Mutual information-based feature selection in studying perturbation of dendritic structure caused by TSC2 inactivation. Academic Article uri icon

Overview

abstract

  • In this study, the effect of protein Tuberous sclerosis 2 (TSC2) on the dendritic spine density and length was demonstrated by using TSC2-RNAinactivation. In addition, the role of rapamycin, an antagonist of the molecular target of rapamycin, in the morphological changes of spine caused by TSC2 silencing was investigated. The features were extracted from highresolution three-dimensional image stacks collected by two-photon laser scanning microscopy of green fluorescing pyramidal cells expressing TSC2-RNA interference (RNAi), or TSC2-RNAi and rapamycin treatment in rat hippocampal slice cultures. We proposed to apply the lognormal distribution method for feature extraction. The extracted features of three cases under investigation, namely, (1) green-fluorescent protein GFP vs TSC2-RNAi, (2) GFP vs TSC2-RNAi and rapamycin, and (3) TSC2-RNAi vs TSC2-RNAi and rapamycin, were analyzed by mutual information-based feature selection and evaluated by three classifiers, K-nearest neighbor, Perceptron, and two-layer neural networks. The results showed that both the spine density and length have significant morphological changes after TSC2-RNAi treatment. However, rapamycin treatment could reverse the effect of TSC2-RNAi on spine length but not on spine density. These results are consistent with the results reported in the scientific literature. Finally, we explored the application of pattern recognition method in a small sample with richer feature properties, namely bootstrap mutual information estimation and a mutual information- based feature selection method.

publication date

  • January 1, 2006

Research

keywords

  • Cell Differentiation
  • Cerebral Cortex
  • Dendritic Spines
  • Image Cytometry
  • Tuberous Sclerosis
  • Tumor Suppressor Proteins

Identity

Scopus Document Identifier

  • 33646700012

Digital Object Identifier (DOI)

  • 10.1385/NI:4:1:81

PubMed ID

  • 16595860

Additional Document Info

volume

  • 4

issue

  • 1