scholarly journals Intrinsic positional memory guides target-specific axon regeneration in the zebrafish vagus nerve

Development ◽  
2021 ◽  
Vol 148 (18) ◽  
Author(s):  
Adam J. Isabella ◽  
Jason A. Stonick ◽  
Julien Dubrulle ◽  
Cecilia B. Moens
Keyword(s):  
Vagus Nerve ◽  
Motor Nerve ◽  
Target Selection ◽  
Branch Points ◽  
Developmental Guidance ◽  
Peripheral Nerve Damage ◽  
Injury Model ◽  
Mechanistic Basis ◽  
The Brain ◽  
Correct Target

ABSTRACT Regeneration after peripheral nerve damage requires that axons re-grow to the correct target tissues in a process called target-specific regeneration. Although much is known about the mechanisms that promote axon re-growth, re-growing axons often fail to reach the correct targets, resulting in impaired nerve function. We know very little about how axons achieve target-specific regeneration, particularly in branched nerves that require distinct targeting decisions at branch points. The zebrafish vagus motor nerve is a branched nerve with a well-defined topographic organization. Here, we track regeneration of individual vagus axons after whole-nerve laser severing and find a robust capacity for target-specific, functional re-growth. We then develop a new single-cell chimera injury model for precise manipulation of axon-environment interactions and find that (1) the guidance mechanism used during regeneration is distinct from the nerve's developmental guidance mechanism, (2) target selection is specified by neurons' intrinsic memory of their position within the brain, and (3) targeting to a branch requires its pre-existing innervation. This work establishes the zebrafish vagus nerve as a tractable regeneration model and reveals the mechanistic basis of target-specific regeneration.

Localization of Adductor and Abductor Motor Nerve Fibers to the Larynx

1977 ◽  
Vol 86 (6) ◽  
pp. 770-776 ◽  
Author(s):  
Richard R. Gacek ◽  
Leslie T. Malmgren ◽  
Michael J. Lyon
Keyword(s):  
Vagus Nerve ◽  
Motor Neurons ◽  
Motor Nerve ◽  
Functional Results ◽  
Nerve Fibers ◽  
Nucleus Ambiguus ◽  
Axoplasmic Flow ◽  
Anterograde Degeneration ◽  
Almost All ◽  
The Brain

Knowledge of the location of motor nerve fibers to the adductor and abductor muscles of the larynx may be useful in the diagnosis and treatment of innervation disorders in this organ. Anterograde degeneration and retrograde tracer anatomical techniques have demonstrated the central and peripheral positions of these two groups of motor nerve fibers in the cat. Traditional nerve fiber degeneration methods applied following intracranial transection of the vagus nerve rootlets indicated that: 1) Most of the fibers in the recurrent laryngeal nerve (RLN) are motor; 2) Almost all of these motor fibers leave the brain stem in the most rostral rootlet(s) of the vagus nerve; and 3) Motor fibers to the larynx form a discrete bundle within the trunk of the vagus nerve before forming the RLN. A tracer (horseradish peroxidase) of retrograde axoplasmic flow in motor neurons has been employed to demonstrate: 1) Dorsoventral division of the adductor and abductor neurons in the nucleus ambiguus; and 2) Diffuse arrangement of both adductor and abductor nerve fibers in the vagus nerve but collection of these fibers into abductor and adductor halves of the RLN prior to entering the larynx. These findings dispel theories of differential cord paralysis (Semon's law) based on a vulnerable position of abductor fibers at the periphery of the RLN. Furthermore, the diffuse arrangement of these fiber groups explains the usually mixed functional results obtained following reimplantation of the RLN into a laryngeal muscle.

