الفهرس 
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Abstract
Laterality of cerebral hemisphere has been well known based
on dominance of higher brain functions in human such as language
processing in the left hemisphere (Broca, 1861; Wernicke, 1874) and
spatial navigation in the right hemisphere (Fenton and Bures, 1993;
Maguire et al., 1996; Bohbot et al., 1998; Czeh et al., 1998; Nunn et
al., 1999; Burgess et al., 2002; Klur et al., 2009; Igloi et al., 2010). L-R
asymmetry of macroscopic structure of the brain has been reported
since 1968 first found in the plenum temporal, which was larger in
the left than the right (Geschwind and Levitsky, 1968). In addition,
dendritic branches were found to be greater in the left hemisphere
speech area than the right, and the central sulcus located in the primary motor cortex was deeper and larger in the right hemisphere
(Toga and Thompson, 2003). Recent technologies such as fMRI, PET
and CT have also demonstrated L-R asymmetry in various brain
regions such as temporal cortex, striatum and amygdala (Maguire et
al., 1996, 1997 and 2000). Studies on the L-R asymmetry extended to
involve the biochemical and molecular basis including asymmetric
distribution of GABA binding sites in the cerebral hemisphere (Oke
et al., 1980), nitric oxide lateralization in the hippocampus (Kristofikova et al., 2008), and dominance of dopaminergic D2
receptor in the right striatum (Afonso et al., 1993). Furthermore, the
first description of L-R asymmetry has been done at the synapse
level in the hippocampal pyramidal cells (Kawakami et al., 2003; Wu
et al., 2005). Density of NMDA glutamatergic receptor subunit
GluN2B and AMPA glutamatergic receptor subunit GluA1 in CA1
pyramidal cells are about 50% higher in synapses receiving afferents
from the left and right CA3 pyramidal cells, respectively (Kawakami et al., 2003; Shinohara et al., 2008). Furthermore, size and shape of
the spine synapses and induction of LTP were also found to be
asymmetrical depending on the side of input in CA1 pyramidal cells
(Kawakami et al., 2003; Wu et al., 2005 and Kohl et al., 2011).
Surprisingly, the asymmetrical allocation of GluN2B disappeared
resulting in right isomerism in inversus viscerum (iv) mutant mice,
which have a point mutation in LrD and randomized laterality in
internal organs (Kawakami et al., 2008). Thus iv mutant can serve as an interesting model to investigate physiological roles of brain
asymmetry (Goto et al., 2010).