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The excitatory glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) contribute to epileptogenesis. Thirty patients with epilepsy and 31 healthy controls are scanned using positron emission tomography with our recently developed radiotracer for AMPARs, [11C]K-2, which measures the density of cell-surface AMPARs. In patients with focal-onset seizures, an increase in AMPAR trafficking augments the amplitude of abnormal gamma activity detected by electroencephalography. In contrast, patients with generalized-onset seizures exhibit a decrease in AMPARs coupled with increased amplitude of abnormal gamma activity. Patients with epilepsy had reduced AMPAR levels compared with healthy controls, and AMPARs are reduced in larger areas of the cortex in patients with generalized-onset seizures compared with those with focal-onset seizures. Thus, epileptic brain function can be regulated by the enhanced trafficking of AMPAR due to Hebbian plasticity with increased simultaneous neuronal firing and compensational downregulation of cell-surface AMPARs by the synaptic scaling.

DOI： 10.1016/j.xcrm.2023.101020

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DOI： 10.1016/j.nucmedbio.2022.04.009

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Presurgical identification of the epileptogenic zone is a critical determinant of seizure control following surgical resection in epilepsy. Excitatory glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor is a major component of neurotransmission. Although elevated α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor levels are observed in surgically resected brain areas of patients with epilepsy, it remains unclear whether increased α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor-mediated currents initiate epileptic discharges. We have recently developed the first PET tracer for α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor, [11C]K-2, to visualize and quantify the density of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors in living human brains. Here, we detected elevated [11C]K-2 uptake in the epileptogenic temporal lobe of patients with mesial temporal lobe epilepsy. Brain areas with high [11C]K-2 uptake are closely colocalized with the location of equivalent current dipoles estimated by magnetoencephalography or with seizure onset zones detected by intracranial electroencephalogram. These results suggest that epileptic discharges initiate from brain areas with increased α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors, providing a biological basis for epileptic discharges and an additional non-invasive option to identify the epileptogenic zone in patients with mesial temporal lobe epilepsy.

DOI： 10.1093/braincomms/fcac023

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The glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) is an important molecule in neurotransmission. We have recently developed the first positron emission tomography (PET) tracer [11C]K-2 to visualize and quantify AMPARs in the living human brain. After injection, [11C]K-2 is hydrolyzed at the terminal amide (and is thus metabolized to a major metabolite, [11C]K-2OH) within 10 min, representing the PET image in rodents and humans. Here, we found that K-2OH did not penetrate the cell membrane but slowly passed through the blood brain barrier (BBB) with paracellular transport. Furthermore, major efflux transporters in the BBB did not carry K-2OH. Logan graphical analysis exhibited reversible binding kinetics of this radiotracer in healthy individuals; these results demonstrated that the PET image of this tracer represents cell surface AMPARs with passive penetration of [11C]K-2OH through the BBB, resulting in reversible binding kinetics. Thus, PET images with this tracer depict the physiologically crucial fraction of AMPARs.

DOI： 10.1016/j.neures.2021.05.009

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

[11C]K-2, a radiotracer exhibiting high affinity and selectivity for α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs), is suitable for the quantification of AMPARs in living human brains and potentially useful in the identification of epileptogenic foci in patients. This study aimed to estimate the radiation doses of [11C]K-2 in various organs and calculate the effective dose after injection of [11C]K-2 in healthy human subjects. Twelve healthy male subjects were registered and divided into two groups (370 or 555 MBq of [11C]K-2), followed by 2 h whole-body scans. We estimated the radiation dose of each organ and then calculated the effective dose for each subject. The highest uptake of [11C]K-2 was observed in the liver, while the brain also showed relatively high uptake. The urinary bladder exhibited the highest radiation dose. The kidneys and liver also showed high radiation doses after [11C]K-2 injections. The effective dose of [11C]K-2 ranged from 5.0 to 5.2 μSv/MBq. Our findings suggest that [11C]K-2 is safe in terms of the radiation dose and adverse effects. The injection of 370-555 MBq (10 to 15 mCi) for PET studies using this radiotracer is applicable in healthy human subjects and enables serial PET scans in a single subject.

