scholarly journals Expression and Localization of C-APP and N-APP in Peripheral Neurons of Rats and Crayfish After Axotomy

Author(s):  
Stanislav Vladimirovich Rodkin ◽  
Valentina Aleksandrovna Dzreyan ◽  
Andrey Mikhailovich Khaitin ◽  
Maria Aleksandrovna Pitinova ◽  
Moez Ali Eid ◽  
...  

Abstract Nerve injury induces a cascade of molecular-cellular events, leading to neuronal death or survival, where amyloid precursor protein (APP) and its proteolytic products play an important role. We studied the localization and expression of C-APP and N-APP in rat dorsal root ganglia (DRG) with transected sciatic nerve, axotomized crayfish stretch receptor neuron (SRN) and ventral nerve cord (VNC) ganglia with transected connectives. C-APP and N-APP localized predominantly in neurons, not in glial cells. Axotomy increased C-APP and N-APP expression in rat and crayfish neurons. The expression of APP in crustaceans confirms its conservative nature. In DRG, C-APP level was higher in neuronal nuclei than in cytoplasm in 24 hours post-axotomy. N-APP accumulation was not observed in DRG and crayfish neuronal nuclei. SRN axotomy resulted in C-APP and N-APP accumulation in 4–8 hours in perikaryon and its extensions, but only С-APP accumulated in nuclei. This indicates that not the whole APP, but its C-terminal product, AICD, enters the nucleus. Also, there was high level of C-APP in SRN nucleolus, suggesting possible AICD involvement in rRNA synthesis and ribosome formation. The APP accumulation in transected axons confirms its involvement in injury-induced axonal events.

1996 ◽  
Vol 199 (8) ◽  
pp. 1781-1789
Author(s):  
H Moser ◽  
N Mair ◽  
F Fresser

1. In the stretch receptor neurones of the crayfish Astacus astacus, the intracellular pH (pHi), the intracellular Na+ concentration ([Na+]i) and the membrane potential (Em) were measured simultaneously using ion-selective and conventional microelectrodes. Normal Astacus saline (NAS), and salines containing varying amounts of Ca2+ (Ca2+-NAS) but of constant ionic strength, with Na+, Mg2+ or Ba2+ as substituting ions, were used to investigate the effects of extracellular Ca2+ concentration ([Ca2+]o) on pHi and pHi regulation, on [Na+]i and on Em. The maximum rate of pHi recovery was used as a measure of pHi regulation. Acid loads were imposed using the NH4+/NH3 rebound technique. 2. [Ca2+]o affected pHi, pHi regulation, [Na+]i and Em. The magnitudes of the effects were inversely related to [Ca2+]o and were specific to the ion used for [Ca2+]o substitution. 3. Compared with controls, increasing [Ca2+]o threefold (in exchange for Na+) elicited some alkalization, a 7 % faster maximum rate of pHi recovery and generally lower values of [Na+]i. 4. In low-Ca2+ or Ca2+-free NAS (substitutions by Na+ or Mg2+), pHi became more acid, the maximum rate of pHi recovery was reduced by up to 50 % and [Na+]i was generally higher. The effects were faster and larger at lower [Ca2+]o, and stronger with Na+ than with Mg2+ as the substituting ion. 5. In Ca2+-free NAS (Ca2+ substituted for by Ba2+), the effects on pHi, on the maximum rate of pHi recovery and on [Na+]i were generally small. In this respect, Ba2+ had similar physiological properties to Ca2+ and was almost equally effective. 6. Changes in Em, including rapid depolarizations and occasional burst activity in Ca2+-free NAS, indicate that alterations in the properties of the membrane, such as a change in its permeability or selectivity, are occurring. Measurements of [Na+]i support this view. In addition, Ba2+ per se induced a (small) depolarization, as shown when Ba2+ was present in NAS or in low-Ca2+ NAS. 7. Changes in [Ca2+]o affected [Na+]i. *[Na+]i is defined as [Na+]i determined at the onset of the maximum rate of pHi recovery, and the ratio *[Na+]i/[Na+]o at that instant was calculated. A linear relationship between the maximum rate of pHi recovery and the *[Na+]i/[Na+]o ratio was found, irrespective of the amount and of the ion species used for [Ca2+]o substitution. This is strong evidence that pHi and pHi regulation were indirectly affected by [Ca2+]o, which altered membrane properties and thus caused a change in [Na+]i. We could find no evidence for a direct contribution of [Ca2+]o to acid extrusion or to a direct modulatory action on the transport protein of the Na+/H+ antiporter.


