GAP‐43, aFGF, CCK and α‐ and β‐CGRP in Rat Spinal Motoneurons Subjected to Axotomy and/or Dorsal Root Severance

Piehl, Fredrik; Arvidsson, Ulf; Johnson, Hans; Cullheim, Staffan; Dagerlind, Å.; Ulfhake, Brun; Cao, Yihai; Elde, Robert; Pettersson, Ralf F.; Terenius, Lars; Hökfelt, Tomas

doi:10.1111/j.1460-9568.1993.tb00918.x

Cited by 68 publications

(46 citation statements)

References 59 publications

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“…Various spinal and cranial nerve motoneurons do express protein and mRNA of FGF-1 Piehl et al, 1993) and of FGF-2 (Grothe et al, 1991a;Gonzalez et al, 1995). In line with these data is the first demonstration of the FGF-2 mRNA in hypoglossal motoneurons in this study in addition to the previously reported presence of FGF-2 protein in hypoglossal motoneurons Grothe and Janet, 1995).…”

Section: Discussionsupporting

confidence: 91%

“…Furthermore, FGFR1 protein and mRNA are highly expressed by hypoglossal motoneurons, as previously demonstrated for other motoneurons as well (Wanaka et al, 1990;Gonzalez et al, 1995;Grothe and Janet, 1995). In contrast to FGF-1, which was not affected after peripheral nerve axotomy (Piehl et al, 1993), both FGF-2 protein and mRNA are changed after hypoglossal nerve lesion. A temporary reduction of FGF-2 protein was followed by a reexpression of FGF-2 11 days after hypoglossal nerve axotomy .…”

Section: Discussionmentioning

confidence: 50%

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Expression of fibroblast growth factor‐2 in hypoglossal motoneurons is stimulated by peripheral nerve injury

1997

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We have studied the expression of basic fibroblast growth factor 2 (FGF-2) and FGF receptor 1 (FGFR1) in the hypoglossal motor system during degeneration and regeneration by using an RNase protection assay, in situ hybridization, and Western blot analysis. The FGF-2 transcript was found to be weakly expressed in the hypoglossal motoneurons of the adult rat. Both peripheral transection and crush injury of the hypoglossal nerve resulted in a marked up-regulation of the FGF-2 mRNA in motoneurons of the hypoglossal nucleus (with a peak at 10 and 11 days postlesion) as well as in the proximal and distal nerve stumps. The FGFR1 transcript was strongly expressed by hypoglossal motoneurons of unlesioned rats. Neither axotomy nor crush lesion of the hypoglossal nerve revealed any alteration of the expression level and cellular localization in the hypoglossal nucleus, but they did result in a significant increase of the FGFR1 mRNA level in the proximal and distal nerve stump. Western blot analysis of the hypoglossal nucleus revealed the presence of the 21 kD and 23 kD isoforms and of a weak expression of the 18 kD isoform. Hypoglossal nerve transection resulted in a complete down-regulation of the FGF-2 protein 3 days after lesion. After 14 days, however, the level of the three isoforms was increased above the control level. The regulation of FGF-2 in hypoglossal motoneurons after experimental nerve injury is in agreement with the idea of a lesion-related function of FGF-2. Together with previously reported neurotrophic effects, these results suggest that FGF-2 provides trophic support for lesioned motoneurons. At the injury site, FGF-2 could be involved in the regulation of the myelination.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 50%

Expression of fibroblast growth factor‐2 in hypoglossal motoneurons is stimulated by peripheral nerve injury

1997

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“…In line with this, CGRP has been involved in the formation of synaptic processes (Sala et al, 1995). Increased CGRP staining has been shown to persist for a long time, and to be still evident when nearly complete reinnervation has been achieved, even when levels of neurotrophin receptors have returned to control levels (Piehl et al, 1993). Therefore, the fact that CGRP protein was expressed in extraocular motoneurons after lesion might suggest that a process of axonal regrowth and reinnervation has been at least initiated (Fig.…”

Section: Induction Of Cgrp Expression By Axotomymentioning

confidence: 87%

“…In motoneurons, a reduction in choline acetyltransferase (ChAT) expression, an enzyme involved in the synthesis of the neurotransmitter acetylcholine, often occurs after nerve damage (Lams et al, 1988;Matsuura et al, 1997;Wang et al, 1997). In contrast, other molecules like calcitonin gene-related peptide (CGRP), a protein related to rearrangement of synaptic connections, increase their expression after lesion (Calderó et al, 1992;Borke et al, 1993;Piehl et al, 1993;Fukuoka et al, 1999).…”

mentioning

confidence: 96%

Differential regulation of the expression of neurotrophin receptors in rat extraocular motoneurons after lesion

