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Vagal Receptor Transport
Published in Sue Ritter, Robert C. Ritter, Charles D. Barnes, Neuroanatomy and Physiology of Abdominal Vagal Afferents, 2020
A variety of neurotransmitters or neuromodulators are released from vagal fibers and the vagus has been demonstrated to contain neurotransmitter and peptide receptors. Since there is no synthesis of proteins in nerve terminals, some neurotransmitter molecules or receptor proteins must be synthesized at the cell body and transported to the locations where they will exert some physiological function. There are axoplasmic transport mechanisms responsible for the delivery of large and small molecules to and from nerve endings. This chapter will focus on the transport of receptors within the vagus, identify the mechanisms by which this transport is carried out, and review the available information on which receptor populations are contained and transported in both the efferent and afferent limbs of the vagus nerve.
Dopamine Receptors, Signaling Pathways, and Drugs
Published in Nira Ben-Jonathan, Dopamine, 2020
In the absence of specific ligands for D1R and D5R, immunohistochemistry could not be used for the purpose of mapping their distribution within the brain. By default, in situ hybridization has been employed as the method of choice. However, interpretation of such data on the brain distribution of these receptors should be made with caution because mRNA abundance does not necessarily reflect the actual level of the encoded protein or the number of ligand-binding sites. Moreover, receptors are synthesized in the neuronal cell body, followed by their delivery by axoplasmic transport to distal neuronal projections. In situ hybridization can only detect mRNA within the cell body and, therefore, data obtained with this technique do not reflect the distribution of the receptors in axons or dendrites.
Regional injuries and patterns of injury
Published in Jason Payne-James, Richard Jones, Simpson's Forensic Medicine, 2019
Jason Payne-James, Richard Jones
The shearing effects are also identifiable on microscopy, where damage to axons can be visualised with the aid of special staining techniques. These changes have been termed traumatic axonal injury which, when present at multiple sites throughout vulnerable areas of the cerebral hemispheres and brain-stem, may be described as diffuse traumatic axonal injury. Axonal injury takes a variable time to develop, or at least to become apparent under the microscope, and in cases of immediate or very rapid death following brain injury the microscopic changes may not be identifiable. β-amyloid precursor protein (β-APP) takes part in the axoplasmic transport system and accumulates at sites of interruption of axoplasmic flow. Where there has been survival for several hours, immunohistochemical staining for β-APP may identify injured axons, although interpretation of such staining may be problematic, given that this stain also highlights axonal injury caused by non-traumatic phenomena including hypoxia-ischaemia (Figure 10.11). Progressive axonal injury, resulting in the formation of axonal retraction ‘bulbs’, can easily be recognised by silver staining techniques after some 12 hours following axonal injury, and subsequently on routine haematoxylin and eosin (H&E) staining.
The therapeutic potential of a calorie-restricted ketogenic diet for the management of Leber hereditary optic neuropathy
Published in Nutritional Neuroscience, 2019
Mithu Storoni, Matthieu P. Robert, Gordon T. Plant
Mitochondrial bioenergetic capacity may partly account for this variation in susceptibility. An axon’s volume determines its capacity for mitochondria, whereas its surface area dictates its energy needs. Small diameter parvocellular type (P cells) have the smallest ratio of volume to surface area, which places them at greater risk from a bioenergetic imbalance. Among non-MCGC cells, P cells appear to be more vulnerable to damage in LHON than magnocellular cells (M cells) that generally have larger diameters.17,18 Impaired axonal transport precedes the death of retinal ganglion cells in LHON. Axoplasmic transport, which shuttles both mitochondria and trophic factors along ganglion cell axons, is ‘energy-expensive’ and becomes compromised in the presence of an energy constraint, which may further predispose small diameter retinal ganglion cells to maximal damage.19,20
Bone marrow mesenchymal stem cell-derived exosome uptake and retrograde transport can occur at peripheral nerve endings
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Rui Ren, Xiao-Hong Tan, Jiu-Hong Zhao, Quan-Peng Zhang, Xian-Fang Zhang, Zhi-Jian Ma, Ya-Nan Peng, Qi-Bing Liu, Hai-Ying Zhang, Yun-Qing Li, Rui He, Zhen-Qiang Zhao, Xi-Nan Yi
In this study, we injected exosomes into the gastrocnemius muscle because the long distance from the nerve endings to the cell body allowed us to exclude any effects of local dispersion upon detecting exosomes in the spinal motor neurons and/or DRG sensory neurons. Thus, we could conclude that there was successful retrograde axoplasmic transport and hematogenous transport of exosomes. To exclude the influence of transport via the bloodstream, we designed two test groups: the normal right gastrocnemius injection group and the transectioned right sciatic nerve followed by ipsilateral gastrocnemius injection group. Detection of GFP-positive cells in both sides of the DRG at day 1 after injection suggests the uptake of exosomes through hematogenous transport. The significantly stronger GFP intensity at the DRG and the ipsilateral (right side) of the spinal cord at day 5 after injection suggests that exogenous exosomes may have undergone retrograde axoplasmic transport. Initially, we examined the bilateral DRG on days 2 and 3 after gastrocnemius muscle injection but observed a much smaller increase in fluorescence intensity compared to day 5 after injection, indicating that axoplasmic transport is slow. Hence, we opted to use a 5-day model and made a deeper incision of the right sciatic nerve of the rat. There was minimal difference in fluorescence intensity between both sides of the DRG, indicating that nerve damage prevented axoplasmic transport and exosome uptake could only occur via hematogenous transport. This confirmed that exosomes undergo both retrograde axoplasmic transport and hematogenous transport. Moreover, the observation of higher CD63 expression in bilateral DRG tissues at the injection side confirmed the confocal microscopy results.
MR neurography showed brachial plexus abnormalities in syringomyelia with shoulder Charcot arthropathy: a case report
Published in British Journal of Neurosurgery, 2023
Kai Chen, Lijing Deng, Hualong She, Fang Hu, Tao Li
The main mechanism might be axonal transport interruption. The majority of axonal proteins are synthesized in the neuron's cell body and transported along axon to the tip, also called anterograde transport. Since the axon depends on axoplasmic transport of vital proteins, anterograde transport is necessary for axon growth and survival. The syrinx may compress the neuronal cell bodies in the spinal cord, impairing synthesis of proteins and causing the distal axons to degenerate.3 As a result, the number of axons and the water content of the nerve roots decrease, these were detected by MR neurography.