Differential response of arcuate proopiomelanocortin- and neuropeptide Y-containing neurons to the lesion produced by gold thioglucose administration

Homma, Akiko; Liu, Hongpeng; Hayashi, Kaori; Kawano, Yukari; Kawano, Hitoshi

doi:10.1002/cne.21097

Cited by 15 publications

(12 citation statements)

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“…b In neonatal and DPY-treated animals, axons regenerate despite of the presence of glial scar and chondroitin sulfate proteoglycan ( CSPG ) (Stichel et al 1999a; Kawano et al 2005). c In the hypothalamic arcuate nucleus ( ARC ) and by chondroitinase ABC ( ChABC ) treatment, upregulation of chondroitin sulfate is prevented and axons regenerate (Homma et al 2006; Li et al 2007). d In olfactory ensheathing cell ( OEC )-transplanted rats, fibrotic scar is not formed and axons regenerate (Teng et al 2008)…”

Section: Fibrotic Scar As An Impediment For Axonal Regenerationmentioning

confidence: 99%

“…This treatment transected axons from arcuate NPY neurons but 2 weeks later, they regenerated and extended across the lesion site (Homma et al 2006). The lesion site was identified by accumulation of reactive astrocytes but a fibrotic scar was not formed, suggesting that the absence of a fibrotic scar may be a permissive factor in the regeneration of the axons of arcuate NPY neurons.…”

Section: Fibrotic Scar As An Impediment For Axonal Regenerationmentioning

confidence: 99%

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Role of the lesion scar in the response to damage and repair of the central nervous system

et al. 2012

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Traumatic damage to the central nervous system (CNS) destroys the blood–brain barrier (BBB) and provokes the invasion of hematogenous cells into the neural tissue. Invading leukocytes, macrophages and lymphocytes secrete various cytokines that induce an inflammatory reaction in the injured CNS and result in local neural degeneration, formation of a cystic cavity and activation of glial cells around the lesion site. As a consequence of these processes, two types of scarring tissue are formed in the lesion site. One is a glial scar that consists in reactive astrocytes, reactive microglia and glial precursor cells. The other is a fibrotic scar formed by fibroblasts, which have invaded the lesion site from adjacent meningeal and perivascular cells. At the interface, the reactive astrocytes and the fibroblasts interact to form an organized tissue, the glia limitans. The astrocytic reaction has a protective role by reconstituting the BBB, preventing neuronal degeneration and limiting the spread of damage. While much attention has been paid to the inhibitory effects of the astrocytic component of the scars on axon regeneration, this review will cover a number of recent studies in which manipulations of the fibroblastic component of the scar by reagents, such as blockers of collagen synthesis have been found to be beneficial for axon regeneration. To what extent these changes in the fibroblasts act via subsequent downstream actions on the astrocytes remains for future investigation.

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Section: Fibrotic Scar As An Impediment For Axonal Regenerationmentioning

confidence: 99%

Section: Fibrotic Scar As An Impediment For Axonal Regenerationmentioning

confidence: 99%

Role of the lesion scar in the response to damage and repair of the central nervous system

et al. 2012

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“…Simultaneously, the fibrotic scar and surrounding glia limitans can be a physical and chemical obstacle for axonal regeneration in the damaged CNS. Elimination of the fibrotic scar has been shown to be required for axonal regeneration in a variety of animal models (reviewed in Klapka and Muller 2006;Kawano et al 2007), such as by suppression of type IV collagen synthesis (Stichel et al 1999;Klapka et al 2005), in newborn mouse (Kawano et al 2005), in the mouse hypothalamic arcuate nucleus (Homma et al 2006), by degradation of glycochains of chondroitin sulfate proteoglycans with chondroitinase ABC , and by transplantation of olfactory ensheathing cells (Teng et al 2008).…”

