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Journal of Korean Neurosurgical Society > Volume 21(6); 1992 > Article
Journal of Korean Neurosurgical Society 1992;21(6): 697-705.
Effects of Experimental Focal Ischemia of PV- and Calbindin-Immunoreactive Neuron of Rat Neocortex.
Sa Joon Kang, Jae Hyoo Kim, Jin Ho Cho, Je Hyuk Lee, Jung Hyun Woo, Kee Young Lee, Choon Sang Bae
1Department of Neurosurgery, Chonnam University Medical School, Kwangju, Korea.
2Department of Biochemisty, Chonnam University Medical School, Kwangju, Korea.
3Department of Anatomy, Chonnam University Medical School, Kwangju, Korea.
To understand the changes in expression of calcium binding proteins(CaBP) during the experimental focal ischemia, expression of two kinds of CaBP, paralvumin(PV) and calbindin D-28K(Calbindin), immunocytochemically, and activities of cytochrome oxidase(CO) and acetylcholinesterase(AchE), histochemically, in focal ischemic brain of the rat were investigated. Two groups of focal ischemic infarction were produced in Sprague Dawley rats(200-350 mg):Group I, Clip compression of left middle cerebral artery(MCA) for 5-10 mins and release;Group II, Electric coagulation of left MCA for 2-24 hrs. In the group I, CO activity and PV- and Calbindin-immunoreactivity(IR) were decreased in the left MCA territory, and decreased in number of PV- and Calbindin-IR neurons and degree of IR, but AchE activity was nearly same as that of control cortex. In the group II, decrease of CO and AchE activities, and marked increase of PV- and Calbindin IRs were noted on neuropil in the layers I through VI of ischemic region. Characteristically pyramidal cells, which did not express the both CaBPs in the control cortex, of layer V of ischemic cortex showed PV- and Calbindin Irs in the cell body and apical dendrite. These findings suggest that 1) PV- and Calbindin-IR neurons, mainly non-pyramidal cells, are more vulnerable than pyramidal cell to ischemic injury, 2) CaBP may have some roles in hypoxic neuronal injury, and 3) PV and Calbindin-immunocytochemistry can be used as useful technique in evaluation of experimental ischemia.
Key Words: Experimental ischemia; Neocortex; Parvalbumin; Calbindin; Immunocyto-chemistrys
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