Differential effects of activity dependent treatments on axonal regeneration and neuropathic pain after peripheral nerve injury

Cobianchi, Stefano; Casals‐Diaz, Laura; Jaramillo, Jessica; Navarro, Xavier

doi:10.1016/j.expneurol.2012.11.023

Cited by 121 publications

(132 citation statements)

References 56 publications

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“…Moreover, activity-dependent therapies can also modulate the plastic changes observed after peripheral nerve injury, as reported for the modulation of the H reflex (Asensio-Pinilla et al, 2009;Udina et al, 2011a;Vivó et al, 2008) and of pain responses (Cobianchi et al, 2010(Cobianchi et al, , 2013. Since synaptic stripping might be a source of poor functional recovery following peripheral nerve injury, these combined effects of treadmill training have the potential for improved functional recovery after injury.…”

Section: Discussionmentioning

confidence: 99%

“…The training protocol was started 3 days after surgery. The highintensity treadmill running program (HTRP) consisted of one session of treadmill running daily for 5 days, with duration and intensity being progressively increased; running started at a locomotion speed of 10 cm/s that was increased 2 cm/s every 5 min, until a maximum speed of 30 cm/s for 60 min was reached during the final training session (Cobianchi et al, 2013). The low-intensity treadmill running program (LTRP) was performed with a constant treadmill speed of 10 cm/s in two sessions of 30 min each with 10 minute resting period, daily during all the follow-up.…”

Section: Treadmill Runningmentioning

confidence: 99%

“…Therefore, either physical activity or exposure to enriched environment promotes neurite outgrowth and functional plasticity (Ghiani et al, 2007;Rampon et al, 2000;Sale et al, 2007;Vaynman and Gomez-Pinilla, 2005). Activity-dependent plasticity has been linked with changes in neurotrophin expression, neuronal growth genes and regulatory substances (Cobianchi et al, 2013;Molteni et al, 2004). However, other studies note the importance of a specific rehabilitation therapy to improve functional recovery after neural damage (García-Alías and Fawcett, 2012;Wang et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Activity dependent therapies modulate the spinal changes that motoneurons suffer after a peripheral nerve injury

Arbat-Plana

Torres-Espín

Navarro

et al. 2015

Experimental Neurology

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Section: Discussionmentioning

confidence: 99%

Section: Treadmill Runningmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Activity dependent therapies modulate the spinal changes that motoneurons suffer after a peripheral nerve injury

Arbat-Plana

Torres-Espín

Navarro

et al. 2015

Experimental Neurology

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“…In fact, single exogenous dosage of BDNF has shown better results than continuous long-term applications [258]. It is reported that muscle regeneration causes the overexpression of GDNF which increases the number of motor axons in the neuromuscular junctions in vivo [259][260][261][262][263][264][265][266]. Also, GDNF is a potent protective factor against axotomy-induced motor and sensory neuron death [267][268][269][270].…”

Section: Neurotrophic Factorsmentioning

confidence: 99%

Scaffolds for Peripheral Nerve Regeneration, the Importance of In Vitro and In Vivo Studies for the Development of Cell-Based Therapies and Biomaterials: State of the Art

Pedrosa¹,

Caseiro²,

Santos³

et al. 2017

Scaffolds in Tissue Engineering - Materials, Technologies and Clinical Applications

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Human adult peripheral nerve injuries are a high incidence clinical problem that greatly affects patients' quality of life. Although peripheral nervous system has intrinsic regenerative capacity, this occurs in an incomplete or poorly functional manner. When a nerve fiber loses its continuity with consequent damage of the basal lamina tubes, axon spontaneous regeneration is disorganized and mismatched. These phenomena translate in an inadequate nerve functional recovery and consequent musculoskeletal incapacity. Nerve grafts still remain the gold standard in peripheral injuries treatment. However, this approach contains its disadvantages such as the necessity of primary surgery to harvest the autografts, loss of a functional nerve, donor site morbidity and longer surgery procedures. Therefore, biomaterials and tissue engineering can provide efficient resources and alternatives to nerve injury repair not only by the development of biocompatible structures but also, introducing neurotrophic factors and cellular systems to stimulate optimum clinical outcome. In this chapter, a comprehensive state-of-the art picture of tissue-engineered nerve grafts scaffolds, their application in nerve regeneration along with latest advances in peripheral nerve repair and future perspectives will be discussed, including our own large experience in this field of knowledge.

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“…Axotomy and glial plasticity have been linked with changes in neurotrophins expression, neuronal growth genes, and several regulatory molecules (Cobianchi et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Astrocytes and Microglia-Mediated Immune Response in Maladaptive Plasticity is Differently Modulated by NGF in the Ventral Horn of the Spinal Cord Following Peripheral Nerve Injury

et al. 2015

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Reactive astrocytes and activated microglia are the key players in several pathophysiologic modifications of the central nervous system. We used the spared nerve injury (SNI) of the sciatic nerve to induce glial maladaptive response in the ventral horn of lumbar spinal cord and examine its role in the remodeling of the tripartite synapse plasticity. Imaging the ventral horn revealed that SNI was associated with both an early microglial and astrocytic activation, assessed, respectively, by analysis of Iba1 and GFAP expression. Microglia, in particular, localized peculiarly surrounding the motor neurons somata. Perineuronal astrocytes, which play a key role in maintaining the homeostasis of neuronal circuitry, underwent a substantial phenotypic change following peripheral axotomy, producing reactive gliosis. The gliosis was associated with the reduction of glial aminoacid transporters (GLT1 and GlyT1) and increase of neuronal glutamate transporter EAAC1. Although the expression of GABAergic neuronal marker GAD65/67 showed no change, glutamate increase, as demonstrated by HPLC analysis, shifted the excitatory/inhibitory balance as showed by the net increase of the glutamate/GABA ratio. Moreover, endogenous NGF levels were altered in SNI animals and not restored by the intrathecal NGF administration. This treatment reverted phenotypic changes associated with reactive astrocytosis, but failed to modify microglia activation. These findings on one hand confirm the correlation between gliopathy and maladaptive plasticity of the spinal synaptic circuitry, on the other hand add new data concerning the complex peculiar behavior of different glial cells in neuronal degenerative processes, defining a special role of microglia in sustaining the inflammatory response.

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Differential effects of activity dependent treatments on axonal regeneration and neuropathic pain after peripheral nerve injury

Cited by 121 publications

References 56 publications

Activity dependent therapies modulate the spinal changes that motoneurons suffer after a peripheral nerve injury

Activity dependent therapies modulate the spinal changes that motoneurons suffer after a peripheral nerve injury

Scaffolds for Peripheral Nerve Regeneration, the Importance of In Vitro and In Vivo Studies for the Development of Cell-Based Therapies and Biomaterials: State of the Art

Astrocytes and Microglia-Mediated Immune Response in Maladaptive Plasticity is Differently Modulated by NGF in the Ventral Horn of the Spinal Cord Following Peripheral Nerve Injury

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