scholarly journals Ocular neuromyotonia

2018 ◽  
Vol 18 (5) ◽  
pp. 389-390 ◽  
Author(s):  
Ricardo Soares-dos-Reis ◽  
Ana Inês Martins ◽  
Ana Brás ◽  
Anabela Matos ◽  
Conceição Bento ◽  
...  
Keyword(s):  
Motor Nerve ◽  
Underlying Mechanism ◽  
Motor Disorder ◽  
Ocular Motor ◽  
Drug Switching ◽  
Ephaptic Transmission ◽  
History Of ◽  
The Brain ◽  
Ocular Neuromyotonia ◽  
Fourth Nerve Palsy

Ocular neuromyotonia is a rare, albeit treatable, ocular motor disorder, characterised by recurrent brief episodes of diplopia due to tonic extraocular muscle contraction. Ephaptic transmission in a chronically damaged ocular motor nerve is the possible underlying mechanism. It usually improves with carbamazepine. A 53-year-old woman presented with a 4-month history of recurrent episodes of binocular vertical diplopia (up to 40/day), either spontaneously or after sustained downward gaze. Between episodes she had a mild left fourth nerve palsy. Sustained downward gaze consistently triggered downward left eye tonic deviation, lasting around 1 min. MR scan of the brain was normal. She improved on starting carbamazepine but developed a rash that necessitated stopping the drug. Switching to lacosamide controlled her symptoms.

scholarly journals Neuropod Cells: The Emerging Biology of Gut-Brain Sensory Transduction

2020 ◽  
Vol 43 (1) ◽  
pp. 337-353 ◽  
Author(s):  
Melanie Maya Kaelberer ◽  
Laura E. Rupprecht ◽  
Winston W. Liu ◽  
Peter Weng ◽  
Diego V. Bohórquez
Keyword(s):  
Epithelial Cells ◽  
Vagus Nerve ◽  
Nutritional Value ◽  
Sensory Systems ◽  
Enteroendocrine Cells ◽  
Sensory Transduction ◽  
Sensory Signals ◽  
Passive Release ◽  
The Brain

Guided by sight, scent, texture, and taste, animals ingest food. Once ingested, it is up to the gut to make sense of the food's nutritional value. Classic sensory systems rely on neuroepithelial circuits to convert stimuli into signals that guide behavior. However, sensation of the gut milieu was thought to be mediated only by the passive release of hormones until the discovery of synapses in enteroendocrine cells. These are gut sensory epithelial cells, and those that form synapses are referred to as neuropod cells. Neuropod cells provide the foundation for the gut to transduce sensory signals from the intestinal milieu to the brain through fast neurotransmission onto neurons, including those of the vagus nerve. These findings have sparked a new field of exploration in sensory neurobiology—that of gut-brain sensory transduction.

Microinjection of TRH analogue into the dorsal vagal complex stimulates pancreatic secretion in rats

1995 ◽  
Vol 269 (3) ◽  
pp. G328-G334 ◽  
Author(s):  
T. Okumura ◽  
I. L. Taylor ◽  
T. N. Pappas
Keyword(s):  
Vagus Nerve ◽  
Pancreatic Secretion ◽  
Exocrine Secretion ◽  
Dependent Manner ◽  
Dorsal Vagal Complex ◽  
Pancreatic Exocrine Secretion ◽  
Pancreatic Fluid ◽  
Neurophysiological Studies ◽  
Pancreatic Exocrine ◽  
The Brain

