Acetylsalicylic acid-induced changes in the chemical coding of extrinsic sensory neurons supplying the prepyloric area of the porcine stomach

2016 ◽  
Vol 617 ◽  
pp. 218-224 ◽  
Author(s):  
L. Rytel ◽  
J. Calka
Keyword(s):  
Acetylsalicylic Acid ◽  
Sensory Neurons ◽  
Chemical Coding ◽  
Induced Changes

Conantokin G-induced changes in the chemical coding of dorsal root ganglion neurons supplying the porcine urinary bladder

2012 ◽  
Vol 15 (1) ◽  
pp. 101-109 ◽  
Author(s):  
A. Bossowska ◽  
M. Majewski
Keyword(s):  
Urinary Bladder ◽  
Dorsal Root Ganglion ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Bladder Wall ◽  
Dorsal Root Ganglion Neurons ◽  
Chemical Coding ◽  
Ganglion Neurons ◽  
Immunofluorescence Labeling ◽  
Induced Changes

Conantokin G-induced changes in the chemical coding of dorsal root ganglion neurons supplying the porcine urinary bladder Conantokin G (CTG), isolated from the venom of the marine cone snail Conus geographus, is an antagonist of N-methyl-d-aspartate receptors (NMDARs), the activation of which, especially those located on the central afferent terminals and dorsal horn neurons, leads to hypersensitivity and pain. Thus, CTG blocking of NMDARs, has an antinociceptive effect, particularly in the case of neurogenic pain treatment. As many urinary bladder disorders are caused by hyperactivity of sensory bladder innervation, it seems useful to estimate the influence of CTG on the plasticity of sensory neurons supplying the organ. Retrograde tracer Fast Blue (FB) was injected into the urinary bladder wall of six juvenile female pigs. Three weeks later, intramural bladder injections of CTG (120 μg per animal) were carried out in all animals. After a week, dorsal root ganglia of interest were harvested from all animals and neurochemical characterization of FB+ neurons was performed using a routine double-immunofluorescence labeling technique on 10-μm-thick cryostat sections. CTG injections led to a significant decrease in the number of FB+ neurons containing substance P (SP), pituitary adenylate cyclase activating polypeptide (PACAP), somatostatin (SOM), calbindin (CB) and nitric oxide synthase (NOS) when compared with healthy animals (20% vs. 45%, 13% vs. 26%, 1.3% vs. 3%, 1.2 vs. 4% and 0.9% vs. 6% respectively) and to an increase in the number of cells immunolabelled for galanin (GAL, 39% vs. 6.5%). These data demonstrated that CTG changed the chemical coding of bladder sensory neurons, thus indicating that CTG could eventually be used in the therapy of selected neurogenic bladder illnesses.

Zearalenone-induced changes in the lymphoid tissue and mucosal nerve fibers in the porcine ileum

2015 ◽  
Vol 18 (2) ◽  
pp. 357-365 ◽  
Author(s):  
K. Obremski ◽  
S. Gonkowski ◽  
P. Wojtacha
Keyword(s):  
Nerve Fibers ◽  
Lower Percentage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Dot Blot ◽  
Chemical Coding ◽  
Tissue Levels ◽  
Intestinal Functions ◽  
Induced Changes ◽  
First Time

Abstract This is the first study to examine zearalenone-(ZEN) induced changes in the immune system of the ileum and substance P-(SP-) and vasoactive intestinal peptide-(VIP-) immunoreactive nerve fibers in the mucosa, which participate in the regulation of intestinal functions under physiological conditions and during pathological processes. The aim of this study was also to identify potential relationships between selected immune and neural elements in ileal Peyer’s patches in pigs that were and were not exposed to ZEN. The experiment was performed on 10 prepubertal gilts divided into two groups: the experimental group (n=5) where ZEN was administered at 0.1 mg kg−1 feed day−1 for 42 days, and the control group (n=5) which was administered a placebo. The tissue levels of cytokines were determined by enzyme-linked immunosorbent assay which revealed elevated concentrations of IL-12/23 40p and IL-1 β in animals exposed to ZEN. Flow cytometry revealed a lower percentage of CD21+ lymphocytes in pigs exposed to ZEN in comparison with control animals. The tissue levels of neuropeptides were evaluated in the dot blot procedure which demonstrated higher concentrations of VIP and SP in experimental pigs. In experimental animals, numerous VIP-like immunoreactive processes were observed, and SP-immunoreactive nerve fibers formed a very dense network. Our results demonstrate for the first time that ZEN can modify the chemical coding of nerve structures in the gastrointestinal system. Those modifications can be attributed to ZEN’s impact on estrogen receptors or its pro-inflammatory properties, and they reflect changes that take place in the nervous system at the transcriptional, translational and metabolic level.

Afferent-Induced Changes in Rhythmic Motor Programs in the Feeding Circuitry of Aplysia

2004 ◽  
Vol 92 (4) ◽  
pp. 2312-2322 ◽  
Author(s):  
Avniel N. Shetreat-Klein ◽  
Elizabeth C. Cropper
Keyword(s):  
Sensory Neurons ◽  
Motor Neurons ◽  
Rhythmic Activity ◽  
Motor Program ◽  
Firing Frequency ◽  
Afferent Activity ◽  
Motor Programs ◽  
Rhythmic Motor ◽  
Induced Changes ◽  
The Impact

A manipulation often used to determine whether a neuron plays a role in the generation of a motor program involves injecting current into the cell during rhythmic activity to determine whether activity is modified. We perform this type of manipulation to study the impact of afferent activity on feeding-like motor programs in Aplysia. We trigger biting-like programs and manipulate sensory neurons that have been implicated in producing the changes in activity that occur when food is ingested, i.e., when bites are converted to bite-swallows. Sensory neurons that are manipulated are the radula mechanoafferent B21 and the retraction proprioceptor B51. Data suggest that both cells are peripherally activated during radula closing/retraction when food is ingested. We found that phasic subthreshold depolarization of a single sensory neuron can significantly prolong radula closing/retraction, as determined by recording both from interneurons (e.g., B64), and motor neurons (e.g., B15 and B8). Additionally, afferent activity produces a delay in the onset of the subsequent radula opening/protraction, and increases the firing frequency of motor neurons. These are the changes in activity that are seen when food is ingested. These results add to the growing data that implicate B21 and B51 in bite to bite-swallow conversions and indicate that afferent activity is important during feeding in Aplysia.

