Immunohistochemical study of vesicle monoamine transporter 2 in the hippocampal region of genetic animal model of schizophrenia

• Published in: Synapse (New York, N.Y.) Vol. 64; no. 12; pp. 948 - 953
• Main Authors: Iritani, Shuji, Sekiguchi, Hirotaka, Habuchi, Chikako, Hikita, Takao, Taya, Shinichiro, Kaibuchi, Kozo, Ozaki, Norio
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.12.2010
• Subjects: 14-3-3 Proteins - genetics; animal model; Animal models; Animals; Axons - metabolism; Biogenic Monoamines - metabolism; Brain; Disease Models, Animal; Etiology; Female; Hippocampus; Hippocampus - metabolism; Immunohistochemistry; Male; Mental disorders; Mice; Mice, 129 Strain; Mice, Knockout; Monoamine transporter; Neural networks; Neurotransmission; Neurotransmitters; Schizophrenia; Schizophrenia - genetics; Schizophrenia - metabolism; Synapses; Vesicles; Vesicular amine transporter; Vesicular Monoamine Transport Proteins - metabolism; VMAT2
• ISSN: 0887-4476; 1098-2396; 1098-2396
• DOI: 10.1002/syn.20846

Recent research in the etiology of schizophrenia revealed that there may be some neurodevelopmental failures such as neuronal network incompetence in the brain of this disease, and neurotransmitters cannot function accurately or adequately. But, it is unknown precisely what kinds of deficit in neurotransmission may be existed histopathologically. We investigated the expression of vesicle monoamine transporter 2 (VMAT2), which has a significant role in neurotransmission, in the hippocampal formation of the animal model of schizophrenia, 14‐3‐3epsilon hetero knockout (KO) mouse, using an immunohistochemical staining technique to clarify the neuronal abnormalities in the model animal. As a result, the expression of VMAT2 was increased significantly in the hippocampal formation of 14‐3‐3epsilon hetero KO mice compared to that of the wild‐type littermates. In conclusion, these findings might be related the pathophysiology of this disease includes a monoaminergic transmission abnormality, based on the investigation in a genetically‐modified mouse as schizophrenic model. Synapse 64:948–953, 2010. © 2010 Wiley‐Liss, Inc.