produce transient functional improvements in the paretic hand [14,48]. One aim of this study was to sensitively assay the bilateral effects of unilateral ischemic SMC damage on performance of a unimanual skilled reaching task (the single pellet retrieval task) that rats had acquired pre-operatively with each forelimb. The second aim was to determine whether partially recovered contralesional reaching function is influenced by anesthetization of the ipsilesional forelimb. Unilateral SMC lesions were found to result in transient ipsilesional impairments in reaching success and significant ipsilesional abnormalities in reaching movements compared with sham-operates. There were major contralesional reaching impairments which improved during a 4 week training period, but movements remained significantly abnormal. Anesthetization of the ipsilesional forelimb with lidocaine at this time attenuated the contralesional movement abnormalities. These findings indicate that unilateral ischemic SMC lesions impair skilled reaching behavior in both forelimbs. Furthermore, after partial recovery in the contralesional forelimb, additional improvements can be induced by transient anesthetization of the ipsilesional forelimb. This is consistent with the effects of unilateral anesthetization in humans which have been attributed to the modulation of competitive interhemispheric interactions. The present findings suggest that such interactions are also likely to influence skilled reaching function in rats.

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Section: Discussionsupporting

confidence: 90%

Abnormalities in skilled reaching movements are improved by peripheral anesthetization of the less-affected forelimb after sensorimotor cortical infarcts in rats

O'Bryant¹,

Bernier²,

Jones³

2007

Behavioural Brain Research

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“…In some previous studies rats were trained in short (10-15 min) daily sessions across 1-2 weeks. 21,39 In other studies, instead, 1-h training sessions were repeated for…”

Section: Single Pellet Reaching Taskmentioning

confidence: 99%

Effects of Skilled Training on Sleep Slow Wave Activity and Cortical Gene Expression in the Rat

Hanlon

Faraguna

Vyazovskiy

et al. 2009

Sleep

141

131

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SO FAR. IN MAMMALS, THE BEST CHARACTERIZED marker of sleep homeostasis is slow wave activity (SWA), the power density in the electroencephalogram (EEG) between 0.5 and 4 Hz during NREM sleep. SWA is high at sleep onset and declines during sleep, suggesting that it may reflect the accumulation of sleep pressure as a function of duration and/or intensity of prior waking. 1,2 Why and how SWA should reflect sleep homeostasis, however, is still unclear.We hypothesized that SWA is high at sleep onset because it reflects the occurrence, during waking, of widespread synaptic potentiation in cortical and subcortical areas. 3,4 This increase would be detrimental in the long term, because stronger synapses need more energy, space, and cellular supplies, and may lead to saturation of the ability to learn. Sleep would thus be crucial to renormalize synaptic strength to an energetically sustainable level. Molecular and electrophysiological markers of synaptic potentiation increase after waking in rat cortex and hippocampus, while markers of synaptic depression do so after sleep. 5,6 Moreover, in rats and humans, procedures presumably leading to synaptic potentiation or depression result in SWA increases and decreases, respectively. 7-12 More specifically, a study in humans using highdensity EEG found that performing a visuomotor learning task produced a local increase in SWA during subsequent sleep. 7 The increase was restricted to the right parietal cortical areas presumably modified by learning. 13 Moreover, it was specific for NREM sleep, reversible within the first 90 minutes of sleep, and correlated with the improvement in performance after sleep. 7 However, there is no direct evidence that the motor adaptation task used in that study activates neurons in parietal cortex, nor that it causes synaptic potentiation specifically in that region.Previous studies have suggested that activity-dependent genes activated during a specific waking experience may be reactivated during sleep, perhaps to potentiate the same synapses previously engaged during waking. 14 Ribeiro and colleagues found that the exposure to a new environment for 3 hours 15 results in the immediate cortical and hippocampal induction, during waking, of plasticity-related gene zif-268, 16 followed by its downregulation during NREM sleep, and then again by its increased expression during REM sleep (relative to NREM sleep). Intriguingly ~ 3 min of NREM sleep were enough to downregulate waking-induced zif-268 expression, and ~ 2 min of REM sleep were sufficient to detect its selective reinduction, even if both NREM and REM rats were awake during the last 30 min before sacrifice. Another study 17 recently found, using fluorescent in situ hybridization, that the number of hippocampal CA1 neurons showing induction of Arc and/or Homer1a was similar during "rest" periods before and after the exploration of a new environment. However, more cells were active during both exploration and post-task rest than during exploration and pre-task rest. Based on these findings, it h...

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“…Quantitative measures, such as reaching success, usually undergo considerable spontaneous improvement after focal ischemia, which is mainly mediated by the use of compensatory adjustments. These include the replacement of distal limb use with proximal and axial movement (Whishaw, 2000;Metz et al, 2005a;Gharbawie et al, 2005). For example, rats will adjust their posture and will perform exaggerated shoulder and body rotation in order to lift, aim and advance the paw to improve their reaching success (Gharbawie et al, 2005).…”

Section: Restraint Stress Impairs Skilled Reaching Ability and Compenmentioning

confidence: 99%

Delayed recovery and exaggerated infarct size by post-lesion stress in a rat model of focal cerebral stroke

et al. 2008

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Stress might be one of the most salient intrinsic factors influencing the risk of stroke and its outcome. Previous studies have linked stress to increased infarct size and exaggerated cognitive deficits in rodent models of stroke. This study compares the effects of chronic restraint stress, representing a psychological stressor, prior to or after motor cortex devascularization lesion on motor recovery in rats. Daily testing in a skilled reaching task revealed initially exaggerated deficits in limb use caused by pre-lesion stress in the absence of increased infarct size. Both preand post-lesion stresses affected movement by delaying recovery and limiting compensation of lesion-induced deficits. Nevertheless, only rats that experienced post-lesion stress showed enlarged infarct size. This was accompanied by enlarged edema formation in the lesion hemisphere of poststress animals on day 2 post-lesion. There were no significant differences in infarct size between post-lesion day 2 and day 15. The data demonstrate that both pre-and post-lesion chronic restraint stresses affect motor recovery after ischemic lesion. Lesion volume, however, is influenced by the timing of a stressful experience relative to the lesion. These findings suggest that stress represents a critical variable determining the outcome after stroke.

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Skilled reaching impairments from the lateral frontal cortex component of middle cerebral artery stroke: a qualitative and quantitative comparison to focal motor cortex lesions in rats

Cited by 79 publications

References 67 publications

Abnormalities in skilled reaching movements are improved by peripheral anesthetization of the less-affected forelimb after sensorimotor cortical infarcts in rats

Abnormalities in skilled reaching movements are improved by peripheral anesthetization of the less-affected forelimb after sensorimotor cortical infarcts in rats

Effects of Skilled Training on Sleep Slow Wave Activity and Cortical Gene Expression in the Rat

Delayed recovery and exaggerated infarct size by post-lesion stress in a rat model of focal cerebral stroke

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