The organization of the rat motor cortex: A microstimulation mapping study

Neafsey, Edward J.; Bold, E. L.; Haas, Gretchen L.; Hurley-Gius, Karen M.; Quirk, Gregory J.; Sievert, Carl; Terreberry, R. R.

doi:10.1016/s0006-8993(86)80191-3

Cited by 411 publications

(475 citation statements)

References 50 publications

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“…In the waking group (n = 8), as expected, Fos nuclear staining was consistently observed throughout the cerebral cortex, including the entire motor cortex as previously defined 27,40 ( Figure 5A). In the frontal areas of both sides Fos positive cells were mostly seen in layers II-III and V-VI, although a few cells were also present in layers I and IV ( Figure 5B).…”

Section: Fos Stainingsupporting

confidence: 84%

“…This area includes the motor cortex as defined both functionally and cytoarchitecturally, 27,28 and its boundaries were confirmed in a subset of sections stained with cresyl violet (10x magnification): the medial/lateral borders of the rostral half of the motor cortex, which closely corresponds 3-5 days. 20 In all cases, most of the learning occurred within the first 2 to 4 days.…”

Section: Fos and Arc Immunolabelingmentioning

confidence: 75%

“…In the rat, the forelimb representation within the motor cortex spans an area from + 3.7 mm anterior to −1.88 mm posterior to bregma and from the midline to +4 mm laterally. 27,40 Thus, only the frontal, but not the parietal LFPs were located within the targeted forelimb region (Figure 2A). Figure 2B shows the NREM relative power spectrum during the first hour after sleep onset (defined as the first sleep epoch after the end of training) for the trained frontal cortex, during the baseline recording (after habituation to the sugar pellets) and following the first training session.…”

Section: Single Pellet Reaching Taskmentioning

confidence: 96%

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

Hanlon

Faraguna

Vyazovskiy

et al. 2009

Sleep

139

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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Section: Fos Stainingsupporting

confidence: 84%

Section: Fos and Arc Immunolabelingmentioning

confidence: 75%

Section: Single Pellet Reaching Taskmentioning

confidence: 96%

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

Hanlon

Faraguna

Vyazovskiy

et al. 2009

Sleep

139

131

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“…In contrast, no correlation was found for AD. This at first glance incongruous observation could be accounted for by different brain substrates underlying different AIMs, because in contrast to forelimb movements, trunk movements are barely represented in the motor cortex (Donoghue and Wise, 1982;Neafsey et al, 1986), and indeed, it is believed that projections to the brain stem rather than to thalamo-cortical circuits are involved in basal ganglia control of locomotion and posture (Grillner et al, 2005).…”

Section: Severity Of Fd Is Related To Striatal and Motor Cortex Boldmentioning

confidence: 99%

Mapping the Effects of Three Dopamine Agonists with Different Dyskinetogenic Potential and Receptor Selectivity Using Pharmacological Functional Magnetic Resonance Imaging

Delfino

Kalisch

Czisch

et al. 2007

Neuropsychopharmacol

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The mechanisms underlying dopamine agonist-induced dyskinesia in Parkinson's disease remain poorly understood. Similar to patients, rats with severe nigrostriatal degeneration induced by 6-hydroxydopamine are more likely to show dyskinesia during chronic treatment with unselective dopamine receptor agonists than with D2 agonists, suggesting that D1 receptor stimulation alone or in conjunction with D2 receptor stimulation increases the chances of experiencing dyskinesia. As a first step towards disclosing drug-induced brain activation in dyskinesia, we examined the effects of dopamine agonists on behavior and blood oxygenation level-dependent (BOLD) signal in the striatum and motor cortex of rats with unilateral nigrostriatal lesions. Rats were rendered dyskinetic before pharmacologic functional magnetic resonance imaging by means of a repeated treatment regime with dopamine agonists. The unselective agonist apomorphine and the selective D1/D5 agonist SKF-81297 induced strong forelimb dyskinesia (FD) and axial dystonia and increased BOLD signal in the denervated striatum. Besides, SKF-81297 produced a significant but smaller BOLD increase in the intact striatum and a symmetric bilateral increase in the motor cortex. The D2 family agonist quinpirole, which induced mild dyskinesia on chronic treatment, did not produce BOLD changes in the striatum or motor cortex. Further evidence to support an association between BOLD changes and dyskinesia comes from a direct correlation between scores of FD and magnitude of drug-induced BOLD increases in the denervated striatum and motor cortex. Our results suggest that striatal and cortical activation induced by stimulation of D1/D5 receptors has a primary role in the induction of peak dose dyskinesia in parkinsonism.

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“…Thus, reaching performance at day three could not be measured and the formal proof of an improvement in performance is consequently lacking. The intact brains were rapidly removed from the skull and the forelimb area of M1 contralateral to the trained forelimb was dissected en-bloc (all cortical layers) at ice temperature according to published coordinates (+2.0 -0.0 mm to bregma, 2.0 -5.0 mm parasagittal; (Neafsey, Bold, Haas, Hurley-Gius, Quirk, Sievert, and Terreberry, 1986). All tissue samples were shock frozen in liquid nitrogen and stored at -80°C until use.…”

Section: Tissue and Rna Preparationmentioning

confidence: 99%

Temporal course of gene expression during motor memory formation in primary motor cortex of rats

Hertler

Buitrago

Luft

et al. 2016

Neurobiology of Learning and Memory

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Motor learning is associated with plastic reorganization of neural networks in primary motor cortex (M1) that depends on changes in gene expression. Here, we investigate the temporal profile of these changes during motor memory formation in response to a skilled reaching task in rats. mRNA-levels were measured 1h, 7h and 24h after the end of a training session using microarray technique. To assure learning specificity, trained animals were compared to a control group. In response to motor learning, genes are sequentially regulated with high time-point specificity and a shift from initial suppression to later activation. The majority of regulated genes can be linked to learning-related plasticity. In the gene-expression cascade following motor learning, three different steps can be defined: (1) an initial suppression of genes influencing gene transcription. (2) Expression of genes that support translation of mRNA in defined compartments. (3) Expression of genes that immediately mediates plastic changes. Gene expression peaks after 24h -this is a much slower time-course when compared to hippocampusdependent learning, where peaks of gene-expression can be observed 6-12h after training ended. AbstractMotor learning is associated with plastic reorganization of neural networks in primary motor cortex (M1) that depends on changes in gene expression. Here, we investigate the temporal profile of these changes during motor memory formation in response to a skilled reaching task in rats. mRNA-levels were measured 1h, 7h and 24h after the end of a training session using microarray technique. To assure learning specificity, trained animals were compared to a control group. In response to motor learning, genes are sequentially regulated with high time-point specificity and a shift from initial suppression to later activation. The majority of regulated genes can be linked to learning-related plasticity. In the gene-expression cascade following motor learning, three different steps can be defined: 1) an initial suppression of genes influencing gene transcription. 2) Expression of genes that support translation of mRNA in defined compartments. 3) Expression of genes that immediately mediates plastic changes. Gene expression peaks after 24 hours -this is a much slower time-course when compared to hippocampus-dependent learning, where peaks of geneexpression can be observed 6 to 12 hours after training ended.3

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The organization of the rat motor cortex: A microstimulation mapping study

Cited by 411 publications

References 50 publications

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

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

Mapping the Effects of Three Dopamine Agonists with Different Dyskinetogenic Potential and Receptor Selectivity Using Pharmacological Functional Magnetic Resonance Imaging

Temporal course of gene expression during motor memory formation in primary motor cortex of rats

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