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Search Results: 1 - 10 of 86 matches for " Shigeyoshi Itohara "
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Analyses of fear memory in Arc/Arg3.1-deficient mice: intact short-term memory and impaired long-term and remote memory  [PDF]
Kazuyuki Yamada, Chihiro Homma, Kentaro Tanemura, Toshio Ikeda, Shigeyoshi Itohara, Yoshiko Nagaoka
World Journal of Neuroscience (WJNS) , 2011, DOI: 10.4236/wjns.2011.11001
Abstract: Activity-regulated cytoskeleton-associated protein (Arc/Arg3.1) was originally identified in patients with seizures. It is densely distributed in the hip-pocampus and amygdala in particular. Because the expression of Arc/Arg3.1 is regulated by nerve in-puts, it is thought to be an immediate early gene. As shown both in vitro and in vivo, Arc/Arg3.1 is in-volved in synaptic consolidation and regulates some forms of learning and memory in rats and mice [1,2]. Furthermore, a recent study suggests that Arc/Arg3.1 may play a significant role in signal transmission via AMPA-type glutamate receptors [3-5]. Therefore, we conducted a detailed analysis of fear memory in Arc/Arg3.1-deficient mice. As previously reported, the knockout animals exhib-ited impaired fear memory in both contextual and cued test situations. Although Arc/Arg3.1-deficient mice showed almost the same performance as wild-type littermates 4 hr after a conditioning trial, their performance was impaired in the retention test after 24 hr or longer, either with or without reconsolidation. Immunohistochemical analyses showed an abnormal density of GluR1 in the hip-pocampus of Arc/Arg3.1-deficient mice; however, an application of AMPA potentiator did not improve memory performance in the mutant mice. Memory impairment in Arc/Arg3.1-deficient mice is so ro-bust that the mice provide a useful tool for devel-oping treatments for memory impairment.
A Novel Form of Memory for Auditory Fear Conditioning at a Low-Intensity Unconditioned Stimulus
Ayumi Kishioka, Fumiaki Fukushima, Tamae Ito, Hirotaka Kataoka, Hisashi Mori, Toshio Ikeda, Shigeyoshi Itohara, Kenji Sakimura, Masayoshi Mishina
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004157
Abstract: Fear is one of the most potent emotional experiences and is an adaptive component of response to potentially threatening stimuli. On the other hand, too much or inappropriate fear accounts for many common psychiatric problems. Cumulative evidence suggests that the amygdala plays a central role in the acquisition, storage and expression of fear memory. Here, we developed an inducible striatal neuron ablation system in transgenic mice. The ablation of striatal neurons in the adult brain hardly affected the auditory fear learning under the standard condition in agreement with previous studies. When conditioned with a low-intensity unconditioned stimulus, however, the formation of long-term fear memory but not short-tem memory was impaired in striatal neuron-ablated mice. Consistently, the ablation of striatal neurons 24 h after conditioning with the low-intensity unconditioned stimulus, when the long-term fear memory was formed, diminished the retention of the long-term memory. Our results reveal a novel form of the auditory fear memory depending on striatal neurons at the low-intensity unconditioned stimulus.
Restoration of Contralateral Representation in the Mouse Somatosensory Cortex after Crossing Nerve Transfer
Haruyoshi Yamashita, Shanlin Chen, Seiji Komagata, Ryuichi Hishida, Takuji Iwasato, Shigeyoshi Itohara, Takeshi Yagi, Naoto Endo, Minoru Shibata, Katsuei Shibuki
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035676
Abstract: Avulsion of spinal nerve roots in the brachial plexus (BP) can be repaired by crossing nerve transfer via a nerve graft to connect injured nerve ends to the BP contralateral to the lesioned side. Sensory recovery in these patients suggests that the contralateral primary somatosensory cortex (S1) is activated by afferent inputs that bypassed to the contralateral BP. To confirm this hypothesis, the present study visualized cortical activity after crossing nerve transfer in mice through the use of transcranial flavoprotein fluorescence imaging. In na?ve mice, vibratory stimuli applied to the forepaw elicited localized fluorescence responses in the S1 contralateral to the stimulated side, with almost no activity in the ipsilateral S1. Four weeks after crossing nerve transfer, forepaw stimulation in the injured and repaired side resulted in cortical responses only in the S1 ipsilateral to the stimulated side. At eight weeks after crossing nerve transfer, forepaw stimulation resulted in S1 cortical responses of both hemispheres. These cortical responses were abolished by cutting the nerve graft used for repair. Exposure of the ipsilateral S1 to blue laser light suppressed cortical responses in the ipsilateral S1, as well as in the contralateral S1, suggesting that ipsilateral responses propagated to the contralateral S1 via cortico-cortical pathways. Direct high-frequency stimulation of the ipsilateral S1 in combination with forepaw stimulation acutely induced S1 bilateral cortical representation of the forepaw area in na?ve mice. Cortical responses in the contralateral S1 after crossing nerve transfer were reduced in cortex-restricted heterotypic GluN1 (NMDAR1) knockout mice. Functional bilateral cortical representation was not clearly observed in genetically manipulated mice with impaired cortico-cortical pathways between S1 of both hemispheres. Taken together, these findings strongly suggest that activity-dependent potentiation of cortico-cortical pathways has a critical role for sensory recovery in patients after crossing nerve transfer.
