**Acknowledgement**

I wish to thank Y. Tanimura (National Museum of Nature and Science, Japan) for kind assistance of preparing the manuscript in various aspects. Thanks are also due to T. Kamiya, S. Tsukawaki, M. Kato, T. Ishii, T. Sato (Kanazawa University), A. Tsukagoshi, S. Yamada (Shizuoka University), R. J. Smith (Lake Biwa Museum), R. M. Karasz (Ludwig-Maximilians-University), T. Irizuki (Shimane University), H. Takata (Pusan University), B. C. Zhou (Shanghai Museum of Natural History), K. Ikehara, H. Katayama (AIST, Japan), H. Domitsu (University of Shiga Prefecture), A. Nojo (Hokkaido University of Education), P. J. Hayward (University of Wales Swansea) and the late N. Ikeya, Y. Kuwano and T. Matsuzaka for many valuable suggestions for ostracod resraches, with help of various aspect for my investigation. I express my gratitude to captain, all crew of the *Tansei-maru* (JAMSTEC, Japan) and *Hakurei-maru* (AIST, Japan) and all onboard scientists for their help of collecting sediment samples during Cruises KT95-14, KT96-17, KT97-15, KT98-17, KT99- 14, KT00-14, KT01-14, KT04-20 and GH98. Thanks are also due to R. J. Smith permitting for using figures of his literature, and to two anonymous reviwers of native English speakers for correcting my manuscript carefully.

#### **6. References**

[1] Butlin RK., Schön I., Griffiths HI. Chapter 1: Intoroduction to reproductive modes. In: Martens K. (ed.) Sex and Parthenogenesis: Evolutionary Ecology of Reproductive Modes in Non-Marine Ostracods. Leiden: Backhuys Publishers; 1998, p. 1–24.

[2] Kamiya T. Different sex-ratios in two Recent species of *Loxoconcha* (Ostracoda). Senckenbergiana Lethaia, 1998, 68: 337–345.

74 Sexual Dimorphism

million years.

**Acknowledgement** 

for correcting my manuscript carefully.

**6. References** 

**Author details** 

Hirokazu Ozawa

*Japan* 

4. To elucidate the functions of sexually dimorphic characteristics in extinct groups; *e*.*g*., the brood pouch of Palaeocopida in the Palaeozoic, fossil eggs or juvenile carapaces in the inner part of the adult carapaces from Palaeozoic sediments must be identified. For Palaeocopida, we must attempt to find fossils resting their appendages, despite their rarity. Furthermore, detailed observation of the ecological behaviour of living species will facilitate understanding of the actual functions of sexually dimorphic morphology in both living and extinct species [31]. Due to the excellent ostracod fossil record from Palaeozoic to Cenozoic, the living ostracod sexual dimorphism data can be applied to extinct species. Combined studies of the ecology and functional morphology of both living and fossil ostracod species will clarify the history of the evolutionary ecology and reproductive modes of organisms during the last ca. 500

*Earth Sciences Laboratory, College of Bioresource Sciences, Nihon University, Fujisawa, Kanagawa,* 

I wish to thank Y. Tanimura (National Museum of Nature and Science, Japan) for kind assistance of preparing the manuscript in various aspects. Thanks are also due to T. Kamiya, S. Tsukawaki, M. Kato, T. Ishii, T. Sato (Kanazawa University), A. Tsukagoshi, S. Yamada (Shizuoka University), R. J. Smith (Lake Biwa Museum), R. M. Karasz (Ludwig-Maximilians-University), T. Irizuki (Shimane University), H. Takata (Pusan University), B. C. Zhou (Shanghai Museum of Natural History), K. Ikehara, H. Katayama (AIST, Japan), H. Domitsu (University of Shiga Prefecture), A. Nojo (Hokkaido University of Education), P. J. Hayward (University of Wales Swansea) and the late N. Ikeya, Y. Kuwano and T. Matsuzaka for many valuable suggestions for ostracod resraches, with help of various aspect for my investigation. I express my gratitude to captain, all crew of the *Tansei-maru* (JAMSTEC, Japan) and *Hakurei-maru* (AIST, Japan) and all onboard scientists for their help of collecting sediment samples during Cruises KT95-14, KT96-17, KT97-15, KT98-17, KT99- 14, KT00-14, KT01-14, KT04-20 and GH98. Thanks are also due to R. J. Smith permitting for using figures of his literature, and to two anonymous reviwers of native English speakers

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**Chapter 5** 

© 2013 Muneoka and Kuwagata , licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is

and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

properly cited.

**Sexual Dimorphism in Monoamine** 

**An Animal Model of Schizophrenia** 

Katsumasa Muneoka and Makiko Kuwagata

Additional information is available at the end of the chapter

phenomenon without sex difference (Figure 1).

http://dx.doi.org/10.5772/55348

**1. Introduction** 

**Metabolism in BrdU-Treated Rats Showing** 

A nucleotide analog 5-bromo-2'-deoxyuridine (BrdU) is a genotoxic compound that is incorporated into DNA [1]. When rodent fetuses are exposed to BrdU prenatally, the cortical development is profoundly affected. Cortical abnormalities induced by prenatal BrdU are shown as a reduction in thickness of the cerebral cortex [2]. An induction of apoptotic cell death in the mouse and rat fetal brain [3, 4] and disturbance to normal migration that induces abnormal composition of cortical glutamatergic or GABAergic neurons have been demonstrated [4]. Mouse data suggest that the prenatal BrdU treatment induced apoptotic

Adult rats that were prenatally treated with BrdU show locomotor hyperactivity. The hyperactivity was observed in both male and female rats and was characterized as an increase in spontaneous motor activity during dark cycles observed in home cages [5] and novelty-induced hyperlocomotion in the open-field [5 - 8]. This abnormal behavior is exacerbated by the treatment with dopamine (DA) agonist, methylphenidate, which indicates that animals acquired hypersensitivity to dopaminergic stimuli [5, 8]. Recently proposed animal models for schizophrenia that knock-out candidate genes for this disease, such as neurotensin receptors [9] or calcium/calmodulin-dependent kinase II alpha [10], show hyperactive phenotypes and abnormal striatal DA function while mice overexpressing DA D2 receptors in the striatum show unaltered locomotor activity [11]. In a major psychiatric disorder schizophrenia, disturbance in cortical development and subcortical dopaminergic abnormality have been proposed [12] and they induces hypothetical

**Behavioral Dopamine Hypersensitivity:** 
