Articles

  • the Korean Society for Brain and Neural Sciences

Article

Original

Exp Neurobiol 2007; 16(2): 61-70

Published online December 31, 2007

© The Korean Society for Brain and Neural Sciences

Neuronal Adhesion Molecules in Neuronal Injury

You-Na Jang1,2,3, Yi-Sook Jung1, Soo Hwan Lee1,3, Chang-Hyun Moon1,3 and Eun Joo Baik1,2,3*

1Department of Physiology, 2Chronic Inflammatory Disease Research Center, 3BK 21 Graduate Program for Medical Sciences, Ajou University School of Medicine, Suwon 443-749, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-31-219-5042, FAX: 82-31-219-5049
e-mail: eunjoo@ajou.ac.kr

Abstract

Cell adhesion molecules (CAMs) play critical roles in development and maintenance of nervous system, but also might be key determinants in neuronal response to injury. Neuronal CAMs include neural cadherin (N-cadherin), neural cell adhesion molecule (NCAM), L1, CHL1 (close homologue of L1), and intercellular adhesion molecule (ICAM). Spinal nerve ligation (SNL) evoked neuropathic pain within 1 day, which is maintained until 3∼5 weeks. In this study, we investigated whether what kinds of CAMs in the dorsal root ganglia (DRG) was changed by in vivo SNL model, and how the CAMs are expressed to inflammatory stimuli or excitotoxic insult in the neuronal cell cultures such as primary cortical neuron, cortical neurons mixed with glial cells, astrocytes and BV microglial cells. In SNL, ICAM-1 mRNA significantly increased 3 days after ligation, and CHL1 mRNA increased after 7 days and until 21 days. In contrast, NCAM mRNA was not changed through 3-21 days. NCAM mRNA was expressed in astrocytes as well as neurons, and CHL1 mRNA was expressed in astrocytes, microglia and neurons, whereas L1 mRNA was expressed only in neurons. In vitro cultures, ICAM-1 mRNA in astrocytes was induced by inflammatory stimuli such as TNF-Ձ, IL-1Ղ and LPS, and it was increased by only LPS in microglial cells. CHL1 mRNA was increased by TNF-Ձ in neurons, however was decreased in the microglial cells. N-cadherin mRNA was significantly reduced by NMDA in neurons. Especially, NMDA reduced N-cadherin with dose-dependent manner, and NMDA receptor antagonist MK-801 restored it. L1 mRNA also was reduced by NMDA in mixed cortical neurons with glial cells and NCAM mRNA expression was not changed significantly by TNF-Ձ, IL-1Ղ and NMDA. Taken together, our data showed that expression of ICAM-1 is associated with inflammatory responses, N-cadherin, L1 and CHL1 in neurons might be modulated during neurodegeneration, but NCAM mRNA, which might play an important roles in the nervous system, is not changed by either kind of stimuli. Especially, N-cadherin expressed in neurons may be correlated with NMDA-dependent neurodegeneration.

Keywords: ICAM-1, CHL1, N-cadherin, NCAM, glial cell, neuron