Cell death and axon regeneration of Purkinje cells after axotomy: Challenges of classical hypotheses of axon regeneration

Dusart, Isabelle; Ghoumari, A.; Wehrlé, Rosine; Morel, Marie-Pierre; Bouslama-Oueghlani, Lamia; Camand, Emeline; Sotelo, Constantino

doi:10.1016/j.brainresrev.2004.11.007

Cited by 49 publications

(40 citation statements)

References 168 publications

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“…In addition, similar to other systems (Thallmair et al, 1998;Bareyre et al, 2002), sprouting from intact Purkinje axons, with aberrant growth into the deep granular layer, can be induced by application of anti-Nogo antibodies in both adult (Buffo et al, 2000) and developing (Gianola et al, 2003) cerebella. This suggests that Purkinje axons are endowed with strong inclination for structural plasticity that is normally restricted by inhibitory environmental cues (Rossi, 2004;Dusart et al, 2005). We show here that CSPGs also contribute to this regulation.…”

Section: Discussionmentioning

confidence: 57%

“…Despite their poor regenerative potential (Rossi et al, 1995b;Dusart et al, 1997;Carulli et al, 2004), Purkinje axons are capable of extensive sprouting at long-term after injury (Dusart and Sotelo, 1994;Dusart et al, 1999;Gianola and Rossi, 2002), when the scar environment acquires growth-promoting/permissive properties, including disappearance of CSPGs (Dusart et al, 1999(Dusart et al, , 2005Morel et al, 2002). In addition, similar to other systems (Thallmair et al, 1998;Bareyre et al, 2002), sprouting from intact Purkinje axons, with aberrant growth into the deep granular layer, can be induced by application of anti-Nogo antibodies in both adult (Buffo et al, 2000) and developing (Gianola et al, 2003) cerebella.…”

Section: Discussionmentioning

confidence: 99%

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Degradation of Chondroitin Sulfate Proteoglycans Induces Sprouting of Intact Purkinje Axons in the Cerebellum of the Adult Rat

Corvetti¹,

Rossi²

2005

J. Neurosci.

123

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Chondroitin sulfate proteoglycans are major constituents of the extracellular matrix and form perineuronal nets. Information regarding the growth-inhibitory activity of these molecules after injury is rapidly expanding. However, less is known about their physiological role in the adult undamaged CNS. Here, we investigated the function of chondroitin sulfate proteoglycans in maintaining the proper structure of Purkinje axons in the cerebellum of adult rats. To this end, we examined the morphology and distribution of intracortical Purkinje neurites after intraparenchymal injection of chondroitinase ABC. Staining with the lectin Wisteria floribunda agglutinin or 2B6 antibodies showed that this treatment efficiently removed chondroitin sulfate proteoglycans from wide areas of the cerebellar cortex. In the same sites, there was a profuse outgrowth of terminal branches from the Purkinje infraganglionic plexus, which invaded the deeper regions of the granular layer. In contrast, myelinated axon segments were not affected and maintained their normal relationship with oligodendroglial sheaths. Purkinje axon sprouting was first evident at 4 d and increased further at 7 d after enzyme application. Within 42 d, the expression pattern of chondroitin sulfate proteoglycans gradually recovered, whereas axonal modifications progressively regressed. Our results show that, in the absence of injury or novel external stimuli, degradation of chondroitin sulfate proteoglycans is sufficient to induce Purkinje axon sprouting but not the formation of long-lasting synaptic contacts. Together with other growth-inhibitory molecules, such as myelin-associated proteins, chondroitin sulfate proteoglycans restrict structural plasticity of intact Purkinje axons to maintain normal wiring patterns in the adult cerebellar cortex.