Physiological Mouse Brain Aβ Levels Are Not Related to the Phosphorylation State of Threonine-668 of Alzheimer's APP
Yoshitake Sano, Tadashi Nakaya, Steve Pedrini, Shizu Takeda, Kanae Iijima-Ando, Koichi Iijima, Paul M. Mathews, Shigeyoshi Itohara, Sam Gandy, Toshiharu Suzuki
PLOS ONE , 2006, DOI: 10.1371/journal.pone.0000051
Abstract: Background Amyloid-β peptide species ending at positions 40 and 42 (Aβ40, Αβ42) are generated by the proteolytic processing of the Alzheimer's amyloid precursor protein (APP). Aβ peptides accumulate in the brain early in the course of Alzheimer's disease (AD), especially Aβ42. The cytoplasmic domain of APP regulates intracellular trafficking and metabolism of APP and its carboxyl-terminal fragments (CTFα, CTFβ). The role of protein phosphorylation in general, and that of the phosphorylation state of APP at threonine-668 (Thr668) in particular, has been investigated in detail by several laboratories (including our own). Some investigators have recently proposed that the phosphorylation state of Thr668 plays a pivotal role in governing brain Aβ levels, prompting the current study. Methodology In order to evaluate whether the phosphorylation state of Thr668 controlled brain Aβ levels, we studied the levels and subcellular distributions of holoAPP, sAPPα, sAPPβ, CTFα, CTFβ, Aβ40 and Aβ42 in brains from “knock-in” mice in which a non-phosphorylatable alanyl residue had been substituted at position 668, replacing the threonyl residue present in the wild-type protein. Conclusions The levels and subcellular distributions of holoAPP, sAPPα, sAPPβ, CTFα, CTFβ, Aβ40 and Aβ42 in the brains of Thr668Ala mutant mice were identical to those observed in wild-type mice. These results indicate that, despite speculation to the contrary, the phosphorylation state of APP at Thr668 does not play an obvious role in governing the physiological levels of brain Aβ40 or Αβ42 in vivo.
Identification of a novel intronic enhancer responsible for the transcriptional regulation of musashi1 in neural stem/progenitor cells
Satoshi Kawase, Takao Imai, Chikako Miyauchi-Hara, Kunio Yaguchi, Yoshinori Nishimoto, Shin-ichi Fukami, Yumi Matsuzaki, Atsushi Miyawaki, Shigeyoshi Itohara, Hideyuki Okano
Molecular Brain , 2011, DOI: 10.1186/1756-6606-4-14
Abstract: To identify the DNA region affecting Msi1 transcription, we inserted the fusion gene ffLuc, comprised of the fluorescent Venus protein and firefly Luciferase, at the translation initiation site of the mouse Msi1 gene locus contained in a 184-kb bacterial artificial chromosome (BAC). Fluorescence and Luciferase activity, reflecting the Msi1 transcriptional activity, were observed in a stable BAC-carrying embryonic stem cell line when it was induced toward neural lineage differentiation by retinoic acid treatment. When neuronal differentiation was induced in embryoid body (EB)-derived neurosphere cells, reporter signals were detected in Msi1-positive NSCs and GFAP-positive astrocytes, but not in MAP2-positive neurons. By introducing deletions into the BAC reporter gene and conducting further reporter experiments using a minimized enhancer region, we identified a region, "D5E2," that is responsible for Msi1 transcription in NS/PCs.A regulatory element for Msi1 transcription in NS/PCs is located in the sixth intron of the Msi1 gene. The 595-bp D5E2 intronic enhancer can transactivate Msi1 gene expression with cell-type specificity markedly similar to the endogenous Msi1 expression patterns.Neural stem cells (NSCs) are one of the most important research targets in developmental neurobiology, and are attracting attention in strategies for central nervous system (CNS) regeneration [1-6]. NSCs are somatic stem cells that exist in both the embryonic and adult CNS, and they can be defined conceptually as cells that possess both multipotency and the ability for self-renewal [1,2]. Selective NSC markers include the intermediate filament protein Nestin and the RNA-binding protein Musashi1 (Msi1) [7,8]. In the mammalian embryonic CNS, neural stem/progenitor cells (NS/PCs), which include NSCs and neural precursor cells, are present in the ventricular zone of the developing neural tube. Immunoreactivity against Nestin and Msi1 are consistently detected in the ventricular zone [7-9]