Chemical Coding of Sensory Neurons Supplying the Hip Joint Capsule in the Sheep

2016 ◽  
Vol 46 (2) ◽  
pp. 121-131 ◽  
Author(s):  
A. Dudek ◽  
W. Sienkiewicz ◽  
A. Chrószcz ◽  
M. Janeczek ◽  
J. Kaleczyc
Keyword(s):  
Sensory Neurons ◽  
Hip Joint ◽  
Joint Capsule ◽  
Chemical Coding

scholarly journals Effects of Axotomy on Cultured Sensory Neurons of Aplysia: Long-Term Injury-Induced Changes in Excitability and Morphology Are Mediated by Different Signaling Pathways

2008 ◽  
Vol 100 (6) ◽  
pp. 3209-3224 ◽  
Author(s):  
Supinder S. Bedi ◽  
Diancai Cai ◽  
David L. Glanzman
Keyword(s):  
Signaling Pathways ◽  
Sensory Neurons ◽  
Specific Inhibitor ◽  
Distinct Pattern ◽  
Extracellular Signal ◽  
Vitro Model ◽  
Induced Changes ◽  
And Control

To facilitate an understanding of injury-induced changes within the nervous system, we used a single-cell, in vitro model of axonal injury. Sensory neurons were individually dissociated from the CNS of Aplysia and placed into cell culture. The major neurite of some neurons was then transected (axotomized neurons). Axotomy in hemolymph-containing culture medium produced long-term hyperexcitability (LTH-E) and enhanced neuritic sprouting (long-term hypermorphogenesis [LTH-M]). Axotomy in the absence of hemolymph induced LTH-E, but not LTH-M. Hemolymph-derived growth factors may activate tyrosine receptor kinase (Trk) receptors in sensory neurons. To examine this possibility, we treated uninjured (control) and axotomized sensory neurons with K252a, an inhibitor of Trk receptor activity. K252a depressed the excitability of both axotomized and control neurons. K252a also produced a distinct pattern of arborizing outgrowth of neurites in both axotomized and control neurons. Protein kinase C (PKC) is an intracellular signal downstream of Trk; accordingly, we tested the effects of bisindolylmaleimide I (Bis-I), a specific inhibitor of PKC, on the axotomy-induced cellular changes. Bis-I blocked LTH-E, but did not disrupt LTH-M. Finally, because Trk activates the extracellular signal regulated kinase pathway in Aplysia sensory neurons, we examined whether this pathway mediates the injury-induced changes. Sensory neurons were axotomized in the presence of U0126, an inhibitor of mitogen-activated/extracellular receptor-regulated kinase. U0126 blocked the LTH-M due to axotomy, but did not impair LTH-E. Therefore distinct cellular signaling pathways mediate the induction of LTH-E and LTH-M in the sensory neurons.

Allergic inflammation-induced neuropeptide production in rapidly adapting afferent nerves in guinea pig airways

2002 ◽  
Vol 282 (4) ◽  
pp. L775-L781 ◽  
Author(s):  
Allen C. Myers ◽  
Radhika Kajekar ◽  
Bradley J. Undem
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Sensory Neurons ◽  
Large Diameter ◽  
Sensory System ◽  
Small Diameter ◽  
Allergic Inflammation ◽  
Primary Afferent ◽  
Chemical Coding ◽  
Low Threshold

In the vagal-sensory system, neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) are synthesized nearly exclusively in small-diameter nociceptive type C-fiber neurons. By definition, these neurons are designed to respond to noxious or tissue-damaging stimuli. A common feature of visceral inflammation is the elevation in production of sensory neuropeptides. Little is known, however, about the physiological characteristics of vagal sensory neurons induced by inflammation to produce substance P. In the present study, we show that allergic inflammation of guinea pig airways leads to the induction of substance P and CGRP production in large-diameter vagal sensory neurons. Electrophysiological and anatomical evidence reveals that the peripheral terminals of these neurons are low-threshold Aδ mechanosensors that are insensitive to nociceptive stimuli such as capsaicin and bradykinin. Thus inflammation causes a qualitative change in chemical coding of vagal primary afferent neurons. The results support the hypothesis that during an inflammatory reaction, sensory neuropeptide release from primary afferent nerve endings in the periphery and central nervous system does not require noxious or nociceptive stimuli but may also occur simply as a result of stimulation of low-threshold mechanosensors. This may contribute to the heightened reflex physiology and pain that often accompany inflammatory diseases.

Acetylsalicylic acid reduces heat responses in rat nociceptive primary sensory neurons – evidence for a new mechanism of action

2002 ◽  
Vol 320 (1-2) ◽  
pp. 61-64 ◽  
Author(s):  
Wolfgang Greffrath ◽  
Timo Kirschstein ◽  
Hermann Nawrath ◽  
Rolf-Detlef Treede
Keyword(s):  
Acetylsalicylic Acid ◽  
Sensory Neurons ◽  
Mechanism Of Action ◽  
Primary Sensory Neurons
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