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Increased galanin expression in the celiac ganglion of BB diabetic rats

Mei, Qi ; Mundinger, Thomas O ; Lernmark, Åke LU and Taborsky, Gerald J (2006) In Neuropeptides 40(1). p.1-10
Abstract

BB rats lose >50% of their islet sympathetic nerve terminals soon after diabetes onset, markedly impairing the glucagon response to activation of these nerves. In this study, we sought evidence that this degree of disease-induced nerve terminal damage affected their neuronal cell bodies. Increased galanin expression was used as a marker of the change of phenotype that occurs in neuronal cell bodies when their axons are severely damaged. The celiac ganglion (CG) was analyzed because it is a major source of the sympathetic nerves that project to the pancreatic islets. But we first needed to determine if damaging nerve terminals could increase galanin expression in this ganglion and, if so, when that expression was maximal. Severe,... (More)

BB rats lose >50% of their islet sympathetic nerve terminals soon after diabetes onset, markedly impairing the glucagon response to activation of these nerves. In this study, we sought evidence that this degree of disease-induced nerve terminal damage affected their neuronal cell bodies. Increased galanin expression was used as a marker of the change of phenotype that occurs in neuronal cell bodies when their axons are severely damaged. The celiac ganglion (CG) was analyzed because it is a major source of the sympathetic nerves that project to the pancreatic islets. But we first needed to determine if damaging nerve terminals could increase galanin expression in this ganglion and, if so, when that expression was maximal. Severe, global nerve terminal damage produced a dramatic increase of CG galanin expression which was maximal 5 days later. We next determined if a global, but partial, nerve terminal loss would also increase galanin expression and found a significant increase of galanin mRNA and its peptide in the CG. Finally, we determined if the disease-induced, partial and islet-selective loss of nerve terminals seen in BB diabetic rats was sufficient to increase galanin: we, again, found a significant increase of galanin mRNA and its peptide in their CG. These increases did not occur in their superior cervical ganglia. We conclude that the selective damage to islet sympathetic nerve terminals seen in BB diabetic rats, rather than the systemic factors of diabetic hyperglycemia or insulin deficiency, causes the increased galanin expression observed in the CG of this animal model of type 1 diabetes.

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author
publishing date
type
Contribution to journal
publication status
published
keywords
Galanin, Ganglia, Islets of Langerhans, Messenger, Oxidopamine, Rats: Inbred BB, Reverse transcription polymerase chain reaction, RNA, Sympathetic, Type 1 Diabetes Mellitus
in
Neuropeptides
volume
40
issue
1
pages
10 pages
publisher
Elsevier
external identifiers
  • scopus:32844471566
  • pmid:16487586
ISSN
0143-4179
DOI
10.1016/j.npep.2005.08.005
language
English
LU publication?
no
id
627ab81a-2ab8-4dc9-a02f-c7c38343946d
date added to LUP
2017-09-07 09:58:17
date last changed
2020-01-13 00:03:10
@article{627ab81a-2ab8-4dc9-a02f-c7c38343946d,
  abstract     = {<p>BB rats lose &gt;50% of their islet sympathetic nerve terminals soon after diabetes onset, markedly impairing the glucagon response to activation of these nerves. In this study, we sought evidence that this degree of disease-induced nerve terminal damage affected their neuronal cell bodies. Increased galanin expression was used as a marker of the change of phenotype that occurs in neuronal cell bodies when their axons are severely damaged. The celiac ganglion (CG) was analyzed because it is a major source of the sympathetic nerves that project to the pancreatic islets. But we first needed to determine if damaging nerve terminals could increase galanin expression in this ganglion and, if so, when that expression was maximal. Severe, global nerve terminal damage produced a dramatic increase of CG galanin expression which was maximal 5 days later. We next determined if a global, but partial, nerve terminal loss would also increase galanin expression and found a significant increase of galanin mRNA and its peptide in the CG. Finally, we determined if the disease-induced, partial and islet-selective loss of nerve terminals seen in BB diabetic rats was sufficient to increase galanin: we, again, found a significant increase of galanin mRNA and its peptide in their CG. These increases did not occur in their superior cervical ganglia. We conclude that the selective damage to islet sympathetic nerve terminals seen in BB diabetic rats, rather than the systemic factors of diabetic hyperglycemia or insulin deficiency, causes the increased galanin expression observed in the CG of this animal model of type 1 diabetes.</p>},
  author       = {Mei, Qi and Mundinger, Thomas O and Lernmark, Åke and Taborsky, Gerald J},
  issn         = {0143-4179},
  language     = {eng},
  number       = {1},
  pages        = {1--10},
  publisher    = {Elsevier},
  series       = {Neuropeptides},
  title        = {Increased galanin expression in the celiac ganglion of BB diabetic rats},
  url          = {http://dx.doi.org/10.1016/j.npep.2005.08.005},
  doi          = {10.1016/j.npep.2005.08.005},
  volume       = {40},
  year         = {2006},
}