Immune-mediated alterations in nociceptive sensory function in Aplysia californica

1999 ◽  
Vol 202 (5) ◽  
pp. 623-630 ◽  
Author(s):  
A.L. Clatworthy ◽  
E. Grose
Keyword(s):  
Sensory Neurons ◽  
Interleukin 1 ◽  
Aplysia Californica ◽  
Sensory Function ◽  
Sensory Cells ◽  
Cellular Defense ◽  
Sensory Axons ◽  
Sensory Plasticity ◽  
Immune Mediated ◽  
Necrosis Factor

Nerve injury in Aplysia californica is accompanied by a profound long-lasting enhancement of the excitability of nociceptive sensory neurons that have axons in injured nerves. It is likely that a variety of signals are involved in triggering this injury-induced sensory plasticity. The objective of the present study was to determine whether cells of the cellular defense system (hemocytes) play a role in the modulation of sensory excitability following injury. In support of such an idea, we have shown previously that the induction of a cellular defense reaction close to sensory axons is accompanied by an increase in the excitability of sensory neurons with axons close to responding hemocytes. Furthermore, in the present study, we verified that, following axonal crush, numerous hemocytes accumulate at the injured site on the nerve. Using a hemocyte/nervous system co-culture preparation, we found that there were no significant differences in the expression of injury-induced sensory plasticity between sensory neurons incubated in the presence or absence of hemocytes. To overcome some potential limitations of our co-culture preparation, we used the endotoxin lipopolysaccharide (LPS) as a tool to activate the hemocytes. Sensory cells incubated in the presence of LPS and hemocytes were significantly more excitable than sensory cells incubated in the presence of LPS alone. We speculate that the addition of LPS to the incubation medium containing hemocytes enhanced the release of hemocyte-derived cytokine-like factors such as interleukin-1 and tumor necrosis factor. These cytokine-like factors may act as signals to modulate the expression of injury-induced sensory hyperexcitability.

scholarly journals Electrical Responses from Dually Innervated Tactile Receptors on the Thorax of the Crayfish

1963 ◽  
Vol 40 (1) ◽  
pp. 137-148
Author(s):  
DEFOREST MELLON
Keyword(s):  
Sensory Neurons ◽  
Vital Staining ◽  
Sensory Cells ◽  
Abrupt Increase ◽  
Fluid Medium ◽  
Water Currents ◽  
Tactile Receptors ◽  
Sensory Axons ◽  
Electrophysiological Recordings ◽  
Spike Initiation

1. Electrophysiological recordings have been obtained from tactile receptors which occur in shallow pits on the crayfish carapace. 2. Controlled mechanical stimulation has established that each receptor is innervated by a pair of sensory neurons. One of these neurons responds when the receptor is moved anteriorly, and the partner cell responds to displacement in the opposite direction. 3. The receptors are sensitive to motion of the fluid medium in which they are immersed, and they may provide the animal with a means for determining the speed and direction of water currents. 4. Vital staining procedures have confirmed the presence of two bipolar sensory cells associated with each receptor. An abrupt increase in the diameter of the sensory axons occurs several hundred microns proximal to the cell bodies of the neurons, and it is suggested that this is the locus of spike initiation.

scholarly journals Cytokine-endothelial interactions in inflammation, immunity, and vascular injury.

1990 ◽  
Vol 1 (3) ◽  
pp. 225-235
Author(s):  
R S Cotran ◽  
J S Pober
Keyword(s):  
Septic Shock ◽  
Immune Responses ◽  
Vascular Injury ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Structural Alterations ◽  
Immune Mediated ◽  
Shwartzman Reaction ◽  
Endothelial Adhesion Molecules ◽  
Necrosis Factor

This paper reviews the evidence that cytokines induce a variety of functional and structural alterations in endothelium and that cytokine-endothelial interactions play important roles in the evolution of inflammatory and immune responses. The effect of cytokines, particularly interleukin-1 and tumor necrosis factor, on leukocyte-endothelial adhesion has led to the discovery of several endothelial adhesion molecules, and the molecular and biological characteristics of these are described. Finally, the review discusses the possible contribution of cytokine-induced activation to vascular injury in such pathological processes as septic shock, the Shwartzman reaction, delayed hypersensitivity, and immune-mediated vasculitis.

scholarly journals Artemin promotes functional long-distance axonal regeneration to the brainstem after dorsal root crush

