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The effects of age and ganglioside composition on the rate of motor nerve terminal regeneration following antibody-mediated injury in mice.

Rupp A, Cunningham ME, Yao D, Furukawa K, Willison HJ - Synapse (2013)

Bottom Line: Gangliosides are glycosphingolipids highly enriched in neural plasma membranes, where they mediate a diverse range of functions and can act as targets for auto-antibodies present in human immune-mediated neuropathy sera.Both aging and ganglioside-deficiency have been linked to impaired axonal regeneration.Five days later, most NMJs, regardless of age and strain, had recovered their mNTs.

View Article: PubMed Central - PubMed

Affiliation: Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, G12 8TA, United Kingdom.

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Examples for injury and regeneration of the presynaptic structures in the different mouse strains. A: Isolated mNT injury in an aged GD3sKO mouse. B: Combined mNT and pSC injury in an aged GM2sKO mouse. C: Young control GD3sKO mouse. Note the selective loss of CFP overlying the NMJ (depicted by the nAChRs) in (A), whereas in (B) both GFP and CFP are lost following induction of the injury. After 5 days of the regeneration, both GFP and CFP are recovered, with an increased number of GFP-positive cell bodies overlying the NMJ in (B). No changes to the fluorescent proteins are noted in the control mouse (C), which only received complement, was subjected the in vivo imaging procedures and also was reimaged after a 5-day interval. Scale bars: 20 μm; pre- and post-injury images were acquired in vivo.
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fig02: Examples for injury and regeneration of the presynaptic structures in the different mouse strains. A: Isolated mNT injury in an aged GD3sKO mouse. B: Combined mNT and pSC injury in an aged GM2sKO mouse. C: Young control GD3sKO mouse. Note the selective loss of CFP overlying the NMJ (depicted by the nAChRs) in (A), whereas in (B) both GFP and CFP are lost following induction of the injury. After 5 days of the regeneration, both GFP and CFP are recovered, with an increased number of GFP-positive cell bodies overlying the NMJ in (B). No changes to the fluorescent proteins are noted in the control mouse (C), which only received complement, was subjected the in vivo imaging procedures and also was reimaged after a 5-day interval. Scale bars: 20 μm; pre- and post-injury images were acquired in vivo.

Mentions: Depending on the binding specificity of the anti-ganglioside Ab applied, a selective injury to the mNTs (loss of CFP overlying the NMJ) or a combined injury to the mNTs and pSCs (loss of both CFP and GFP overlying the NMJ) was observed (Fig. 2). In WT mice, the application of TBG3 and complement was associated with a selective mNT injury (WT-1), whereas the combined application of TBG3 and EG1 lead to a combined mNT and pSC injury (WT-2). In GM2sKO mice, the application of EG1 and complement elicited a loss of both CFP and GFP, thus inducing a combined mNT and pSC injury, and in GD3sKO mice, the application of TBG3 and complement lead to a selective loss of CFP, thus inducing a selective mNT injury. The application of human serum as a source of complement (in the absence of anti-ganglioside Ab) and exposure of muscles to in vivo imaging procedures did not induce any changes to the fluorescent proteins of the NMJ (Table1; Fig. 2).


The effects of age and ganglioside composition on the rate of motor nerve terminal regeneration following antibody-mediated injury in mice.

Rupp A, Cunningham ME, Yao D, Furukawa K, Willison HJ - Synapse (2013)

Examples for injury and regeneration of the presynaptic structures in the different mouse strains. A: Isolated mNT injury in an aged GD3sKO mouse. B: Combined mNT and pSC injury in an aged GM2sKO mouse. C: Young control GD3sKO mouse. Note the selective loss of CFP overlying the NMJ (depicted by the nAChRs) in (A), whereas in (B) both GFP and CFP are lost following induction of the injury. After 5 days of the regeneration, both GFP and CFP are recovered, with an increased number of GFP-positive cell bodies overlying the NMJ in (B). No changes to the fluorescent proteins are noted in the control mouse (C), which only received complement, was subjected the in vivo imaging procedures and also was reimaged after a 5-day interval. Scale bars: 20 μm; pre- and post-injury images were acquired in vivo.
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Related In: Results  -  Collection

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fig02: Examples for injury and regeneration of the presynaptic structures in the different mouse strains. A: Isolated mNT injury in an aged GD3sKO mouse. B: Combined mNT and pSC injury in an aged GM2sKO mouse. C: Young control GD3sKO mouse. Note the selective loss of CFP overlying the NMJ (depicted by the nAChRs) in (A), whereas in (B) both GFP and CFP are lost following induction of the injury. After 5 days of the regeneration, both GFP and CFP are recovered, with an increased number of GFP-positive cell bodies overlying the NMJ in (B). No changes to the fluorescent proteins are noted in the control mouse (C), which only received complement, was subjected the in vivo imaging procedures and also was reimaged after a 5-day interval. Scale bars: 20 μm; pre- and post-injury images were acquired in vivo.
Mentions: Depending on the binding specificity of the anti-ganglioside Ab applied, a selective injury to the mNTs (loss of CFP overlying the NMJ) or a combined injury to the mNTs and pSCs (loss of both CFP and GFP overlying the NMJ) was observed (Fig. 2). In WT mice, the application of TBG3 and complement was associated with a selective mNT injury (WT-1), whereas the combined application of TBG3 and EG1 lead to a combined mNT and pSC injury (WT-2). In GM2sKO mice, the application of EG1 and complement elicited a loss of both CFP and GFP, thus inducing a combined mNT and pSC injury, and in GD3sKO mice, the application of TBG3 and complement lead to a selective loss of CFP, thus inducing a selective mNT injury. The application of human serum as a source of complement (in the absence of anti-ganglioside Ab) and exposure of muscles to in vivo imaging procedures did not induce any changes to the fluorescent proteins of the NMJ (Table1; Fig. 2).

Bottom Line: Gangliosides are glycosphingolipids highly enriched in neural plasma membranes, where they mediate a diverse range of functions and can act as targets for auto-antibodies present in human immune-mediated neuropathy sera.Both aging and ganglioside-deficiency have been linked to impaired axonal regeneration.Five days later, most NMJs, regardless of age and strain, had recovered their mNTs.

View Article: PubMed Central - PubMed

Affiliation: Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, G12 8TA, United Kingdom.

Show MeSH
Related in: MedlinePlus