Journals / Marmara Medical Journal / 2000 / Cilt: 13 - Sayı: 1

SUPEROXIDE RADICAL GENERATION IN RAT STRIATAL SLICES EFFECTS OF DEPOLARIZATION AND CALCIUM ION DEFICIENCY CONDITIONS

Pages
11–14
Publication Date
2016-12-03
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Suppression of free radical generation from different sources in the neuron may help to develop new therapeutical approaches and can prevent neurodegeneration in the striatum.Key Words: Striatal slices, superoxide radical, chemiluminescence recording, calcium ion deficiency

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Oxidative stress is thought to be responsible for neurotoxicity through the generation of oxygen radicals.
📊
Key Findings & Data:We also investigated the effect of intracellular and extracellular calcium ion concentrations on superoxide radical formation.Methods: Striatal slices were obtained using a vibroslicer and after incubation of slices in appropriate incubation media the formation of superoxide radicals was detected by the chemiluminescence technique using a luminometer.Results: Depolarization conditions (50 mM-K+) were used to induce superoxide radical generation in striatal slices.
💡
Conclusion & Impact:Suppression of free radical generation from different sources in the neuron may help to develop new therapeutical approaches and can prevent neurodegeneration in the striatum.Key Words: Striatal slices, superoxide radical, chemiluminescence recording, calcium ion deficiency
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Oxidative stress is thought to be responsible for neurotoxicity through the generation of oxygen radicals. The aim of the current study was to determine the generation of superoxide radicals under depolarization conditions in rat striatal slices. We also investigated the effect of intracellular and extracellular calcium ion concentrations on superoxide radical formation.Methods: Striatal slices were obtained using a vibroslicer and after incubation of slices in appropriate incubation media the formation of superoxide radicals was detected by the chemiluminescence technique using a luminometer.Results: Depolarization conditions (50 mM-K+) were used to induce superoxide radical generation in striatal slices. Under depolarization conditions lactate dehydrogenase activity (LDH) was also increased. Incubation of striatal slices in calcium chelator EGTA and intracellular calcium release blocker ryanodine increased superoxide generation compared to depolarization conditions.Conclusion: Under calcium ion deficiency conditions, increased superoxide generation may be related with the suppression of LTD in striatum. Suppression of free radical generation from different sources in the neuron may help to develop new therapeutical approaches and can prevent neurodegeneration in the striatum.Key Words: Striatal slices, superoxide radical, chemiluminescence recording, calcium ion deficiency

🔖

Cite This Article

Saybaşılı, H., Yüksel, M., Haklar, G., Yalçın, S. (2016). SUPEROXIDE RADICAL GENERATION IN RAT STRIATAL SLICES EFFECTS OF DEPOLARIZATION AND CALCIUM ION DEFICIENCY CONDITIONS. Marmara Medical Journal, Cilt: 13 - Sayı: 1, 11–14. https://ajindex.com/articles/688744

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Calabresi P, Pisani A, Mercury ÎÏB, Bernardi G. Postsynaptic mechanisms underlying striatal long-term depression. J Heurosci 1994; 14:4871-4881.
  2. Jiang Z-G, Horth RA. Membrane properties and synaptic responses of rat striatal neurons in vitro. J Phys 1991;443:533-553.
  3. Monoghan DT, Holds VR, Toy DW, Cotman CW. Anatomical distributions of four pharmacologically distinct 3H-L-glutamate binding sites, nature 1983;306:176-179
  4. Sladeczek P, Pin JP, Recasens M, Bockaert J, Weiss S. Glutamate stimulates inositol trisphosphate formation in striatal neurons. nature 1985;317:717-719.
  5. Bashir Zi, Bortolotto ZA, Davies CPI et al. Induction of the LTP in hippocampus needs synaptic activation of glutamate metabotropic receptors, nature 1993;363:347-350.
  6. Bliss TVP, Collingridge GL. A synaptic model of memory: Long-term potentiation in the hippocampus, nature 1993;361 -.31-39.
  7. Patel M, Day BJ, Crapo JD, Fridovich I, Mcnamara JO. Requirement for superoxide in excitotoxic cell death, neuron 1996; 16:345-355.
  8. Liu J, Shigenaga MR, Mori A, Ames B. Free radicals and neurodegenerative diseases: Stress and oxidative damage. In: Packer L, fliramatsu M, Yoshikawa T, eds. Free Radicals in Brain Physiology and Disorders, new York: Academic Press,:403-407.
  9. Harris ME, Carney JM, Cole PS, et al. jl-Amyloid peptide-derived, oxygen-dependent free radicals inhibit glutamate uptake in cultured astrocytes: implications for Alzheimer's disease, neuro Report 1995;6:1875-1879.
  10. Reiderer P, Sofic E, Reusch W-D, et al. Transition metals, ferritin, glutathione and ascorbic acid in Parkinson s disease. J Meurochem 1989;52:381 - Yalçın /İS, Haklar G, Küçükkaya B, Yüksel M, Dalaman G. Chemiluminescence measurements for the detection of free radical species. In: Özben T, ed. Free Radicals, Oxidative Stress, and Antioxidants, new York: Plenum Press, 1998:385- Calabresi P, Mercury nB, Bernardi G. Synaptic and intrinsic control of membrane excitability of striata! neurons. II. An in vitro analysis. J neurophys 1990;63:663-675. Miller RJ. Calcium signalling in neurons. Tins 1988,11:415-419.
  11. Lovinger DM, Tyler EC, Merritt A. Short- and longterm synaptic depression in rat neostriatum. J neurophys 1993; 70:1937-1949.
  12. Calabresi P, Pisani A, Mercury nB, Bernardi G. Lithium treatment blocks long-term synaptic depression in the striatum, neuron 1993; 10:955- 962. Calabresi P, Maj R, Pisani A, Mercury nB, Bernardi G. Long-term synaptic depression in the striatum: physiological and pharmacological characterization. J