2015 ◽  
Vol 112 (19) ◽  
pp. 6170-6175 ◽  
Author(s):  
Laura Elisabeth Wong ◽  
Molly E. Gibson ◽  
H. Moore Arnold ◽  
Blake Pepinsky ◽  
Eric Frank
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Sensory Function ◽  
Long Distance ◽  
Adult Rats ◽  
Sensory Axons ◽  
Sorting Technique ◽  
Cord Injury

Recovery after a spinal cord injury often requires that axons restore synaptic connectivity with denervated targets several centimeters from the site of injury. Here we report that systemic artemin (ARTN) treatment promotes the regeneration of sensory axons to the brainstem after brachial dorsal root crush in adult rats. ARTN not only stimulates robust regeneration of large, myelinated sensory axons to the brainstem, but also promotes functional reinnervation of the appropriate target region, the cuneate nucleus. ARTN signals primarily through the RET tyrosine kinase, an interaction that requires the nonsignaling coreceptor GDNF family receptor (GFRα3). Previous studies reported limited GFRα3 expression on large sensory neurons, but our findings demonstrate that ARTN promotes robust regeneration of large, myelinated sensory afferents. Using a cell sorting technique, we demonstrate that GFRα3 expression is similar in myelinated and unmyelinated adult sensory neurons, suggesting that ARTN likely induces long-distance regeneration by binding GFRα3 and RET. Although ARTN is delivered for just 2 wk, regeneration to the brainstem requires more than 3 mo, suggesting that brief trophic support may initiate intrinsic growth programs that remain active until targets are reached. Given its ability to promote targeted functional regeneration to the brainstem, ARTN may represent a promising therapy for restoring sensory function after spinal cord injury.

Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1

Diabetes ◽  
1993 ◽  
Vol 42 (7) ◽  
pp. 1026-1031 ◽  
Author(s):  
K. Yamada ◽  
N. Takane ◽  
S. Otabe ◽  
C. Inada ◽  
M. Inoue ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Beta Cell ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Pancreatic Beta Cell ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Local mechanisms for acupoint sensitization in gall bladder meridian of foot shaoyang-a gene chip study

2019 ◽  
Vol 44 (2) ◽  
pp. 77-87
Author(s):  
Koichi Ishida ◽  
Liyue Qin ◽  
Ting Wang ◽  
Ying Lei ◽  
Weiwei Hu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gall Bladder ◽  
Interleukin 1 ◽  
Gene Chip ◽  
Molecular Evidence ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Bladder Meridian ◽  
Integrin Linked Kinase ◽  
Necrosis Factor

Acupuncture manipulations are clinically important to traditional Chinese medicine, yet the biological mechanisms have not been fully understood. This study aimed to investigate continuous stimulation-induced gene expression changes at stimulated and non-stimulated adjacent acupoints in the same meridian. Catgut embedding into acupoint (CEP) was conducted at acupoint Yanglingquan (gall bladder meridian of foot-shaoyang 34, GB34) of Sprague Dawley rats once or continuously for eight weeks, and gene expression changes at GB34 were assessed by gene chip array analysis 72 h after the last CEP treatment. A total of 688 genes exhibited opposite changes in expression between the two treatments, and 1,336 genes were regulated only by the eight-week CEP treatment. Ingenuity Pathway Analysis revealed that among these differentially regulated genes by one-time and eight-week CEP treatment, insulin-like growth factor-1 pathway and integrin-linked kinase pathway, and Wnt/~ catenin signaling pathway match the observed gene changes to predicted up/down regulation patterns. Upstream analysis further predicted six molecules, namely, tumor necrosis factor, interleukin 1~, interleukin la, kallikrein-related peptidase 5, protein kinase Ca, and catenin ~1. On the other hand, continuous eight-week CEP stimulation at acupoint Xuanzhong (GB39) caused similar changes in the expression of 32 genes at acupoints GB34 and Fengshi (GB31) on the same meridian. Taken together, our results provide the first molecular evidence for the local acupoints' mechanisms for acupoint sensitization theory, and implicate the existence of signaling pathways, either direct or indirect, between acupoints within the meridian GB.

