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Expression of MARCKS mRNA in lateral geniculate nucleus and visual cortex of normal and monocularly deprived macaque monkeys

Published online by Cambridge University Press:  12 November 2002

NORIYUKI HIGO
Affiliation:
Neuroscience Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan
TAKAO OISHI
Affiliation:
Neuroscience Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan Currently: Department of Cellular and Molecular Biology, Primate Research Institute, Kyoto University
AKIKO YAMASHITA
Affiliation:
Department of Anatomy, Nihon University School of Medicine, Tokyo, Japan
KEIJI MATSUDA
Affiliation:
Neuroscience Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan
MOTOHARU HAYASHI
Affiliation:
Department of Cellular and Molecular Biology, Primate Research Institute, Kyoto University, Inuyama, Japan

Abstract

We performed a nonradioactive in situ hybridization histochemistry (ISH) study of the lateral geniculate nucleus (LGN) and the primary visual area (area 17) of the macaque monkey to investigate mRNA expression of the myristoylated alanine-rich C-kinase substrate (MARCKS), a major protein kinase C (PKC) substrate. In the LGN, intense hybridization signals were observed in both magnocellular neurons (layers 1 and 2) and parvocellular neurons (layers 3 to 6). Double labeling using ISH and immunofluorescence revealed that MARCKS mRNA was coexpressed with the α-subunit of type II calcium/calmodulin-dependent protein kinase, indicating that MARCKS mRNA is also expressed in koniocellular neurons in the LGN. GABA-immunoreactive neurons in the LGN did not contain MARCKS mRNA, indicating that MARCKS mRNA is not expressed in inhibitory interneurons. The signals were generally weak in area 17, and intense signals were restricted to large neurons in layers IVB, V, and VI. GABA-immunoreactive neurons in layers II–VI of area 17 did not contain MARCKS mRNA. Double-label ISH revealed that MARCKS mRNA was coexpressed with mRNA of GAP-43, another PKC substrate, in neurons of both the LGN and area 17. To determine whether the expression of MARCKS mRNA is regulated by retinal activity, we performed ISH in the LGN and area 17 of monkeys deprived of monocular visual input by tetrodotoxin. After monocular deprivation for 5 to 30 days, MARCKS mRNA was down-regulated in the LGN, but not in area 17. These results suggest that MARCKS mediates the activity-dependent changes in the excitatory relay neurons in the LGN.

Type
Research Article
Copyright
2002 Cambridge University Press

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