DOI： 10.1038/s41598-021-81002-3

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Other Link： http://www.nature.com/articles/s41598-021-81002-3

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Although aberrations in the number and function of glutamate AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors are thought to underlie neuropsychiatric disorders, no methods are currently available for visualizing AMPA receptors in the living human brain. Here we developed a positron emission tomography (PET) tracer for AMPA receptors. A derivative of 4-[2-(phenylsulfonylamino)ethylthio]-2,6-difluoro-phenoxyacetamide radiolabeled with 11C ([11C]K-2) showed specific binding to AMPA receptors. Our clinical trial with healthy human participants confirmed reversible binding of [11C]K-2 in the brain according to Logan graphical analysis (UMIN000020975; study design: non-randomized, single arm; primary outcome: dynamics and distribution volumes of [11C]K-2 in the brain; secondary outcome: adverse events of [11C]K-2 during the 4-10 d following dosing; this trial met prespecified endpoints). In an exploratory clinical study including patients with epilepsy, we detected increased [11C]K-2 uptake in the epileptogenic focus of patients with mesial temporal lobe epilepsy, which was closely correlated with the local AMPA receptor protein distribution in surgical specimens from the same individuals (UMIN000025090; study design: non-randomized, single arm; primary outcome: correlation between [11C]K-2 uptake measured with PET before surgery and AMPA receptor protein density examined by biochemical study after surgery; secondary outcome: adverse events during the 7 d following PET scan; this trial met prespecified endpoints). Thus, [11C]K-2 is a potent PET tracer for AMPA receptors, potentially providing a tool to examine the involvement of AMPA receptors in neuropsychiatric disorders.

DOI： 10.1038/s41591-019-0723-9

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Association for the Advancement of Science  

DOI： 10.1126/science.aao2300

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Although the alteration of glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) distribution is believed to underlie physiologic and pathologic neuronal function, there has been no modality to evaluate AMPARs in a living human. [11C]K-2, the PET tracer we previously developed, is the first and only technology, to the best of our knowledge, to visualize AMPAR densities in the living human brain. Despite its favorable kinetics as a PET tracer, the short half-life of 11C limits the potential of [11C]K-2. We recently developed an 18F-labeled PET tracer, [18F]K-40, which demonstrated AMPAR-specific binding properties and brain distribution similar to that of [11C]K-2 in preclinical studies. The purpose of this first-in-human study is to evaluate the properties of [18F]K-40 in humans and to compare the kinetics and PET images of [18F]K-40 with those of [11C]K-2. Methods: Five healthy volunteers were enrolled and underwent dynamic PET imaging using [18F]K-40 and [11C]K-2. The nondisplaceable binding potential (BPND) with white matter as the reference was calculated by Logan graphical analysis using tissue time-activity curves (TACs), and the total distribution volume of [18F]K-40 was calculated using plasma TACs. The intraindividual correlation between BPND values obtained for [18F]K-40 and [11C]K-2 was examined. To optimize the time window for PET scanning, BPND and SUV ratio were evaluated. Results: The tissue TACs of [18F]K-40 showed curves similar to those of [11C]K-2. Logan graphical analysis using plasma TACs revealed reversible binding of [18F]K-40. The BPND obtained with [18F]K-40 and [11C]K-2 significantly correlated in each corresponding region and showed very good correlation, which indicated that K-40, as observed with K-2, can provide PET images that reflect the amount of AMPARs. A good linear relationship was observed between BPND and the summation image of SUV ratios between 40 and 50 min after radiotracer injection. Conclusion: [18F]K-40, as with [11C]K-2, has favorable binding properties as an AMPAR PET tracer. Thus, [18F]K-40 could characterize AMPAR distribution in pathophysiologic conditions of the brain and facilitate the development of novel diagnostics of neuropsychiatric disorders.

DOI： 10.2967/jnumed.124.269405

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DOI： 10.1093/braincomms/fcaf036

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Publishing type：Research paper (scientific journal)   Publisher：Frontiers Media SA  

Functional recovery from brain damage, such as stroke, is a plastic process in the brain. The excitatory glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) plays a crucial role in neuronal functions, and the synaptic trafficking of AMPAR is a fundamental mechanism underlying synaptic plasticity. We recently identified a collapsin response mediator protein 2 (CRMP2)-binding compound, edonerpic maleate, which augments rehabilitative training-dependent functional recovery from brain damage by facilitating experience-driven synaptic delivery of AMPARs. In animals recovering from cryogenic brain injury, a potential compensatory area adjacent to the injured region was observed, where the injection of CNQX, an AMPAR antagonist, significantly attenuated functional recovery. In the compensatory brain area of animals recovering from cryogenic injury, the administration of edonerpic maleate enhanced both excitatory and inhibitory synaptic inputs at pyramidal neurons. In contrast, recovered animals that did not receive the drug exhibited augmentation of only excitatory synaptic input. The threshold of picrotoxin-induced epileptic seizure in recovered animals without edonerpic maleate treatment was lower than in intact animals and recovered animals with edonerpic maleate. Thus, edonerpic maleate enhances motor function recovery from brain damage by balancing excitatory and inhibitory synaptic inputs, which helps prevent epileptic seizures during recovery.