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Degradation of Chondroitin Sulfate Proteoglycans Induces Sprouting of Intact Purkinje Axons in the Cerebellum of the Adult Rat

Corvetti¹,

Rossi²

2005

J. Neurosci.

123

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“…Manipulations of the growth cone protein GAP43 enhance the ability of a neuron to grow a new axon after injury but also increase the level of cell death from that very same injury 62, 63. Neuronal cell types with the greatest resistance to cell death after injury usually also have the lowest regenerative capacity, such as Purkinje cells, whereas neuronal cell types with the greatest regenerative capacity after injury also suffer the most cell death when injured, such as inferior olivary neurons 64. In neuronal sites as diverse as the optic nerve, dorsal root ganglion, and cortex, lesions closest to the cell body provoke the greatest amount of cell death, but also induce a greater regenerative response—compared to lesions distant from the cell body, in which there is little cell death and also little regeneration 64, 65, 66.…”

Section: Plasticity Is a Risk For Neuroprotection: Timing For A Neuramentioning

confidence: 99%

Emergent properties of neural repair: elemental biology to therapeutic concepts

Carmichael

2016

Annals of Neurology

118

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Stroke is the leading cause of adult disability. The past decade has seen advances in basic science research of neural repair in stroke. The brain forms new connections after stroke, which have a causal role in recovery of function. Brain progenitors, including neuronal and glial progenitors, respond to stroke and initiate a partial formation of new neurons and glial cells. The molecular systems that underlie axonal sprouting, neurogenesis, and gliogenesis after stroke have recently been identified. Importantly, tractable drug targets exist within these molecular systems that might stimulate tissue repair. These basic science advances have taken the field to its first scientific milestone; the elemental principles of neural repair in stroke have been identified. The next stages in this field involve understanding how these elemental principles of recovery interact in the dynamic cellular systems of the repairing brain. Emergent principles arise out of the interaction of the fundamental or elemental principles in a system. In neural repair, the elemental principles of brain reorganization after stroke interact to generate higher order and distinct concepts of regenerative brain niches in cellular repair, neuronal networks in synaptic plasticity, and the distinction of molecular systems of neuroregeneration. Many of these emergent principles directly guide the development of new therapies, such as the necessity for spatial and temporal control in neural repair therapy delivery and the overlap of cancer and neural repair mechanisms. This review discusses the emergent principles of neural repair in stroke as they relate to scientific and therapeutic concepts in this field. Ann Neurol 2016;79:895–906

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“…Although this treatment also induces robust neuritic growth (Buffo et al, 2000;Bareyre et al, 2002), it does not improve the regenerative abilities of refractory neurons such as Purkinje cells. In addition, myelin ablation does not prevent the developmental decline of Purkinje cell regenerative capabilities (BouslamaOueghlani et al, 2003;Dusart et al, 2005). Together, these observations indicate that myelin-associated molecules exert a strong action on local neuritic plasticity, but their effect on the expression of growth genes is milder and might require extensive demyelination (Hiebert et al, 2000).…”

Section: Factors Acting Along the Axonmentioning

confidence: 99%

“…Although this remains the most compelling example of such a mechanism, there is correlative evidence that it may also operate on other neurons. For instance, the decline of regenerative capacity of cerebellar Purkinje cells in vivo (Gianola and Rossi, 2001) correlates with the late phase of dendritogenesis when these neurons engage in extensive synaptogenesis with parallel fibers (Armengol and Sotelo, 1991;Dusart et al, 2005).…”

Section: 34mentioning

confidence: 99%

Intrinsic Factors Contributing to Axon Regeneration in the Mammalian Nervous System

Rossi

2006

Model Organisms in Spinal Cord Regeneration

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Cell death and axon regeneration of Purkinje cells after axotomy: Challenges of classical hypotheses of axon regeneration

Cited by 49 publications

References 168 publications

Degradation of Chondroitin Sulfate Proteoglycans Induces Sprouting of Intact Purkinje Axons in the Cerebellum of the Adult Rat

Degradation of Chondroitin Sulfate Proteoglycans Induces Sprouting of Intact Purkinje Axons in the Cerebellum of the Adult Rat

Emergent properties of neural repair: elemental biology to therapeutic concepts

Intrinsic Factors Contributing to Axon Regeneration in the Mammalian Nervous System

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