A second forelimb motor area exists in rat frontal cortex

Neafsey, Edward J.; Sievert, Carl

doi:10.1016/0006-8993(82)90617-5

Cited by 246 publications

(137 citation statements)

References 14 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%

“…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

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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Section: Fos Stainingsupporting

confidence: 84%

Section: Single Pellet Reaching Taskmentioning

confidence: 96%

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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“…As a secondary motor area has been described in rats (Fig. 2) (Neafsey and Sievert, 1982;Reep et al, 1990), further study in tree shrews may reveal additional premotor areas. As in most mammals, the thalamic ventroposterior nucleus projects strongly to both S1 and S2, providing an independent source of activation for both of these areas (Garraghty et al, 1991).…”

Section: Tree Shrews: Close Relatives Of Primatesmentioning

confidence: 70%

Evolution of somatosensory and motor cortex in primates

2004

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Inferences about how the complex somatosensory systems of anthropoid primates evolved are based on comparative studies of such systems in extant mammals. Experimental studies of members of the major clades of extant mammals suggest that somatosensory cortex of early mammals consisted of only a few areas, including a primary area, S1, bordered by strip-like rostral and caudal somatosensory fields, SR and SC. In addition, the second somatosensory area, S2, and the parietal ventral area, PV, were probably present. S1, S2, and PV were activated independently via parallel projections from the ventroposterior nucleus, VP. Little posterior parietal cortex existed, and it was unlikely that a separate primary motor area, M1, existed until placental mammals evolved. Early primates retained this basic organization and also had a larger posterior parietal region that mediated sensorimotor functions via connections with motor and premotor areas. The frontal cortex included M1, dorsal and ventral premotor areas, supplementary motor area, and cingulate motor fields. Ventroposterior superior and ventroposterior inferior nuclei were distinct from the ventroposterior nucleus in the thalamus. In early anthropoid primates, areas S1, SR, and SC had differentiated into the fields now recognized as areas 3b, 3a, and 1. Areas 3b and 1 contained parallel mirror-image representations of cutaneous receptors and a parallel representation in area 2 was probable. Serial processing became dominant, so that neurons in areas 1, S2, and PV became dependent on area 3b for activation. Posterior parietal cortex expanded into more areas that related to frontal cortex. Less is known about changes that might have occurred with the emergence of apes and humans, but their brains were larger and posed scaling problems most likely solved by increasing the number of cortical areas and reducing the proportion of long connections. © 2004 Wiley-Liss, Inc. Key words: galago; premotor; sensorimotor; tarsier; thalamus; ventroposterior nucleusHumans have exceptional sensorimotor skills that appear to be unique in the extent to which they can be individualized and specialized by experience and training. We commonly observe remarkable skills as we view highly trained athletes and musicians, and there are many examples from other activities as well. Such performances stand in contrast to the simple and sometimes clumsy sensorimotor behavior of opossums and laboratory rats. However, vast differences in abilities are to be expected if we consider the differences in the sensorimotor systems of various mammals.The first premise of this review is that early mammals had small brains in proportion to body size, and these brains contained rather simple sensorimotor systems. Furthermore, these simple sensorimotor systems have been retained with little modification in a range of distantly related extant mammals. By using the methods of modern neuroscience to study the sensorimotor systems of these mammals, together with a cladistic character anal-*Correspondence to:

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“…This suggests their origin in the motor rather than the sensory cortex (Kuang and Kalil, 1990;Bareyre et al, 2002). A motor bias of the midlinecrossing CST is also demonstrated by the high proportion of neurons that originated from the RFA, which is suggested to be primarily motor (Neafsey and Sievert, 1982;Sanderson et al, 1984;Rouiller et al, 1993).…”

Section: Increase In Size Of Sensory Activation Map Of the Unimpairedmentioning

confidence: 94%

Functional and Anatomical Reorganization of the Sensory-Motor Cortex after Incomplete Spinal Cord Injury in Adult Rats

Ghosh¹,

Sydekum²,

Haiss³

et al. 2009

J. Neurosci.

157

112

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A lateral hemisection injury of the cervical spinal cord results in Brown-Séquard syndrome in humans and rats. The hands/forelimbs on the injured side are rendered permanently impaired, but the legs/hindlimbs recover locomotor functions. This is accompanied by increased use of the forelimb on the uninjured side. Nothing is known about the cortical circuits that correspond to these behavioral adaptations. In this study, on adult rats with cervical spinal cord lateral hemisection lesions (at segment C3/4), we explored the sensory representation and corticospinal projection of the intact (ipsilesional) cortex. Using blood oxygenation level-dependent functional magnetic resonance imaging and voltage-sensitive dye (VSD) imaging, we found that the cortex develops an enhanced representation of the unimpaired forepaw by 12 weeks after injury. VSD imaging also revealed the cortical spatio-temporal dynamics in response to electrical stimulation of the ipsilateral forepaw or hindpaw. Interestingly, stimulation of the ipsilesional hindpaw at 12 weeks showed a distinct activation of the hindlimb area in the intact, ipsilateral cortex, probably via the injury-spared spinothalamic pathway. Anterograde tracing of corticospinal axons from the intact cortex showed sprouting to recross the midline, innervating the spinal segments below the injury in both cervical and lumbar segments. Retrograde tracing of these midline-crossing axons from the cervical spinal cord (at segment C6/7) revealed the formation of a new ipsilateral forelimb representation in the cortex. Our results demonstrate profound reorganizations of the intact sensory-motor cortex after unilateral spinal cord injury. These changes may contribute to the behavioral adaptations, notably for the recovery of the ipsilesional hindlimb.

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A second forelimb motor area exists in rat frontal cortex

Cited by 246 publications

References 14 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

Evolution of somatosensory and motor cortex in primates

Functional and Anatomical Reorganization of the Sensory-Motor Cortex after Incomplete Spinal Cord Injury in Adult Rats

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