Section: Introductionmentioning

confidence: 98%

Expression of Transforming Growth Factor-β Receptors in Meningeal Fibroblasts of the Injured Mouse Brain

et al. 2009

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The fibrotic scar which is formed after traumatic damage of the central nervous system (CNS) is considered as a major impediment for axonal regeneration. In the process of the fibrotic scar formation, meningeal fibroblasts invade and proliferate in the lesion site to secrete extracellular matrix proteins, such as collagen and laminin. Thereafter, end feet of reactive astrocytes elaborate a glia limitans surrounding the fibrotic scar. Transforming growth factor-beta1 (TGF-beta1), a potent scar-inducing factor, which is upregulated after CNS injury, has been implicated in the formation of the fibrotic scar and glia limitans. In the present study, expression of receptors to TGF-beta1 was examined by in situ hybridization histochemistry in transcortical knife lesions of the striatum in the mouse brain in combination with immunofluorescent staining for fibroblasts and astrocytes. Type I and type II TGF-beta receptor mRNAs were barely detected in the intact brain and first found in meningeal cells near the lesion 1 day postinjury. Many cells expressing TGF-beta receptors were found around the lesion site 3 days postinjury, and some of them were immunoreactive for fibronectin. After 5 days postinjury, many fibroblasts migrated from the meninges to the lesion site formed the fibrotic scar, and most of them expressed TGF-beta receptors. In contrast, few of reactive astrocytes expressed the receptors throughout the postinjury period examined. These results indicate that meningeal fibroblasts not reactive astrocytes are a major target of TGF-beta1 that is upregulated after CNS injury.

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“…The physiological importance of central glucose sensing has been further highlighted in a number of studies whereby peripheral injection of gold thioglucose, which selectively destroys glucose‐responsive neurones in brain regions with a restricted blood‐brain barrier, results in impaired feeding regulation and the subsequent onset of obesity (Bergen et al. 1996; Homma et al. 2006).…”

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Functional magnetic resonance imaging and c‐Fos mapping in rats following a glucoprivic dose of 2‐deoxy‐d‐glucose

Dodd¹,

Williams²,

Luckman³

2010

Journal of Neurochemistry

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J. Neurochem. (2010) 113, 1123–1132. Abstract The glucose analogue, 2‐deoxy‐d‐glucose (2‐DG) is an inhibitor of glycolysis and, when administered systemically or centrally, induces glucoprivation leading to counter‐regulatory responses, including increased feeding behaviour. Investigations into how the brain responds to glucoprivation could have important therapeutic potential, as disruptions or defects in the defence of the brain’s ‘glucostatic’ circuitry may be partly responsible for pathological conditions resulting from diabetes and obesity. To define the ‘glucostat’ brain circuitry further we have combined blood‐oxygen‐level‐dependent pharmacological‐challenge magnetic resonance imaging (phMRI) with whole‐brain c‐Fos functional activity mapping to characterise brain regions responsive to an orexigenic dose of 2‐DG [200 mg/kg; subcutaneous (s.c.)]. For phMRI, rats were imaged using a T2*‐weighted gradient echo in a 7T magnet for 60 min under α‐chloralose anaesthesia, whereas animals for immunohistochemistry were unanaesthetised and freely behaving. These complementary methods demonstrated functional brain activity in a number of previously characterised glucose‐sensing brain regions such as those in the hypothalamus and brainstem following administration of 2‐DG compared with vehicle. As the study mapped whole‐brain functional responses, it also identified the orbitofrontal cortex and striatum (nucleus accumbens and ventral pallidum) as novel 2‐DG‐responsive brain regions. These regions make up a corticostriatal connection with the hypothalamus, by which aspects of motivation, salience and reward can impinge on the hypothalamic control of feeding behaviour. This study, therefore, provides further evidence for a common integrated circuit involved in the induction of feeding behaviour, and illustrates the valuable potential of phMRI in investigating central pharmacological actions.

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Differential response of arcuate proopiomelanocortin- and neuropeptide Y-containing neurons to the lesion produced by gold thioglucose administration

Cited by 15 publications

References 50 publications

Role of the lesion scar in the response to damage and repair of the central nervous system

Role of the lesion scar in the response to damage and repair of the central nervous system

Expression of Transforming Growth Factor-β Receptors in Meningeal Fibroblasts of the Injured Mouse Brain

Functional magnetic resonance imaging and c‐Fos mapping in rats following a glucoprivic dose of 2‐deoxy‐d‐glucose

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