scholarly journals Impact of the Sensory and Sympathetic Nervous System on Fracture Healing in Ovariectomized Mice

2020 ◽  
Vol 21 (2) ◽  
pp. 405 ◽  
Author(s):  
Tanja Niedermair ◽  
Rainer H. Straub ◽  
Christoph Brochhausen ◽  
Susanne Grässel
Keyword(s):  
Nervous System ◽  
Fracture Healing ◽  
Pain Threshold ◽  
Callus Tissue ◽  
Tissue Remodeling ◽  
Nerve Fibers ◽  
M2 Macrophage ◽  
Ovariectomized Mice ◽  
Bony Callus ◽  
Deficient Mice

The peripheral nervous system modulates bone repair under physiological and pathophysiological conditions. Previously, we reported an essential role for sensory neuropeptide substance P (SP) and sympathetic nerve fibers (SNF) for proper fracture healing and bone structure in a murine tibial fracture model. A similar distortion of bone microarchitecture has been described for mice lacking the sensory neuropeptide α-calcitonin gene-related peptide (α-CGRP). Here, we hypothesize that loss of SP, α-CGRP, and SNF modulates inflammatory and pain-related processes and also affects bone regeneration during fracture healing under postmenopausal conditions. Intramedullary fixed femoral fractures were set to 28 days after bilateral ovariectomy (OVX) in female wild type (WT), SP-, α-CGRP-deficient, and sympathectomized (SYX) mice. Locomotion, paw withdrawal threshold, fracture callus maturation and numbers of TRAP-, CD4-, CD8-, F4/80-, iNos-, and Arg1-positive cells within the callus were analyzed. Nightly locomotion was reduced in unfractured SP-deficient and SYX mice after fracture. Resistance to pressure was increased for the fractured leg in SP-deficient mice during the later stages of fracture healing, but was decreased in α-CGRP-deficient mice. Hypertrophic cartilage area was increased nine days after fracture in SP-deficient mice. Bony callus maturation was delayed in SYX mice during the later healing stages. In addition, the number of CD 4-positive cells was reduced after five days and the number of CD 8-positive cells was additionally reduced after 21 days in SYX mice. The number of Arg1-positive M2 macrophages was higher in α-CGRP-deficient mice five days after fracture. The alkaline phosphatase level was increased in SYX mice 16 days after fracture. Absence of α-CGRP appears to promote M2 macrophage polarization and reduces the pain threshold, but has no effect on callus tissue maturation. Absence of SP reduces locomotion, increases the pain-threshold, and accelerates hypertrophic callus tissue remodeling. Destruction of SNF reduces locomotion after fracture and influences bony callus tissue remodeling during the later stages of fracture repair, whereas pain-related processes are not affected.

scholarly journals Linalool odor‐induced analgesia is triggered by TRPA1-independent pathway in mice

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Hideki Kashiwadani ◽  
Yurina Higa ◽  
Mitsutaka Sugimura ◽  
Tomoyuki Kuwaki
Keyword(s):  
Pain Threshold ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Analgesic Effects ◽  
Neuronal Mechanisms ◽  
Odor Exposure ◽  
Noxious Mechanical Stimulation ◽  
Transient Receptor ◽  
Deficient Mice

AbstractWe had recently reported that linalool odor exposure induced significant analgesic effects in mice and that the effects were disappeared in olfactory-deprived mice in which the olfactory epithelium was damaged, thus indicating that the effects were triggered by chemical senses evoked by linalool odor exposure. However, the peripheral neuronal mechanisms, including linalool receptors that contribute toward triggering the linalool odor-induced analgesia, still remain unexplored. In vitro studies have shown that the transient receptor potential ankyrin 1 (TRPA1) responded to linalool, thus raising the possibility that TRPA1 expressed on the trigeminal nerve terminal detects linalool odor inhaled into the nostril and triggers the analgesic effects. To address this hypothesis, we measured the behavioral pain threshold for noxious mechanical stimulation in TRPA1-deficient mice. In contrast to our expectation, we found a significant increase in the threshold after linalool odor exposure in TRPA1-deficient mice, indicating the analgesic effects of linalool odor even in TRPA1-deficient mice. Furthermore, intranasal application of TRPA1 selective antagonist did not alter the analgesic effect of linalool odor. These results showed that the linalool odor-induced analgesia was triggered by a TRPA1-independent pathway in mice.

scholarly journals Effects of Electroacupuncture on Pain Threshold of Laboring Rats and the Expression of Norepinephrine Transporter andα2 Adrenergic Receptor in the Central Nervous System

