The strange case of Purkinje axon regeneration and plasticity

Rossi, Ferdinando; Gianola, Sara; Corvetti, Luigi

doi:10.1080/14734220600786444

Cited by 36 publications

(40 citation statements)

References 56 publications

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“…In addition, Pk axons were immunolabeled with anti-Calbindin (a major Pk cells marker) in the mutant mice, revealing a normal axon patterning. Furthermore, the collateral branching of Pk axons in the infraganglionic plexus, which is normally confined in the most superficial portion of the granular layer [23], did not show any abnormality (see Figure 6B, F). Also, the dendritic arborization of Pk cell in the molecular layer appeared normal in the mutant mice (not shown).…”

Section: Resultsmentioning

confidence: 99%

Plexin-B1 plays a redundant role during mouse development and in tumour angiogenesis

et al. 2007

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Background: Plexins are a large family of transmembrane receptors for the Semaphorins, known for their role in the assembly of neural circuitry. More recently, Plexins have been implicated in diverse biological functions, including vascular growth, epithelial tissue morphogenesis and tumour development. In particular, PlexinB1, the receptor for Sema4D, has been suggested to play a role in neural development and in tumour angiogenesis, based on in vitro studies. However, the tissue distribution of PlexinB1 has not been extensively studied and the functional relevance of this receptor in vivo still awaits experimental testing. In order to shed light on PlexinB1 function in vivo, we therefore undertook the genomic targeting of the mouse gene to obtain loss of function mutants.

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Section: Resultsmentioning

confidence: 99%

Plexin-B1 plays a redundant role during mouse development and in tumour angiogenesis

et al. 2007

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“…The aging process of different brain regions has been suggested to be different, and the cerebellum might be the most resistant to aging (Boukhtouche et al 2006;Rodrigo et al 2005;Rossi et al 2006). One of the reasons behind this could be the special function of the cerebellum, which plays a crucial role in motor control as it integrates information that relates to coordination from different brain regions and sensory systems.…”

Section: Introductionmentioning

confidence: 97%

Aging and exercise affect the level of protein acetylation and SIRT1 activity in cerebellum of male rats

et al. 2010

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Aging is associated with a gradual decline in cognitive and motor functions, the result of complex biochemical processes including pre- and posttranslational modifications of proteins. Sirtuins are NAD(+) dependent protein deacetylases. These enzymes modulate the aging process by lysine deacetylation, which alters the activity and stability of proteins. Exercise can increase mean life-span and improve quality of life. Data from our laboratories revealed that 4 weeks of treadmill running improves performance in the Morris Maze test for young (4 months, old) but not old (30 months, old) male rats, and the exercise could not prevent the age-associated loss in muscle strength assessed by a gripping test. The positive correlation between protein acetylation and the gripping test suggests that the age-dependent decrease in relative activity of SIRT1 in the cerebellum impairs motor function. Similarly to the acetylation level of total proteins, the acetylation of ά -tubulin is also increased with aging, while the effect of exercise training was not found to be significant. Moreover, the protein content of nicotinamide phosphoribosyltransferase, one of the key enzymes of NAD biosynthesis, decreased in the young exercise group. These data suggest that aging results in decreased specific activity of SIRT1 in cerebellum, which could lead to increased acetylation of protein residues, including ά-tubulin, that interfere with motor function.

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“…It is known that axonal destruction does not necessarily cause retrograde atrophy of Purkinje cells. These neurons have much greater inherent resistance to axonal interruption than other nerve cells whose eVerent Wbers begin and end within the CNS [27]. The morphological preservation of Purkinje cells in FRDA does not imply functional integrity, and the deaVerentation of the dentate nucleus points to a primary problem in Purkinje cells.…”

Section: Ferroportin In the Dentate Nucleusmentioning

confidence: 99%

The dentate nucleus in Friedreich’s ataxia: the role of iron-responsive proteins

et al. 2007

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Frataxin deWciency in Friedreich's ataxia (FRDA) causes cardiac, endocrine, and nervous system manifestations. Frataxin is a mitochondrial protein, and adequate amounts are essential for cellular iron homeostasis. The main histological lesion in the brain of FRDA patients is neuronal atrophy and a peculiar proliferation of synaptic terminals in the dentate nucleus termed grumose degeneration. This cerebellar nucleus may be especially susceptible to FRDA because it contains abundant iron. We examined total iron and selected iron-responsive proteins in the dentate nucleus of nine patients with FRDA and nine normal controls by biochemical and microscopic techniques. Total iron (1.53 § 0.53 mol/g wet weight) and ferritin (206.9 § 46.6 g/g wet weight) in FRDA did not signiWcantly diVer from normal controls (iron: 1.78 § 0.88 mol/g; ferritin: 210.9 § 9.0 g/g) but Western blots exhibited a shift to light ferritin subunits. Immunocytochemistry of the dentate nucleus revealed loss of juxtaneuronal ferritin-containing oligodendroglia and prominent ferritin immunoreactivity in microglia and astrocytes. Mitochondrial ferritin was not detectable by immunocytochemistry. Stains for the divalent metal transporter 1 conWrmed neuronal loss while endothelial cells reacting with antibodies to transferrin receptor 1 protein showed crowding of blood vessels due to collapse of the normal neuropil. Regions of grumose degeneration were strongly reactive for ferroportin. Purkinje cell bodies, their dendrites and axons, were also ferroportin-positive, and it is likely that grumose degeneration is the morphological manifestation of mitochondrial iron dysmetabolism in the terminals

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The strange case of Purkinje axon regeneration and plasticity

Cited by 36 publications

References 56 publications

Plexin-B1 plays a redundant role during mouse development and in tumour angiogenesis

Plexin-B1 plays a redundant role during mouse development and in tumour angiogenesis

Aging and exercise affect the level of protein acetylation and SIRT1 activity in cerebellum of male rats

The dentate nucleus in Friedreich’s ataxia: the role of iron-responsive proteins

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