Thyrotropin-releasing hormone (TRH) stimulates pancreatic exocrine secretion through the vagus nerve when injected into rat cerebrospinal fluid. However, little is known about the exact site of action of TRH in the brain to stimulate pancreatic secretion. Recent neuroimmunochemical and neurophysiological studies suggest that TRH could be a neurotransmitter in the dorsal vagal complex, which sends fibers to the pancreas through the vagus nerve. We therefore hypothesized that TRH may act centrally in the dorsal vagal complex to stimulate pancreatic exocrine secretion. To address this question, a TRH analogue, [1-methyl-(S)-4,5-dihydroorotyl]-L-histidyl-L-prolinamide- NH2, was microinjected into the dorsal vagal complex, and basal pancreatic fluid flow and protein secretion were measured in urethan-anesthetized rats. Microinjection of TRH analogue (0.2-2 ng/site) into the dorsal vagal complex significantly stimulated pancreatic flow and protein output in a dose-dependent manner. As a control, microinjection of the TRH analogue into the brain stem outside the vagal complex failed to stimulate pancreatic secretion. Either bilateral subdiaphragmatic vagotomy or atropine abolished the ability of the TRH analogue to stimulate pancreatic secretion. Our data suggest that TRH acts in the dorsal vagal complex to stimulate pancreatic secretion through vagus-dependent and cholinergic pathways. The dorsal vagal complex may play an important role as a central site for control of the exocrine pancreas.

scholarly journals Glial restricted precursor delivery of dendrimer N-acetylcysteine promotes migration and differentiation following transplant in mouse white matter injury model

Nanoscale ◽  
2020 ◽  
Vol 12 (30) ◽  
pp. 16063-16068
Author(s):  
Christina L. Nemeth ◽  
Sophia N. Tomlinson ◽  
Rishi Sharma ◽  
Anjali Sharma ◽  
Sujatha Kannan ◽  
...  
Keyword(s):  
White Matter ◽  
White Matter Injury ◽  
Invasive Procedures ◽  
Injury Model ◽  
Regenerative Therapies ◽  
The Brain

Dendrimer-NAC improves the long-term engraftment of transplanted cells to the brain, suggesting targeted nanotherapeutic support may eliminate the need for overt immunosuppression or multiple invasive procedures in regenerative therapies.

Protective effects of Lactobacillus reuteri and Bifidobacterium infantis in murine models for colitis do not involve the vagus nerve

2008 ◽  
Vol 295 (4) ◽  
pp. R1131-R1137 ◽  
Author(s):  
Hanneke van der Kleij ◽  
Caitlin O'Mahony ◽  
Fergus Shanahan ◽  
Liam O'Mahony ◽  
John Bienenstock
Keyword(s):  
Vagus Nerve ◽  
Lactobacillus Reuteri ◽  
Transfer Model ◽  
Cell Transfer ◽  
Protective Effects ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
T Cell Transfer ◽  
The Brain

The vagus nerve is an important pathway signaling immune activation of the gastrointestinal tract to the brain. Probiotics are live organisms that may engage signaling pathways of the brain-gut axis to modulate inflammation. The protective effects of Lactobacillus reuteri ( LR) and Bifidobacterium infantis ( BI) during intestinal inflammation were studied after subdiaphragmatic vagotomy in acute dextran sulfate sodium (DSS) colitis in BALB/c mice and chronic colitis induced by transfer of CD4+ CD62L+ T lymphocytes from BALB/c into SCID mice. LR and BI (1 × 109) were given daily. Clinical score, myeloperoxidase (MPO) levels, and in vivo and in vitro secreted inflammatory cytokine levels were found to be more severe in mice that were vagotomized compared with sham-operated animals. LR in the acute DSS model was effective in decreasing the MPO and cytokine levels in the tissue in sham and vagotomized mice. BI had a strong downregulatory effect on secreted in vitro cytokine levels and had a greater anti-inflammatory effect in vagotomized- compared with sham-operated mice. Both LR and BI retained anti-inflammatory effects in vagotomized mice. In SCID mice, vagotomy did not enhance inflammation, but BI was more effective in vagotomized mice than shams. Taken together, the intact vagus has a protective role in acute DSS-induced colitis in mice but not in the chronic T cell transfer model of colitis. Furthermore, LR and BI do not seem to engage their protective effects via this cholinergic anti-inflammatory pathway, but the results interestingly show that, in the T cell, transfer model vagotomy had a biological effect, since it increased the effectiveness of the BI in downregulation of colonic inflammation.

