ArticleJournal of anatomy1995
An ultrastructural study of the submucous plexus of guinea pig intestine after unilateral vagotomy.
Article in Journal of anatomy, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Microglia-derived IL-1β contributes to axon development disorders and synaptic deficit through p38-MAPK signal pathway in septic neonatal rats.Journal of neuroinflammation · 2017Article
- Immunohistochemical localization of glycogen phosphorylase isozymes in the rat gastrointestinal muscle layers and enteric nervous system.Neurochemical research · 2009Article
- Ultrastructural localization of NADPH-diaphorase activity in the submucous ganglia of the guinea-pig intestine after vagotomy.Anatomy and embryology · 1996Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study describes the degenerative changes of the axon terminals making synaptic contacts with the neurons in the submucous ganglia of guinea pig small and large intestines following left or right cervical vagotomy. There were no noticeable ultrastructural changes 1 d after the operation. Beginning at the 3rd postoperative day for the small intestines and the 5th day for the large intestines, some of the axon terminals presynaptic to the submucous neurons displayed different stages of degeneration. The most obvious feature of the degenerating terminals was the swelling and vacuolation of mitochondria with disrupted cristae; another change was the clumping of synaptic vesicles. In the animals killed 7 d after vagotomy, besides the above changes, the degenerating axon terminals also showed an accumulation of a variable amount of glycogen-like particles. The changes were most severe in the guinea pigs killed on the 10th postoperative day. The synaptic vesicles in some degenerating terminals were depleted. There were occasional degenerating nerve cell bodies in the submucous ganglia in the period studied. A variable number of lamellated bodies were found in some of the submucous neurons of 10 and 15 d postoperative animals. By 30 d after vagotomy, all the terminals presynaptic to the submucous neurons appeared normal. There was no significant difference in the total number of axon terminals between 10 d and 30 d after operation (P > 0.05). This suggests that either there had been successful reinnervation or new synaptic contacts had been established by sprouting from the unoperated vagus or other intrinsic neurons. The present quantitative studies also showed that the number of degenerating axon terminals in the submucous ganglia of duodenum after left vagotomy was higher than right vagotomy (P < 0.05). This feature was particularly evident in animals killed 10 d after the operation. The larger number of degenerating terminals in the submucous ganglia of duodenum after left vagotomy suggests that the presynaptic axon terminals in the submucous ganglia of different gut regions are not evenly distributed. Finally, the present study showed that the degenerative changes in the small intestine preceded the large intestine.
Indexed as
Identifiers
8586560PMC1167464W207875015What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.