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Mol. Cells 2004; 18(1): 30-39

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Nitric Oxide Synthase and Calcium-binding Protein-containing Neurons in the Hamster Visual Cortex

Jee-Eun Lee, Chang-Hyun Ahn, Jea-Young Lee, Eun-Sun Chung, Chang-Jin Jeon

Abstract

The distribution and morphology of neurons containing neuronal nitric oxide synthase (NOS), and calcium-binding proteins calbindin D28K and calretinin in the hamster visual cortex were compared by immunocytochemistry. Staining for NOS, calbindin D28K and calretinin was seen both in the specific layers and in the selective cell types. The densest concentration of anti-NOS-immunoreactive (IR) neurons was found in layer VI. Most of the calbindin D28K-IR neurons were located in layers II/III and V while the calretinin-IR neurons were predominantly located in layers II/III. The labeled neurons varied in morphology. The large majority of NOS-IR neurons were round or oval cells with many dendrites coursing in all directions. The majority of the calbindin D28K-IR neurons were stellate and round or oval cells with multipolar dendrites. The majority of the calretinin-IR neurons were vertical fusiform cells with long processes traveling perpendicular to the pial surface. Our study showed that 14.7% and 27.5% of the NOS-IR cells in the hamster visual cortex contained calbindin D28K or calretinin, respectively. These results indicate that NOS, calbindin and calretinin are located in specific layers and specific cell types and the vast majority of NOS-containing neurons are limited to neurons that do not express calbindin D28K or calretinin.

Keywords Calcium-binding Protein; Immunocytochemistry; Localization; Nitric Oxide Synthase; Visual Cortex

Article

Research Article

Mol. Cells 2004; 18(1): 30-39

Published online August 31, 2004

Copyright © The Korean Society for Molecular and Cellular Biology.

Nitric Oxide Synthase and Calcium-binding Protein-containing Neurons in the Hamster Visual Cortex

Jee-Eun Lee, Chang-Hyun Ahn, Jea-Young Lee, Eun-Sun Chung, Chang-Jin Jeon

Abstract

The distribution and morphology of neurons containing neuronal nitric oxide synthase (NOS), and calcium-binding proteins calbindin D28K and calretinin in the hamster visual cortex were compared by immunocytochemistry. Staining for NOS, calbindin D28K and calretinin was seen both in the specific layers and in the selective cell types. The densest concentration of anti-NOS-immunoreactive (IR) neurons was found in layer VI. Most of the calbindin D28K-IR neurons were located in layers II/III and V while the calretinin-IR neurons were predominantly located in layers II/III. The labeled neurons varied in morphology. The large majority of NOS-IR neurons were round or oval cells with many dendrites coursing in all directions. The majority of the calbindin D28K-IR neurons were stellate and round or oval cells with multipolar dendrites. The majority of the calretinin-IR neurons were vertical fusiform cells with long processes traveling perpendicular to the pial surface. Our study showed that 14.7% and 27.5% of the NOS-IR cells in the hamster visual cortex contained calbindin D28K or calretinin, respectively. These results indicate that NOS, calbindin and calretinin are located in specific layers and specific cell types and the vast majority of NOS-containing neurons are limited to neurons that do not express calbindin D28K or calretinin.

Keywords: Calcium-binding Protein, Immunocytochemistry, Localization, Nitric Oxide Synthase, Visual Cortex

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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