DOI： 10.3389/fncir.2024.1492043

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BACKGROUND: While altered expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) type receptor has been reported in postmortem studies of schizophrenia, these findings are inconsistent. Therefore, we aimed to systematically review postmortem studies that investigated AMPA receptor expressions in schizophrenia. METHODS: A systematic literature search was conducted for postmortem studies that measured AMPA receptor subunit expressions or receptor bindings in schizophrenia compared to healthy individuals on February 3, 2021, using Medline and Embase. RESULTS: A total of 39 relevant articles were identified from 1360 initial reports. The dorsolateral prefrontal cortex (DLPFC) was the most investigated region (15 studies), followed by the medial temporal lobe (8 studies). For the DLPFC, 4/15 studies (26.7%) showed increased AMPA receptor binding or subunit expression in patients with schizophrenia compared to that in controls, especially in GRIA1 and GRIA4, 2/15 studies (13.3%) reported a decrease, particularly in GRIA2, and 8/15 studies (56.7%) found no significant differences. A decreased expression or receptor binding was observed in 6/8 studies (75.0%) in the subregions of the hippocampus in patients with schizophrenia compared to that in controls, whereas the other two studies found no significant differences. CONCLUSION: Published data have reported decreased subunit expression or receptor binding in the hippocampus in schizophrenia. These findings were inconsistent in other brain regions, which might be due to the heterogeneity of this population, various study design, physiological changes after death, and limited number of studies. Future in vivo studies are warranted to examine AMPA receptor expressions in human brains, together with their comprehensive clinical characterization.

DOI： 10.1016/j.schres.2022.02.033

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Collapsin response mediator proteins (CRMPs) have been identified as mediating proteins of repulsive axon guidance cue Semaphorin-3A (Sema3A). Phosphorylation of CRMPs plays a crucial role in the Sema3A signaling cascade. It has been shown that Fyn phosphorylates CRMP1 at Tyrosine 504 residue (Tyr504); however, the physiological role of this phosphorylation has not been examined. We found that CRMP1 was the most strongly phosphorylated by Fyn among the five members of CRMPs. We confirmed Tyr504 phosphorylation of CRMP1 by Fyn. Immunocytochemistry of mouse dorsal root ganglion (DRG) neurons showed that phosphotyrosine signal in the growth cones was transiently increased in the growth cones upon Sema3A stimulation. Tyr504-phosphorylated CRMP1 also tended to increase after Sema3A simulation. Ectopic expression of a single amino acid mutant of CRMP1 replacing Tyr504 with phenylalanine (CRMP1-Tyr504Phe) suppressed Sema3A-induced growth cone collapse response in chick DRG neurons. CRMP1-Tyr504Phe expression in mouse hippocampal neurons also suppressed Sema3A but not Sema3F-induced growth cone collapse response. Immunohistochemistry showed that Tyr504-phosphorylated CRMP1 was present in the cell bodies and in the dendritic processes of mouse cortical neurons. CRMP1-Tyr504Phe suppressed Sema3A-induced dendritic growth of primary cultured mouse cortical neurons as well as the dendritic development of cortical pyramidal neurons in vivo. Fyn± ; Crmp1± double heterozygous mutant mice exhibited poor development of cortical layer V basal dendrites, which was the similar phenotype observed in Sema3a-/- , Fyn-/- , and Crmp1-/- mice. These findings demonstrate that Tyr504 phosphorylation of CRMP1 by Fyn is an essential step of Sema3A-regulated dendritic development of cortical pyramidal neurons. (247 words).

