An investigation of neuromorphological alterations in the auditory cortex of Akt1 knockout mice
演題番号 : P1-p13
Yi-Wen Chen:1 Ju-Chun Pei:1 Wen-Sung Lai:1,2
1:Dept Psychology, National Taiwan University, Taipei, Taiwan 2:Neurobiology and Cognitive Science Center, National Taiwan University, Taipei, Taiwan
Accumulating evidence suggests that Akt1 might contribute to susceptibility for schizophrenia and schizophrenia-related phenotypes. AKT1 is also involved in the neurite outgrowth (e.g., elongation, branching, and caliber) which might lead to the neuromorphological abnormality found in schizophrenic patients. Based on our recent finding of an impairment of acoustic prepulse inhibition (PPI) in the female AKT1 knockout mice, the objective of this study is to investigate whether there is any phenotype-related neuromorphological alteration in AKT1 knockout mice. AKT1 heterozygous mice were intercrossed with a reporter strain (C57Bl6-Tg(GFPm)) to partially label the pyramidal neurons with GFP in the auditory cortex. Each available neuron in the auditory cortex (between Bregma -2.30 and -2.80 mm) of AKT1 knockout and wild-type female mice was surveyed with a morphometric analysis using a total of 14 morphological variables. Our data revealed that there are several neuromorphological alterations in AKT1 knockout mice compared with wild-type littermate controls. In the apical dendrites, there are (1) a 31% increase in the length of dendritic shafts, (2) a 55% enhancement in the branch angle of the primary dendrites, and (3) a 51% increase in the apical dendritic field area. In the basal dendrites, these alterations include (1) a slight (22%) but significant increase in soma size, (2) a 31% reduction in the number of branches, (3) a 18% decrease in the number of tips, and (4) a 25% decline in the total length. These decreases in complexity were confirmed by Sholl analysis. Our data indicate the involvement of AKT1 in neuromorphology in vivo and also suggest its potential relevance to the PPI deficit.