scholarly journals Protein, amino acids, vagus nerve signaling, and the brain

2009 ◽  
Vol 90 (3) ◽  
pp. 838S-843S ◽  
Author(s):  
Daniel Tomé ◽  
Jessica Schwarz ◽  
Nicolas Darcel ◽  
Gilles Fromentin
Keyword(s):  
Amino Acids ◽  
Vagus Nerve ◽  
Protein Amino Acids ◽  
The Brain

scholarly journals Interactions of ghrelin signaling pathways with the GH neuroendocrine axis: a new and experimentally tested model

2009 ◽  
Vol 43 (3) ◽  
pp. 105-119 ◽  
Author(s):  
Clemens Wagner ◽  
S Roy Caplan ◽  
Gloria S Tannenbaum
Keyword(s):  
Growth Hormone ◽  
Vagus Nerve ◽  
Present Model ◽  
Male Rat ◽  
Extended Model ◽  
Growth Hormone Releasing Hormone ◽  
Hypothalamic Neuropeptides ◽  
Neuroendocrine Axis ◽  
The Brain

Growth hormone (GH) is secreted in a pulsatile fashion from the pituitary gland into the circulation. Release is governed by two hypothalamic neuropeptides, growth hormone-releasing hormone (GHRH) and somatostatin (SRIF), resulting in secretion episodes with a periodicity of 3.3 h in the male rat. Ghrelin is an additional recently identified potent GH-secretagogue. However, its in vivo interactions with the GH neuroendocrine axis remain to be elucidated. Moreover, two different sites of ghrelin synthesis are involved, the stomach and the hypothalamus. We used our previously developed core model of GH oscillations and added the sites of ghrelin action at the pituitary and in the hypothalamus. With this extended model, we simulated the effects of central and peripheral ghrelin injections, monitored the GH profile and compared it with existing experimental results. Systemically administered ghrelin elicits a GH pulse independent of SRIF, but only in the presence of GHRH. The peripheral ghrelin signal is mediated to the brain via the vagus nerve, where it augments the release of GHRH and stimulates the secretion of neuropeptide-Y (NPY). By contrast, centrally administered ghrelin initiates a GH pulse by increasing the GHRH level and by antagonizing the SRIF block at the pituitary. In addition, NPY neurons are activated, which trigger a delayed SRIF surge. The major novel features of the present model are a) the role played by NPY, and b) the dissimilar functions of ghrelin in the hypothalamus and at the pituitary. Furthermore, the predictions of the model were experimentally examined and confirmed.

Transcutaneous Vagus Nerve Stimulation Enhances Post-error Slowing

2015 ◽  
Vol 27 (11) ◽  
pp. 2126-2132 ◽  
Author(s):  
Roberta Sellaro ◽  
Jelle W. R. van Leusden ◽  
Klodiana-Daphne Tona ◽  
Bart Verkuil ◽  
Sander Nieuwenhuis ◽  
...  
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Direct Evidence ◽  
Noradrenergic System ◽  
Group Design ◽  
Transcutaneous Vagus Nerve Stimulation ◽  
The Brain ◽  
Single Blind

People tend to slow down after they commit an error, a phenomenon known as post-error slowing (PES). It has been proposed that slowing after negative feedback or unforeseen errors is linked to the activity of the locus coeruleus–norepinephrine (LC–NE) system, but there is little direct evidence for this hypothesis. Here, we assessed the causal role of the noradrenergic system in modulating PES by applying transcutaneous vagus nerve stimulation (tVNS), a new noninvasive and safe method to stimulate the vagus nerve and to increase NE concentrations in the brain. A single-blind, sham-controlled, between-group design was used to assess the effect of tVNS in healthy young volunteers (n = 40) during two cognitive tasks designed to measure PES. Results showed increased PES during active tVNS, as compared with sham stimulation. This effect was of similar magnitude for the two tasks. These findings provide evidence for an important role of the noradrenergic system in PES.

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