Tissue preparation & Golgi-Cox Staining with FD Rapid GolgiStain™ Kit

Cat. # SS201 

Golgi-Cox impregnation1,2 has been one of the most effective techniques for studying both the normal and abnormal morphology of neurons as well as glia. Using Golgi technique, subtle morphological alterations in neuronal dendrites and dendritic spines have been discovered in the brains of animals treated with drugs as well as in the postmortem brains of patients with neurological diseases3,4. However, the complex and time-consuming process of Golgi staining has been a major obstacle to the widespread application of this technique.

FD Rapid GolgiStain™ kit (Cat. # PK401), designed based on the principle of the methods described by Ramón-Moliner2, Glaser and Van der Loos5, has overcome most problems associated with the Golgi-Cox technique. The FD Rapid GolgiStain™ kit has been tested extensively in the brains from several species of animals as well as in specimens of the postmortem human brain. This kit has not only significantly simplified and improved the Golgi-Cox technique but also proven to be extremely sensitive and reliable for demonstrating morphological details of neurons and glia, especially dendritic spines (cf. photo samples). 

This service includes tissue preparation, sectioning, staining, coverslipping and slide labeling. As a result, you will receive up to all sections from each brain or  block which are Golgi-Cox-impregnated and ready for microscopic observations.

Procedure: Following cryoprotection, tissue will be rapidly frozen in isopentane pre-cooled to -70°C. The frozen tissue will be cut on a cryostat and mounted on gelatin-coated microscope slides. Subsequently, sections cut through various levels (or the levels of your choice) will be processed with FD Rapid GolgiStain™ kit (cf. Products, Cat. # PK401 for details).

 
          

Remarks: 

  • A quotation is required before placing an order.

  • The investigator needs to provide tissue fixed with special fixative provided by FD Neurotechnologies, Inc.

  • Please contact us for more information.

References using FD Rapid Golgistain™ kit:

  1. Dahl JP, Wang-Dunlop J, Gonzales C, Goad MEP, Mark RJ and Kwak SP: Characterization of the WAVE1 knock-out  mouse: implications for CNS development. J. Neuroscience 23: 3343-3352, 2003.

  2. Beggs HE, Schahin-Reed D, Zang K, Goebbels S, Nave KA, Gorski J, Jones KR, Sretavan D and Reichardt LF: FAK deficiency in cells contributing to the basal lamina results in cortical abnormalities resembling congenital muscular dystrophies. Neuron 40:501-514, 2003.

  3. Milatovic D, Zaja-Milatovic S, Montine KS, Horner PJ, and Montine TJ: Pharmacologic suppression of neuronal oxidative damage and dendritic degeneration following direct activation of glial innate immunity in mouse cerebrum. J. Neurochem. 87: 1518-1526, 2003.

  4. Amateau SK and McCarthy MM: Induction of PGE2 by estradiol mediates developmental masculinization of sex behavior. Nature Neuroscience 7:643-650, 2004.

  5. Ishikura N, Clever JL, Bouzamondo-Bernstein E, Samayoa E, Prusiner SB, Huang EJ, and DeArmond SJ: Notch-1 activation and dendritic atrophy in prion disease. Proc. Natl. Acad. Sci. USA 102:886-891, 2005.

  6. Ren-Patterson RF, Cochran LW, Holmes A, Sherrill S, Huang SJ, Tolliver T, Lesch KP, Lu B and Murphy DL: Loss of brain-derived neurotrophic factor gene allele exacerbates brain monoamine deficiencies and increases stress abnormalities of serotonin transporter knockout mice. J. Neurosci. Res. 79:756-771, 2005.

  7. Grillet N, Pattyn A, Contet C, Kieffer BL, Goridis C and JF Brunet: Generation and characterization of Rgs4 mutant mice. Molecular and Cellular Biology 25:4221-4228, 2005.

  8. Laub F, Lei L, Sumiyoshi H, Kajimura D, Dragomir C, Smaldone S, Puche AC, Petros TJ, Mason C, Parada LF, and Ramirez F: Transcription factor KLF7 is important for neuronal morphogenesis in selected regions of the nervous system. Molecular and Cellular Biology 25:5699-5711, 2005.

  9. Pyter LM, Reader BF and Nelson RJ: Short photoperiods impair spatial learning and alter hippocampal dendritic morphology in adult male white-footed mice (peromyscus leucopus). J. Neuroscience 25:4521-4526, 2005.

  10. Gu X, Li C, Wei W, Lo V, Gong S, Li SH, Iwasato T, Itohara S, Li XJ, Mody I, Heintz N and Yang XW: Pathological cell-cell interactions elicited by a neuropathogenic form of mutant huntingtin contribute to cortical pathogenesis in HD mice. Neuron 46:433-444, 2005.

  11. Ramanan N, Shen Y, Sarsfield S, Lemberger T, Schütz G, Linden DJ and Ginty DD: SRF mediates activity-induced gene expression and synaptic plasticity but not neuronal viability. Nature Neuroscience 8:759-767, 2005.

  12. Björkblom B, Östman N, Hongisto V, Komarovski V, Filén JJ, Nyman TA, Kallunki T, Courtney MJ and Coffey ET: Constitutively active cytoplasmic c-jun N-terminal kinase 1 is a dominant regulator of dendritic architecture: role of microtubule-associated protein 2 as an effector. J. Neuroscience 25:6350-6361, 2005.

  13. Niewmierzycka A, Mills J, St-Arnaud R, Dedhar S and Reichardt LF: Integrin-linked kinase deletion from mouse cortex results in cortical lamination defects resembling cobblestone lissencephaly. J. Neuroscience 25:7022-7031, 2005.

  14. McLaughlin KJ, Baran SE, Wright RL and Conrad CD: Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: possible involvement of CA1 neurons. Neuroscience 135:1045-1054, 2005.