Functional mapping of the motor cortex of the white mouse by a microstimulation method

Pronichev, I. V.; Lenkov, D. N.

doi:10.1007/bf02461916

Cited by 55 publications

(37 citation statements)

References 15 publications

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“…The stroke-lesion induced by pMCAo in mouse affects cortical brain areas controlling the contralateral front limb/paw and hindlimb/paw (Pronichev and Lenkov, 1998). We analyzed the grip strength in individual paws to measure the severity of the pMCAo-induced asymmetry.…”

Section: Methodsmentioning

confidence: 99%

Microglia Protect Neurons against Ischemia by Synthesis of Tumor Necrosis Factor

Lambertsen¹,

Clausen²,

Babcock³

et al. 2009

J. Neurosci.

335

352

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Microglia and infiltrating leukocytes are considered major producers of tumor necrosis factor (TNF), which is a crucial player in cerebral ischemia and brain inflammation. We have identified a neuroprotective role for microglial-derived TNF in cerebral ischemia in mice. We show that cortical infarction and behavioral deficit are significantly exacerbated in TNF-knock-out (KO) mice compared with wild-type mice. By using in situ hybridization, immunohistochemistry, and green fluorescent protein bone marrow (BM)-chimeric mice, TNF was shown to be produced by microglia and infiltrating leukocytes. Additional analysis demonstrating that BM-chimeric TNF-KO mice grafted with wild-type BM cells developed larger infarcts than BM-chimeric wild-type mice grafted with TNF-KO BM cells provided evidence that the neuroprotective effect of TNF was attributable to microglial-not leukocyte-derived TNF. In addition, observation of increased infarction in TNF-p55 receptor (TNF-p55R)-KO mice compared with TNF-p75R and wild-type mice suggested that microglialderived TNF exerts neuroprotective effects through TNF-p55R. We finally report that TNF deficiency is associated with reduced microglial population size and Toll-like receptor 2 expression in unmanipulated brain, which might also influence the neuronal response to injury. Our results identify microglia and microglial-derived TNF as playing a key role in determining the survival of endangered neurons in cerebral ischemia.

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Section: Methodsmentioning

confidence: 99%

Microglia Protect Neurons against Ischemia by Synthesis of Tumor Necrosis Factor

Lambertsen¹,

Clausen²,

Babcock³

et al. 2009

J. Neurosci.

335

352

View full text Add to dashboard Cite

show abstract

“…The skull overlying the right primary motor cortex was carefully removed with a drill. To visualize the uninjured CST and CRT, the anterograde tracer biotinylated dextran amine (BDA) (molecular weight, 10,000; dilution, 10% in PBS; Invitrogen) was injected at 4 sites (0.4 l/site) within the forelimb motor area, as guided by a functional map of the motor cortex (Pronichev and Lenkov, 1998).…”

Section: Methodsmentioning

confidence: 99%

Genetic Deletion of Paired Immunoglobulin-Like Receptor B Does Not Promote Axonal Plasticity or Functional Recovery after Traumatic Brain Injury

et al. 2010

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The rewiring of neural networks is a fundamental step in recovering behavioral functions after brain injury. However, there is limited potential for axonal plasticity in the adult CNS. The myelin-associated proteins Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp) are known to inhibit axonal plasticity, and thus targeting the inhibitory pathways they participate in is a potential means of promoting plasticity and functional recovery. Each of Nogo, MAG, and OMgp interacts with both the Nogo receptor (NgR) and paired immunoglobulin-like receptor B (PirB). Here, we determined whether blocking PirB activity enhances axonal reorganization and functional recovery after cortical injury. We found that axons of the contralesional corticospinal tract sprouted into the denervated side of the cervical spinal cord after unilateral injury of the motor cortex. The extent to which this axonal reorganization occurred was far greater in mice lesioned during early postnatal days than in mice lesioned at an age when myelin had begun to form. This suggests that myelin-associated proteins might limit axonal remodeling in vivo. However, the number of sprouting fibers within either the corticospinal or corticorubral tract was not enhanced in PirB Ϫ/Ϫ mice. Blocking PirB signaling also failed to enhance functional recovery with three motor tests. Our results suggest that blocking the function of PirB is not sufficient to promote axonal reorganization or functional recovery after cortical injury.

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“…Twelve weeks after injury, descending CST fibers were labeled with biotinylated dextran amine (BDA) (MW 10,000, 10% in saline, 2 ll per cortex; Molecular Probes) [21,22] by injection into the left and right motor cortices [23]. The skulls of anesthetized mice were tightly fixed to a stereotaxic apparatus (Narishige).…”

Section: Anterograde Labeling Of the Cstmentioning

confidence: 99%

“…Scalping and craniotomy over the motor cortex area were carried out using a micromotor system (Nakanishi). The injection site was 2.1 mm posterior to the bregma, 2 mm lateral to the bregma, and 0.7 mm in depth [23]. For pressure injections with a 20-lm outer diameter glass capillary attached to a microsyringe (Narishige), we used 0.1-ll steps per minute until the desired volume (1 ll per injection site) was injected.…”

Section: Anterograde Labeling Of the Cstmentioning

confidence: 99%

Treatment of a Mouse Model of Spinal Cord Injury by Transplantation of Human Induced Pluripotent Stem Cell-Derived Long-Term Self-Renewing Neuroepithelial-Like Stem Cells

et al. 2012

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Because of their ability to self-renew, to differentiate into multiple lineages, and to migrate toward a damaged site, neural stem cells (NSCs), which can be derived from various sources such as fetal tissues and embryonic stem cells, are currently considered to be promising components of cell replacement strategies aimed at treating injuries of the central nervous system, including the spinal cord. Despite their efficiency in promoting functional recovery, these NSCs are not homogeneous and possess variable characteristics depending on their derivation protocols. The advent of induced pluripotent stem (iPS) cells has provided new prospects for regenerative medicine. We used a recently developed robust and stable protocol for the generation of long-term, self-renewing, neuroepithelial-like stem cells from human iPS cells (hiPS-lt-NES cells), which can provide a homogeneous and well-defined population of NSCs for standardized analysis. Here, we show that transplanted hiPS-lt-NES cells differentiate into neural lineages in the mouse model of spinal cord injury (SCI) and promote functional recovery of hind limb motor function. Furthermore, using two different neuronal tracers and ablation of the transplanted cells, we revealed that transplanted hiPS-lt-NES cell-derived neurons, together with the surviving endogenous neurons, contributed to restored motor function. Both types of neurons reconstructed the corticospinal tract by forming synaptic connections and integrating neuronal circuits. Our findings indicate that hiPS-lt-NES transplantation represents a promising avenue for effective cell-based treatment of SCI. Disclosure of potential conflicts of interest is found at the end of this article.

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Functional mapping of the motor cortex of the white mouse by a microstimulation method

Cited by 55 publications

References 15 publications

Microglia Protect Neurons against Ischemia by Synthesis of Tumor Necrosis Factor

Microglia Protect Neurons against Ischemia by Synthesis of Tumor Necrosis Factor

Genetic Deletion of Paired Immunoglobulin-Like Receptor B Does Not Promote Axonal Plasticity or Functional Recovery after Traumatic Brain Injury

Treatment of a Mouse Model of Spinal Cord Injury by Transplantation of Human Induced Pluripotent Stem Cell-Derived Long-Term Self-Renewing Neuroepithelial-Like Stem Cells

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