Morcuende

Matarredona

Benítez‐Temiño

et al. 2011

J of Comparative Neurology

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Neurotrophins acting through high-affinity tyrosine kinase receptors (trkA, trkB, and trkC) play a crucial role in regulating survival and maintenance of specific neuronal functions after injury. Adult motoneurons supplying extraocular muscles survive after disconnection from the target, but suffer dramatic changes in morphological and physiological properties, due in part to the loss of their trophic support from the muscle. To investigate the dependence of the adult rat extraocular motoneurons on neurotrophins, we examined trkA, trkB, and trkC mRNA expression after axotomy by in situ hybridization. trkA mRNA expression was detectable at low levels in unlesioned motoneurons, and its expression was downregulated 1 and 3 days after injury. Expression of trkB and trkC mRNAs was stronger, and after axotomy a simultaneous, but inverse regulation of both receptors was observed. Thus, whereas a considerable increase in trkB expression was seen about 2 weeks after axotomy, the expression of trkC mRNA had decreased at the same post-lesion period. Injured extraocular motoneurons also experienced an initial induction in expression of calcitonin gene-related peptide and a transient downregulation of cholinergic characteristics, indicating a switch in the phenotype from a transmitter-specific to a regenerative state. These results suggest that specific neurotrophins may contribute differentially to the survival and regenerative responses of extraocular motoneurons after lesion.

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“…Compared to other neuronal types, motor neurons contain high levels of FGF-1 [35][36][37] , which represent approximately 0.1% of soluble protein in the cytoplasmic compartment [35] . FGF-1 levels in motor neurons are altered following spinal cord injury or nerve lesions [38,39] , which might be due to an increased rate of release. FGF-1 is not released by a classical secretion pathway but rather by an alternative mechanism triggered by cell damage.…”

Section: Fibroblast Growth Factor-1 Induces Astrocyte Activationmentioning

confidence: 99%

Complexity of Astrocyte-Motor Neuron Interactions in Amyotrophic Lateral Sclerosis

Pehar¹,

Vargas²,

Cassina³

et al. 2005

Neurodegener Dis

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Neurons and surrounding glial cells compose a highly specialized functional unit. In amyotrophic lateral sclerosis (ALS) astrocytes interact with motor neurons in a complex manner to modulate neuronal survival. Experiments using chimeric mice expressing ALS-linked mutations to Cu,Zn superoxide dismutase (SOD-1) suggest a critical modulation exerted by neighboring non-neuronal cell types on disease phenotype. When perturbed by primary neuronal damage, e.g. expression of SOD-1 mutations, neurons can signal astrocytes to proliferate and become reactive. Fibroblast growth factor-1 (FGF-1) can be released by motor neurons in response to damage to induce astrocyte activation by signaling through the receptor FGFR1. FGF-1 stimulates nerve growth factor (NGF) expression and secretion, as well as activity of the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor. Nrf2 leads to the expression of antioxidant and cytoprotective enzymes such as heme oxygenase-1 and a group of enzymes involved in glutathione metabolism that prevent motor neuron degeneration. However, prolonged stimulation with FGF-1 or SOD-mediated oxidative stress in astrocytes may disrupt the normal neuron-glia interactions and lead to progressive neuronal degeneration. The re-expression of p75 neurotrophin receptor and neuronal NOS in motor neurons in parallel with increased NGF secretion by reactive astrocytes may be a mechanism to eliminate critically damaged neurons. Consequently, astrocyte activation in ALS may have a complex pathogenic role.

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GAP‐43, aFGF, CCK and α‐ and β‐CGRP in Rat Spinal Motoneurons Subjected to Axotomy and/or Dorsal Root Severance

Cited by 68 publications

References 59 publications

Expression of fibroblast growth factor‐2 in hypoglossal motoneurons is stimulated by peripheral nerve injury

Expression of fibroblast growth factor‐2 in hypoglossal motoneurons is stimulated by peripheral nerve injury

Differential regulation of the expression of neurotrophin receptors in rat extraocular motoneurons after lesion

Complexity of Astrocyte-Motor Neuron Interactions in Amyotrophic Lateral Sclerosis

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