Differential effects of cytokines on thermosensitive neurons in guinea pig preoptic area slices

1991 ◽  
Vol 261 (5) ◽  
pp. R1096-R1103 ◽  
Author(s):  
M. Shibata ◽  
C. M. Blatteis
Keyword(s):  
Guinea Pig ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Firing Rates ◽  
Artificial Cerebrospinal Fluid ◽  
Cold Sensitive ◽  
Factor Alpha ◽  
Necrosis Factor

This study was undertaken to determine whether the reported different courses of the febrile responses to the cytokines interleukin-1 beta (IL-1), interferon-alpha 2 (IFN), and tumor necrosis factor-alpha (TNF) might have neuroelectrophysiological correlates. The reactions of individual thermosensitive neurons in the preoptic area (POA) were evaluated by recording their extracellular single-unit firing rates (FR) in slices of guinea pig POA perfused with artificial cerebrospinal fluid (aCSF), human recombinant IL-1 (50-500 ng), IFN (1,000-8,000 U), and TNF (400-5,000 ng) (all doses per min/ml aCSF); thermosensitivity was assessed by FR responses to changes of perfusate temperature (32-42 degrees C). Overall, these cytokines depressed the FR of warm-sensitive units and excited those of cold-sensitive units, in agreement with expectations. However, the responses of individual neurons treated with two or all three cytokines were dissimilar: 61% of the units tested reacted differentially to two or three cytokines, 32% exhibited identical responses, and 7% had no response to any cytokine. These results support the possibility that IL-1, IFN, and TNF may affect not the same but rather distinct neurons functionally connected to common pyrogenic effectors. Thus they suggest that differential neuronal substrates may be utilized by each cytokine to exert its pyrogenic effect.

scholarly journals Bone marrow-derived neural crest precursors improve nerve defect repair partially through secreted trophic factors

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Haiyan Shi ◽  
Xiaoli Li ◽  
Junling Yang ◽  
Yahong Zhao ◽  
Chengbin Xue ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Peripheral Nerve ◽  
Neural Crest ◽  
Sensory Neurons ◽  
Sensory Function ◽  
Trophic Factors ◽  
Factor Alpha ◽  
Bone Marrow Origin ◽  
Rat Bone

Abstract Background Emerging evidence suggests that neural crest-derived cells (NCCs) present important functions in peripheral nerve regeneration to correct the insufficiency of autogenous Schwann cells. Postmigratory NCCs have been successfully isolated from adult rat bone marrow in our previous work. In this study, we aim to provide neural crest-derived Schwann cell precursors (SCPs) for repair of nerve defects in adult rats, and partially reveal the mechanisms involved in neuroregeneration of cell therapy. Methods A clonal cell line of neural crest precursors of rat bone marrow origin (rBM-NCPs) with SCP identity was expanded in adherent monolayer culture to ensure the stable cell viability of NCPs and potentiate the repair of nerve defects after rBM-NCPs implantation based on tissue engineering nerve grafts (TENG). Here the behavioral, morphological, and electrophysiological detection was performed to evaluate the therapy efficacy. We further investigated the treatment with NCP-conditioned medium (NCP-CM) to sensory neurons after exposure to oxygen-glucose-deprivation (OGD) and partially compared the expression of trophic factor genes in rBM-NCPs with that in mesenchymal stem cells of bone marrow origin (rBM-MSCs). Results It was showed that the constructed TENG with rBM-NCPs loaded into silk fibroin fiber scaffolds/chitosan conduits repaired 10-mm long sciatic nerve defects more efficiently than conduits alone. The axonal regrowth, remyelination promoted the reinnervation of the denervated hind limb muscle and skin and thereby alleviated muscle atrophy and facilitated the rehabilitation of motor and sensory function. Moreover, it was demonstrated that treatment with NCP-CM could restore the cultured primary sensory neurons after OGD through trophic factors including epidermal growth factor (EGF), platelet-derived growth factor alpha (PDGFα), ciliary neurotrophic factor (CNTF), and vascular endothelial growth factor alpha (VEGFα). Conclusions In summary, our findings indicated that monolayer-cultured rBM-NCPs cell-based therapy might effectively repair peripheral nerve defects partially through secreted trophic factors, which represented the secretome of rBM-NCPs differing from that of rBM-MSCs.

scholarly journals Interdependence between Interleukin-1 and Tumor Necrosis Factor Regulates TNF-Dependent Control of Mycobacterium tuberculosis Infection

Immunity ◽  
2015 ◽  
Vol 43 (6) ◽  
pp. 1125-1136 ◽  
Author(s):  
Nelson C. Di Paolo ◽  
Shahin Shafiani ◽  
Tracey Day ◽  
Thalia Papayannopoulou ◽  
David W. Russell ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Tuberculosis Infection ◽  
Mycobacterium Tuberculosis Infection ◽  
Necrosis Factor
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