DOI： 10.1111/jnc.15304

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The semaphorin family is a well-characterized family of secreted or membrane-bound proteins that are involved in activity-independent neurodevelopmental processes, such as axon guidance, cell migration, and immune functions. Although semaphorins have recently been demonstrated to regulate activity-dependent synaptic scaling, their roles in Hebbian synaptic plasticity as well as learning and memory remain poorly understood. Here, using a rodent model, we found that an inhibitory avoidance task, a hippocampus-dependent contextual learning paradigm, increased secretion of semaphorin 3A in the hippocampus. Furthermore, the secreted semaphorin 3A in the hippocampus mediated contextual memory formation likely by driving AMPA receptors into hippocampal synapses via the neuropilin1-plexin A4-semaphorin receptor complex. This signaling process involves alteration of the phosphorylation status of collapsin response mediator protein 2, which has been characterized as a downstream molecule in semaphorin signaling. These findings implicate semaphorin family as a regulator of Hebbian synaptic plasticity and learning.

DOI： 10.1111/ejn.15210

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Publishing type：Research paper (scientific journal)   Publisher：Japan Academy  

Psychiatric and neurological disorders severely hamper patient's quality of life. Despite their high unmet needs, the development of diagnostics and therapeutics has only made slow progress. This is due to limited evidence on the biological basis of these disorders in humans. Synapses are essential structural units of neurotransmission, and neuropsychiatric disorders are considered as "synapse diseases". Thus, a translational approach with synaptic physiology is crucial to tackle these disorders. Among a variety of synapses, excitatory glutamatergic synapses play central roles in neuronal functions. The glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) is a principal component of glutamatergic neurotransmission; therefore, it is considered to be a promising translational target. Here, we review the limitations of current diagnostics and therapeutics of neuropsychiatric disorders and advocate the urgent need for the promotion of translational medicine based on the synaptic physiology of AMPAR. Furthermore, we introduce our recent translational approach to these disorders by targeting at AMPARs.

DOI： 10.2183/pjab.97.001

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Language：Japanese   Publisher：(株)ニュー・サイエンス社  

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PURPOSE OF REVIEW: Stroke is a devastating illness which severely attenuates quality of life because of paralysis. Despite recent advances in therapies during acute phase such as thrombolytic therapy, clinical option to intervene the process of rehabilitation is limited. No pharmacological intervention that could enhance the effect of rehabilitation has not been established. Recent articles, which are summarized in the review article, reported novel small compound which accelerates training-dependent motor function recovery after brain damage. RECENT FINDINGS: A novel small compound, edonerpic maleate, binds to collapsin response mediator protein 2 (CRMP2) and enhance synaptic plasticity leading to the acceleration of rehabilitative training-dependent functional recovery after brain damage in rodent and nonhuman primate. The clinical trial to test this effect in human is now ongoing. Future preclinical and clinical studies will delineate the potentials of this compound. SUMMARY: A novel CRMP2-binding small compound, edonerpic maleate, accelerates motor function recovery after brain damage in rodent and nonhuman primate.

DOI： 10.1097/WCO.0000000000000748

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DOI： 10.1161/STROKEAHA.119.023720

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Neuropsychopharmacology Reports  

BACKGROUND AND OBJECTIVES: Altered trafficking of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors has been reported in postmortem studies and suggested the involvement of AMPA receptors in the pathophysiology underpinning addictive disorders. However, these findings seemed mixed. METHODS: A systematic literature search was conducted, using PubMed and Embase (last search, August 2018), to identify human postmortem studies that examined the expression of proteins and mRNA of AMPA receptor subunits in patients with addictive disorders in comparison with healthy controls. RESULTS: Twelve (18 studies) out of 954 articles were identified to be relevant. Eight studies included alcohol use disorders, and four studies included heroin/cocaine abusers. The most frequently investigated regions were the hippocampus (three studies), amygdala (three studies), and putamen (three studies). In summary, two out of the three studies showed an increase in the expression of AMPA receptors in the hippocampus, while the other study found no change. Two studies to examine the amygdala demonstrated either a decreased or no change in receptor expression or binding. Concerning putamen, two studies showed no significant change whereas an overexpression of receptors was observed in the other. CONCLUSIONS AND SCIENTIFIC SIGNIFICANCE: The hippocampus and amygdala may be pertinent to addictive disorders through their functions on learning and memory, whereas findings in other regions were inconsistent across the studies. Human postmortem studies are prone to degenerative changes after death. Moreover, only qualitative assessment was conducted because of the limited, heterogenous data. These limitations emphasize the need to investigate AMPA receptors in the living human brains.