Genetic dissection of medial habenula–interpeduncular nucleus pathway function in mice
Yuki Kobayashi,Yoshitake Sano,Elisabetta Vannoni,Hiromichi Goto,Hitomi Suzuki,Atsuko Oba,Hiroaki Kawasaki,Shigenobu Kanba,Hans-Peter Lipp,Niall P. Murphy,David P. Wolfer,Shigeyoshi Itohara
Frontiers in Behavioral Neuroscience , 2013, DOI: 10.3389/fnbeh.2013.00017
Abstract: The habenular complex linking forebrain and midbrain structures is subdivided into the medial (mHb) and the lateral nuclei (lHb). The mHb is characterized by the expression of specific nicotinic acetylcholine receptor isoforms and the release of acetylcholine to the interpeduncular nucleus (IPN), the sole output region of the mHb. The specific function of this circuit, however, is poorly understood. Here we generated transgenic mice in which mHb cells were selectively ablated postnatally. These lesions led to large reductions in acetylcholine levels within the IPN. The mutant mice exhibited abnormalities in a wide range of behavioral domains. They tended to be hyperactive during the early night period and were maladapted when repeatedly exposed to new environments. Mutant mice also showed a high rate of premature responses in the 5-choice serial reaction time task (5-CSRTT), indicating impulsive and compulsive behavior. Additionally, mice also exhibited delay and effort aversion in a decision-making test, deficits in spatial memory, a subtle increase in anxiety levels, and attenuated sensorimotor gating. IntelliCage studies under social housing conditions confirmed hyperactivity, environmental maladaptation, and impulsive/compulsive behavior, delay discounting, deficits in long-term spatial memory, and reduced flexibility in complex learning paradigms. In 5-CSRTT and adaptation tasks, systemic administration of nicotine slowed down nose-poke reaction and enhanced adaptation in control but not mutant mice. These findings demonstrate that the mHb–IPN pathway plays a crucial role in inhibitory control and cognition-dependent executive functions.
Partial sums of certain analytic functions
Shigeyoshi Owa
International Journal of Mathematics and Mathematical Sciences , 2001, DOI: 10.1155/s0161171201005099
Abstract: The object of the present paper is to consider the starlikeness and convexity of partial sums of certain analytic functions in the open unit disk.
On certain Bazilevi functions of order 2
Shigeyoshi Owa
International Journal of Mathematics and Mathematical Sciences , 1992, DOI: 10.1155/s0161171292000796
Abstract: A certain class B(n, ±, 2) of Bazilevi functions of order 2 in the unit disk is introduced. The object of the present paper is to derive some properties of functions belonging to the class B(n, ±, 2). Our result for the class B(n, ±, 2) is the improvement of the theorem by N. E. Cho ([1]).
Generalization properties for certain analytic functions
Shigeyoshi Owa
International Journal of Mathematics and Mathematical Sciences , 1998, DOI: 10.1155/s0161171298000982
Abstract: The object ofthe present paper is to give some generalizations of results for certain analytic functions which were proved by Saitoh (Math. Japon. 35 (1990), 1073-1076). Our results contain some corollaries as the special cases.
On new classes of analytic functions with negative coefficients
Shigeyoshi Owa
International Journal of Mathematics and Mathematical Sciences , 1984, DOI: 10.1155/s0161171284000752
Abstract: We introduce the classes Kn* of analytic functions with negative coefficients by using the nth order Ruscheweyh derivative. The object of the present paper is to show coefficient inequalities and some closure theorems for functions f(z) in Kn*. Further we consider the modified Hadamard product of functions fi(z) in Kni*(n=1,2, ¢ € |,m).
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