Time course, localization and pharmacological modulation of immediate early inducible genes, brain-derived neurotrophic factor and trkB messenger RNAs in the rat brain following photochemical stroke

Comelli, Maria Cristina; Guidolin, Diego; Seren, M.S.; Zanoni, R.; Canella, R.; Rubini, R.; Manev, Hari

doi:10.1016/0306-4522(93)90517-j

Cited by 109 publications

(26 citation statements)

References 48 publications

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“…The outgrowth of lesioned CST axons can be promoted by application of neurotrophic growth factors, such as vascular endothelial growth factor (VEGF) (Facchiano et al, 2002), brain-derived neurotrophic factor (BDNF) (Vavrek et al, 2006), or by knockout or neutralization of inhibitory signals such as Nogo (Schwab, 2004) and Nogo receptors (GrandPre et al, 2002). Following ischemic lesions, the adult CNS can induce cellular responses needed for neurite growth and synaptic formation (Cramer and Chopp, 2000), including the expression of growth-promoting factors, such as BDNF (Comelli et al, 1993) and basic fibroblast growth factor (bFGF) (Lin et al, 1997) that could lead to partial spontaneous functional recovery. Related studies have indicated that functional recovery in rodent ischemic stroke models is associated with collateral sprouting of the uninjured CST to the denervated side of spinal cord and is enhanced by treatment of inosine , bFGF (Kawamata et al, 1997), Nogo antibody (Papadopoulos et al, 2002) and Nogo receptor antagonist (Lee et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Axonal sprouting into the denervated spinal cord and synaptic and postsynaptic protein expression in the spinal cord after transplantation of bone marrow stromal cell in stroke rats

Liu¹,

Li²,

Qu³

et al. 2007

Brain Research

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We investigated whether compensatory reinnervation in the corticospinal tract (CST) and the corticorubral tract (CRT) is enhanced by administration of bone marrow stromal cells (BMSCs) after experimental stroke. Adult male Wistar rats were subjected to permanent right middle cerebral artery occlusion (MCAo). Phosphate-buffered saline (PBS, control, n=7) or 3 × 10 6 BMSCs in PBS (n=8) were injected into a tail vein at 1 day postischemia. The CST of the left sensorimotor cortices was labeled with DiI 2 days prior to MCAo. Functional recovery was measured. Rats were sacrificed at 28 days after MCAo. The brain and spinal cord were removed and processed for vibratome sections for laser-scanning confocal analysis and paraffin sections for immunohistochemistry. Normal rats (n=4) exhibited a predominantly unilateral pattern of innervation of CST and CRT axons. After stroke, bilateral innervation occurred through axonal sprouting of the uninjured CRT and CST. Administration of BMSCs significantly increased the axonal restructuring on the de-afferented red nucleus and the denervated spinal motoneurons (p<0.05). BMSC treatment also significantly increased synaptic proteins in the denervated motoneurons. These results were highly correlated with improved functional outcome after stroke (r>0.81, p<0.01). We conclude that the transplantation of BMSCs enhance axonal sprouting and rewiring into the denervated spinal cord which may facilitate functional recovery after focal cerebral ischemia.

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Section: Discussionmentioning

confidence: 99%

Axonal sprouting into the denervated spinal cord and synaptic and postsynaptic protein expression in the spinal cord after transplantation of bone marrow stromal cell in stroke rats

Liu¹,

Li²,

Qu³

et al. 2007

Brain Research

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“…In adjacent areas, the facilitation of long-term potentiation 3 and synaptic plasticity occurs, as demonstrated by a sequential increase in markers for axonal sprouting and synaptogenesis. 23 First, the expression of the growth cone marker growth-associated protein 43 24 and other growth-associated markers 25,26 has been observed in rodents between 3 and 14 days post cortical infarction and was followed by increased expression of the synapse marker synaptophysin until 60 days postinfarction. Positive signals for axonal sprouting have been found to be sequentially replaced by negative factors such as Nogo, [27][28][29] chondroitin sulfate proteoglycan, 30 ephrin-A5, semaphorin-3A, and neuropilin-1 24 to balance the initial reaction.…”

Section: Functional Considerationsmentioning

confidence: 99%

Restoring Neuronal Function After Stroke by Cell Replacement

Dihné

Hartung

Seitz

2011

Stroke

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Background and Purpose-A major challenge to effective treatment after stroke is the restoration of neuronal function.In recent years, cell-based therapies for stroke have been explored in experimental animal models, and the results have suggested behavioral improvements. However, the anatomic targets of a cell-based stroke therapy and the relationship of cell grafts to post stroke reorganization are poorly understood, which results in difficulties defining strategies for neuronal substitution. Given that stroke causes a variety of secondary changes at locations beyond the infarct lesion, overcoming these difficulties is even more important. Summary of Review-We describe which brain structures and cell types are candidates for substitution and how new neuronal functionality could be implemented in a damaged brain by capitalizing on current concepts of post stroke plasticity. (Stroke. 2011;42:2342-2350.)

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“…In animal models of stroke an increase in the levels of BDNF mRNA is observed, starting approximately two hours after stroke commencement. 82 The mRNA was observed predominantly in cells which have normal morphological appearance. 82 Subsequent studies showed that administration of BDNF via an osmotic pump directly into the infarct following middle cerebral artery occlusion (MCAO), could lead to a significant reduction in infarct size.…”

Section: Vector-mediated Transportmentioning

confidence: 99%

“…82 The mRNA was observed predominantly in cells which have normal morphological appearance. 82 Subsequent studies showed that administration of BDNF via an osmotic pump directly into the infarct following middle cerebral artery occlusion (MCAO), could lead to a significant reduction in infarct size. 83 Studies in single allele BDNF knockout mice confirmed these findings.…”

Section: Vector-mediated Transportmentioning

confidence: 99%