DOI： 10.1002/npr2.12058

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AIM: While emotional processing is implicated in various psychiatric illnesses, its differences among diagnoses are unclear. We compared associative learning of social values in patients with depression and schizophrenia by measuring skin conductance response to interpersonal stimuli. METHODS: We included 20 female outpatients each with depression and schizophrenia. They underwent Pavlovian conditioning experiments in response to a classical aversive sound, and an interpersonal stimulus that was designed to cause aversive social conditioning with actors' faces coupled with negative verbal messages. Multiple regression analysis was performed to examine the associations between the degree of conditioned response and the clinical characteristics of the participants. RESULTS: Conditioned responses during the acquisition phase in both conditions were higher in depression compared to schizophrenia. Patients with depression successfully showed fear conditioning in both conditions, and they exhibited slower extinction in the interpersonal condition. The conditioned response during the extinction phase showed a positive association with Emotion Regulation Questionnaire Expressive Suppression score, and a negative association with the Emotion Regulation Questionnaire Cognitive Reappraisal score and the use of antidepressants. Patients with schizophrenia did not become conditioned in either of the conditions. The Positive and Negative Syndrome Scale Negative Syndrome score was negatively associated with the degree of conditioned response during the acquisition phase in the interpersonal condition. CONCLUSION: Female patients with schizophrenia, especially those who prominently demonstrated negative symptoms, suggested their intrinsic impairments in the associative learning of social context. Antidepressants and adaptive emotional regulation strategy may enhance the extinction learning of aversive social conditioning in depression.

DOI： 10.1111/pcn.12805

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Throughout life, individuals learn to predict a punishment via its association with sensory stimuli. This process ultimately prompts goal-directed actions to prevent the danger, a behavior defined as avoidance. Neurons in the lateral habenula (LHb) respond to aversive events as well as to environmental cues predicting them, supporting LHb contribution to cue-punishment association. However, whether synaptic adaptations at discrete habenular circuits underlie such associative learning to instruct avoidance remains elusive. Here, we find that, in mice, contingent association of an auditory cue (tone) with a punishment (foot shock) progressively causes cue-driven LHb neuronal excitation during avoidance learning. This process is concomitant with the strengthening of LHb AMPA receptor-mediated neurotransmission. Such a phenomenon occludes long-term potentiation and occurs specifically at hypothalamus-to-habenula synapses. Silencing hypothalamic-to-habenulainputs or optically inactivating postsynaptic AMPA receptors within the LHb disrupts avoidance learning. Altogether, synaptic strengthening at a discrete habenular circuit transforms neutral stimuli into salient punishment-predictive cues to guide avoidance.

DOI： 10.1016/j.neuron.2019.01.025

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DOI： 10.1038/s41598-017-08849-3

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DOI： 10.1038/nbt.3710

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DOI： 10.1073/pnas.1606351113

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DOI： 10.1186/s13041-016-0267-6

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DOI： 10.1016/j.stemcr.2016.01.010

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DOI： 10.1371/journal.pone.0149068

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Experience-dependent plasticity is limited in the adult brain, and its molecular and cellular mechanisms are poorly understood. Removal of the myelin-inhibiting signaling protein, Nogo receptor (NgR1), restores adult neural plasticity. Here we found that, in NgR1-deficient mice, whisker experience-driven synaptic α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) insertion in the barrel cortex, which is normally complete by 2 weeks after birth, lasts into adulthood. In vivo live imaging by two-photon microscopy revealed more AMPAR on the surface of spines in the adult barrel cortex of NgR1-deficient than on those of wild-type (WT) mice. Furthermore, we observed that whisker stimulation produced new spines in the adult barrel cortex of mutant but not WT mice, and that the newly synthesized spines contained surface AMPAR. These results suggest that Nogo signaling limits plasticity by restricting synaptic AMPAR delivery in coordination with anatomical plasticity.