2019 ◽  
pp. 76-98
Author(s):  
Gordon L. Fain

“Mechanoreceptors and touch” is the fifth chapter of the book Sensory Transduction and describes general mechanisms of touch sensitivity in animals. It begins with a review of mechanoreception in the single-celled protozoan Paramecium and transduction of touch in the round worm Caenorhabditis elegans. A thorough treatment is next given of the crayfish stretch receptor and insect mechanoreceptors, including a description of NOMPC channels in Drosophila. The chapter then reviews the anatomy and physiology of mechanoreceptors and touch in mammals, both in glabrous and hairy skin. It concludes with recent discoveries of the molecular biology and physiology of Merkel cells, known to be responsible for much of mammalian touch sensation.


1968 ◽  
Vol 51 (5) ◽  
pp. 635-654 ◽  
Author(s):  
Shosaku Obara ◽  
Harry Grundfest

Unlike several other varieties of input membrane, that of the crayfish stretch receptor develops a generator potential in response to stretch when all the Na of the medium is replaced with Li. However, Li depolarizes the receptor neuron, the soma membrane becoming more depolarized than that of the axon. During exposure to Li the cell usually fires spontaneously for a period, and when it becomes quiescent spike electrogenesis fails in the soma but persists in the axon. These effects are seen in the rapidly adapting as well as the slowly adapting cells. The block of spike electrogenesis of the soma membrane is only partly due to the Li-induced depolarization and a significant role must be ascribed to a specific effect of Li.


2016 ◽  
Vol 125 (4) ◽  
pp. 765-778 ◽  
Author(s):  
Jun Zhang ◽  
Lingli Liang ◽  
Xuerong Miao ◽  
Shaogen Wu ◽  
Jing Cao ◽  
...  

Abstract Background Peripheral nerve injury–induced gene alterations in the dorsal root ganglion (DRG) and spinal cord likely participate in neuropathic pain genesis. Histone methylation gates gene expression. Whether the suppressor of variegation 3-9 homolog 1 (SUV39H1), a histone methyltransferase, contributes to nerve injury–induced nociceptive hypersensitivity is unknown. Methods Quantitative real-time reverse transcription polymerase chain reaction analysis, Western blot analysis, or immunohistochemistry were carried out to examine the expression of SUV39H1 mRNA and protein in rat DRG and dorsal horn and its colocalization with DRG μ-opioid receptor (MOR). The effects of a SUV39H1 inhibitor (chaetocin) or SUV39H1 siRNA on fifth lumbar spinal nerve ligation (SNL)–induced DRG MOR down-regulation and nociceptive hypersensitivity were examined. Results SUV39H1 was detected in neuronal nuclei of the DRG and dorsal horn. It was distributed predominantly in small DRG neurons, in which it coexpressed with MOR. The level of SUV39H1 protein in both injured DRG and ipsilateral fifth lumbar dorsal horn was time dependently increased after SNL. SNL also produced an increase in the amount of SUV39H1 mRNA in the injured DRG (n = 6/time point). Intrathecal chaetocin or SUV39H1 siRNA as well as DRG or intraspinal microinjection of SUV39H1 siRNA impaired SNL-induced allodynia and hyperalgesia (n = 5/group/treatment). DRG microinjection of SUV39H1 siRNA also restored SNL-induced DRG MOR down-regulation (n = 6/group). Conclusions The findings of this study suggest that SUV39H1 contributes to nerve injury–induced allodynia and hyperalgesia through gating MOR expression in the injured DRG. SUV39H1 may be a potential target for the therapeutic treatment of nerve injury–induced nociceptive hypersensitivity.


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