2016 ◽  
Vol 2016 ◽  
pp. 1-8
Author(s):  
Qianli Tang ◽  
Qiuyan Jiang ◽  
Suren R. Sooranna ◽  
Shike Lin ◽  
Yuanyuan Feng ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adrenergic Receptor ◽  
Pain Threshold ◽  
Norepinephrine Transporter ◽  
Control Group ◽  
Tail Flick ◽  
Pregnant Rats ◽  
Tail Flick Test ◽  
The Central Nervous System

To observe the effects of electroacupuncture on pain threshold of laboring rats and the expression of norepinephrine transporter andα2 adrenergic receptor in the central nervous system to determine the mechanism of the analgesic effect of labor. 120 pregnant rats were divided into 6 groups: a control group, 4 electroacupuncture groups, and a meperidine group. After interventions, the warm water tail-flick test was used to observe pain threshold. NE levels in serum, NET, andα2AR mRNA and protein expression levels in the central nervous system were measured. No difference in pain threshold was observed between the 6 groups before intervention. After intervention, increased pain thresholds were observed in all groups except the control group with a higher threshold seen in the electroacupuncture groups. Serum NE levels decreased in the electroacupuncture and MP groups. Increases in NET andα2AR expression in the cerebral cortex and decreases in enlarged segments of the spinal cord were seen. Acupuncture increases uptake of NE via cerebral NET and decreases its uptake by spinal NET. The levels ofα2AR are also increased and decreased, respectively, in both tissues. This results in a decrease in systemic NE levels and may be the mechanism for its analgesic effects.

Amitriptyline Neurotoxicity

2004 ◽  
Vol 100 (6) ◽  
pp. 1519-1525 ◽  
Author(s):  
Jean-Pierre Estebe ◽  
Robert R. Myers
Keyword(s):  
Nervous System ◽  
Sciatic Nerve ◽  
Local Anesthetic ◽  
Dose Range ◽  
Antidepressant Drug ◽  
Nerve Fibers ◽  
Anesthetic Agent ◽  
Sprague Dawley ◽  
Neurotoxic Effect ◽  
Local Anesthetic Agent

Background Amitriptyline is a tricyclic antidepressant drug used systemically for the management of neuropathic pain. Antidepressants, as a class of drugs with direct neurologic actions, are becoming widely used for the management of chronic pain, although their mechanisms are not entirely understood. Amitriptyline exerts potent effects on reuptake of norepinephrine and serotonin and blocks alpha 2A adrenoreceptors and N-methyl-D-aspartate receptors. Because amitriptyline is also a particularly potent blocker of sodium channels and voltage-gated potassium and calcium channels, it has been recommended as a long-acting local anesthetic agent. Unfortunately, amitriptyline has significant toxic side effects in the central nervous system and cardiovascular system that are dose-related to its systemic administration. Therefore, before amitriptyline can be used clinically as a local anesthetic agent, it should be thoroughly explored with respect to its direct neurotoxic effect in the peripheral nervous system. Methods The left sciatic nerve of Sprague-Dawley rats (12/ group) received a single topical amitriptyline dose of 0.625, 1.25, 2.5, or 5 mg; a saline group (n = 2) was used as control. Neuropathologic evaluations were conducted in separate animals (n = 4) 1, 3, and 7 days later. Results Amitriptyline topically applied in vivo to rat sciatic nerve causes a dose-related neurotoxic effect. Drug doses of 0.625-5 mg all caused Wallerian degeneration of peripheral nerve fibers, with the number of affected fibers and the severity of the injury directly related to the dose. Conclusion Because the effective local anesthetic dose is within this dose range, the authors strongly recommend that amitriptyline not be used as a local anesthetic agent.

scholarly journals Diminished Callus Size and Cartilage Synthesis in α1β1 Integrin-Deficient Mice during Bone Fracture Healing

2002 ◽  
Vol 160 (5) ◽  
pp. 1779-1785 ◽  
Author(s):  
Erika Ekholm ◽  
Kurt D. Hankenson ◽  
Hannele Uusitalo ◽  
Ari Hiltunen ◽  
Humphrey Gardner ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Bone Fracture ◽  
Bone Fracture Healing ◽  
Callus Size ◽  
Deficient Mice ◽  
And Cartilage

Understanding Neuropathic Pain

CNS Spectrums ◽  
2005 ◽  
Vol 10 (4) ◽  
pp. 298-308 ◽  
Author(s):  
Walter Zieglgänsberger ◽  
Achim Berthele ◽  
Thomas R. Tölle
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Neuronal Excitability ◽  
Traumatic Injury ◽  
Nerve Fibers ◽  
Cellular Events ◽  
Excitatory Neurotransmitters ◽  
The Central Nervous System ◽  
Activity Dependent

AbstractNeuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.

scholarly journals α2 -Adrenoceptors in the enteric nervous system: a study in α2A -adrenoceptor-deficient mice

2002 ◽  
Vol 135 (3) ◽  
pp. 697-704 ◽  
Author(s):  
Jens Scheibner ◽  
Anne-Ulrike Trendelenburg ◽  
Lutz Hein ◽  
Klaus Starke ◽  
Corrado Blandizzi
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Α2 Adrenoceptors ◽  
System A ◽  
Deficient Mice

scholarly journals STAG2 promotes the myelination transcriptional program in oligodendrocytes

2021 ◽  
Author(s):  
Ningyan Cheng ◽  
Mohammed Kanchwala ◽  
Bret M. Evers ◽  
Chao Xing ◽  
Hongtao Yu
Keyword(s):  
Nervous System ◽  
Growth Retardation ◽  
Premature Death ◽  
Nerve Fibers ◽  
Conditional Knockout ◽  
Cell Type ◽  
Transcriptional Program ◽  
Dna Loop ◽  
Delayed Maturation ◽  
Relevant Cell Type

SUMMARYCohesin folds chromosomes via DNA loop extrusion. Cohesin-mediated chromosome loops regulate transcription by shaping long-range enhancer-promoter interactions, among other mechanisms. Mutations of cohesin subunits and regulators cause human developmental diseases termed cohesinopathy. Vertebrate cohesin consists of SMC1, SMC3, RAD21, and either STAG1 or STAG2. To probe the physiological functions of cohesin, we created conditional knockout (cKO) mice with Stag2 deleted in the nervous system. Stag2 cKO mice exhibit growth retardation, neurological defects, and premature death, in part due to insufficient myelination of nerve fibers. Stag2 cKO oligodendrocytes exhibit delayed maturation and downregulation of myelination-related genes. Stag2 loss reduces promoter-anchored loops at downregulated genes in oligodendrocytes. Thus, STAG2-cohesin generates promoter-anchored loops at myelination-promoting genes to facilitate their transcription. Our study implicates defective myelination as a contributing factor to cohesinopathy and establishes oligodendrocytes as a relevant cell type to explore the mechanisms by which cohesin regulates transcription.

The Biology of Bothrimonus (=Diplocotyle) (Pseudophyllidea: Cestoda): Detailed Morphology and Fine Structure

1974 ◽  
Vol 31 (2) ◽  
pp. 147-153 ◽  
Author(s):  
M. D. B. Burt ◽  
I. M. Sandeman
Keyword(s):  
Electron Microscopy ◽  
Nervous System ◽  
Fine Structure ◽  
Functional Morphology ◽  
Light And Electron Microscopy ◽  
Nerve Fibers ◽  
Fish Host ◽  
Extensive System ◽  
And Function

Light and electron microscopy were used to describe the functional morphology of Bothrimonus sturionis in detail. In particular, the musculature, nervous system, osmoregulatory system, and tegument are dealt with, and the findings compared with those of other workers. The musculature of the scolex consists of several interrelated systems, the structure of each being discussed in relation to its function. Associated with the regular nervous system, considered typical of cestodes, is an extensive system of giant nerve fibers. The osmoregulatory system is unusual in that there are lateral "excretory" pores in many proglottides which open directly to the exterior of the worm. The microtriches of the tegument are long, like those of other primitive cestodes, and are covered by a noncellular sheath while the worm is in its gammarid host. The sheath is lost when the worm becomes established in its fish host; the nature and function of the sheath are discussed.

Development of the Nervous System of Invertebrates

2018 ◽  
pp. 70-122
Author(s):  
Volker Hartenstein
Keyword(s):  
Nervous System ◽  
Molecular Genetic ◽  
Early Embryo ◽  
Nerve Fibers ◽  
Model Systems ◽  
Animal Phyla ◽  
Invertebrate Animals ◽  
Genetic Mechanisms ◽  
And Migration ◽  
Complex Architecture

The complex architecture of the nervous system is the result of a stereotyped pattern of proliferation and migration of neural progenitors in the early embryo, followed by the outgrowth of nerve fibers along rigidly controlled pathways, and the formation of synaptic connections between specific neurons during later stages. Detailed studies of these events in several experimentally amenable model systems indicated that many of the genetic mechanisms involved are highly conserved. This realization, in conjunction with new molecular-genetic techniques, has led to a surge in comparative neurodevelopmental research covering a wide variety of animal phyla over the past two decades. This chapter attempts to provide an overview of the diverse neural architectures that one encounters among invertebrate animals, and the developmental steps shaping these architectures.

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