DOI： 10.1093/cercor/bhv232

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DOI： 10.1371/journal.pone.0131359

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DOI： 10.1371/journal.pone.0125729

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DOI： 10.1097/ALN.0000000000000269

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DOI： 10.1016/j.neuroscience.2013.06.040

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DOI： 10.1111/ejn.12188

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DOI： 10.1038/ncomms3760

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DOI： 10.1172/JCI63060

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DOI： 10.1016/j.brainres.2011.11.033

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DOI： 10.1073/pnas.1104558108

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DOI： 10.4161/cib.4.4.15470

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DOI： 10.1016/j.neuron.2011.01.016

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DOI： 10.1074/jbc.M109.046284

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DOI： 10.1016/j.neures.2010.07.1261

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DOI： 10.1111/j.1460-9568.2009.07002.x

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Acetylcholine (ACh) release in the dorsal hippocampus increases during stress, exploration or learning, exhibiting sex-specific 24-h release profile. We review the role of gonadal steroids on the ACh release in the dorsal hippocampus. In our studies, we found that male rats showed higher extracellular ACh levels than females, but gonadectomy decreased ACh levels in both sexes of rats and subsequently eliminated the sex difference. To examine the sex difference under comparable gonadal steroid levels, we implanted steroid capsules after gonadectomy. Oestradiol supplementation maintained circulating oestradiol to the levels in proestrous female rats, whereas testosterone capsules maintained circulating testosterone to the levels similar to intact male rats. Under comparable gonadal steroids levels, ACh levels were sex-specific. Testosterone replacement in orchidectomised rats clearly restored ACh levels, which were greater than ovariectomised testosterone-primed rats. Similarly, oestradiol replacement in ovariectomised rats successfully restored ACh levels, which were higher than orchidectomised oestradiol-primed rats. These results suggest sex-specific activational effects of gonadal steroids on ACh release. To further examine the organisational effect, female pups were neonatally treated with oil, testosterone, oestradiol, or dihydrotestosterone. These rats were bilaterally ovariectomised and a testosterone capsule was implanted at postnatal week 8. Neonatal treatment of either testosterone or oestradiol clearly increased ACh levels, whereas neonatal dihydrotestosterone treatment failed to change levels. These results suggest that: (i) gonadal steroids maintain the sex-specific ACh release in the dorsal hippocampus and (ii) neonatal activation of oestrogen receptors is sufficient to mediate masculinisation of the septo-hippocampal cholinergic system.

DOI： 10.1111/j.1365-2826.2009.01848.x

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Acetylcholine (ACh) release in the dorsal hippocampus increases during stress, exploration or learning, exhibiting sex-specific 24-h release profile. We review the role of gonadal steroids on the ACh release in the dorsal hippocampus. In our studies, we found that male rats showed higher extracellular ACh levels than females, but gonadectomy decreased ACh levels in both sexes of rats and subsequently eliminated the sex difference. To examine the sex difference under comparable gonadal steroid levels, we implanted steroid capsules after gonadectomy. Oestradiol supplementation maintained circulating oestradiol to the levels in proestrous female rats, whereas testosterone capsules maintained circulating testosterone to the levels similar to intact male rats. Under comparable gonadal steroids levels, ACh levels were sex-specific. Testosterone replacement in orchidectomised rats clearly restored ACh levels, which were greater than ovariectomised testosterone-primed rats. Similarly, oestradiol replacement in ovariectomised rats successfully restored ACh levels, which were higher than orchidectomised oestradiol-primed rats. These results suggest sex-specific activational effects of gonadal steroids on ACh release. To further examine the organisational effect, female pups were neonatally treated with oil, testosterone, oestradiol, or dihydrotestosterone. These rats were bilaterally ovariectomised and a testosterone capsule was implanted at postnatal week 8. Neonatal treatment of either testosterone or oestradiol clearly increased ACh levels, whereas neonatal dihydrotestosterone treatment failed to change levels. These results suggest that: (i) gonadal steroids maintain the sex-specific ACh release in the dorsal hippocampus and (ii) neonatal activation of oestrogen receptors is sufficient to mediate masculinisation of the septo-hippocampal cholinergic system.

DOI： 10.1111/j.1365-2826.2009.01848.x

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DOI： 10.1016/j.brainres.2008.12.084

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DOI： 10.1016/j.neulet.2008.06.077

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DOI： 10.1523/JNEUROSCI.3463-07.2007

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DOI： 10.1523/JNEUROSCI.4276-06.2006

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DOI： 10.1126/science.1079886

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DOI： 10.1016/S0896-6273(01)00216-1

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DOI： 10.1016/S0092-8674(00)80062-8

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DOI： 10.1002/(SICI)1097-4695(19990615)39:4<579::AID-NEU11>3.0.CO;2-9

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DOI： 10.1016/S0896-6273(00)80626-1

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DOI： 10.1016/0378-1119(94)90690-4

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DOI： 10.1007/BF01233381

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Language：Japanese   Publisher：(公社)日本リハビリテーション医学会  

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Language：Japanese   Publisher：(株)アドスリー  

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Language：Japanese   Publisher：(株)ニュー・サイエンス社  

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Language：Japanese   Publisher：(株)ニュー・サイエンス社  

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Language：Japanese   Publisher：(一社)日本頭痛学会  

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Language：Japanese   Publisher：(公社)日本精神神経学会  

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Language：Japanese   Publisher：日本うつ病学会・日本認知療法・認知行動療法学会  

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Language：Japanese   Publisher：医歯薬出版(株)  

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Language：Japanese   Publisher：(株)中外医学社  

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Language：Japanese   Publisher：日本臨床外科学会  

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Language：Japanese   Publisher：Japanese Association of Physical Therapy Fundamentals  

DOI： 10.24780/jptf.23.1_37

CiNii Research

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Other Link： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2021&ichushi_jid=J05805&link_issn=&doc_id=20210319280006&doc_link_id=%2Fch1thrpy%2F2020%2F002301%2F006%2F0037-0045%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fch1thrpy%2F2020%2F002301%2F006%2F0037-0045%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(株)中外医学社  

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Language：Japanese   Publisher：(一社)日本認知症学会  

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Language：Japanese   Publisher：(株)ニュー・サイエンス社  

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Language：Japanese   Publisher：(一社)日本小児神経学会  

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Language：Japanese   Publisher：エーザイ(株)  

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Language：Japanese   Publisher：(株)ニュー・サイエンス社  

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Language：Japanese   Publisher：エーザイ(株)  

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Language：Japanese   Publisher：メディカルレビュー社  

CiNii Books

CiNii Research

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Language：Japanese   Publisher：(株)メディカルレビュー社  

CiNii Books

CiNii Research

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Other Link： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2019&ichushi_jid=J05023&link_issn=&doc_id=20191113270003&doc_link_id=%2Fai1epild%2F2019%2F001302%2F004%2F0081-0086%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fai1epild%2F2019%2F001302%2F004%2F0081-0086%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：日本臨床精神神経薬理学会・日本神経精神薬理学会  

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Language：Japanese   Publisher：(一社)日本核医学会  

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Language：Japanese   Publisher：(公社)日本リハビリテーション医学会  

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Language：Japanese   Publisher：(公社)日本リハビリテーション医学会  

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Language：Japanese   Publisher：日本臨床分子医学会  

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Language：Japanese   Publisher：医歯薬出版(株)  

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Other Link： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2019&ichushi_jid=J00060&link_issn=&doc_id=20190218030009&doc_link_id=issn%3D0039-2359%26volume%3D268%26issue%3D7%26spage%3D585&url=http%3A%2F%2Fwww.pieronline.jp%2Fopenurl%3Fissn%3D0039-2359%26volume%3D268%26issue%3D7%26spage%3D585&type=PierOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00005_2.gif

Language：Japanese   Publisher：(一社)日本核医学会  

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Language：Japanese   Publisher：日本臨床精神神経薬理学会・日本神経精神薬理学会  

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Language：Japanese   Publisher：(株)先端医学社  

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Language：Japanese   Publisher：(公社)日本リハビリテーション医学会  

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Language：Japanese   Publisher：生命科学系学会合同年次大会運営事務局  

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Language：English   Publisher：(一社)日本てんかん学会  

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Language：Japanese   Publisher：(一社)日本理学療法学会連合  

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Language：Japanese  

CiNii Books

CiNii Research

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Language：Japanese  

J-GLOBAL

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Language：Japanese   Publisher：(株)羊土社  

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：Japanese   Publisher：Japanese Society of Neurological Therapeutics  

DOI： 10.15082/jsnt.33.3_394

CiNii Research

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Other Link： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2016&ichushi_jid=J02615&link_issn=&doc_id=20170202470030&doc_link_id=10.15082%2Fjsnt.33.3_394&url=https%3A%2F%2Fdoi.org%2F10.15082%2Fjsnt.33.3_394&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

Language：Japanese   Publisher：金原一郎記念医学医療振興財団 ; 1949-  

DOI： 10.11477/mf.2425200397

CiNii Books

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Language：Japanese   Publisher：日本神経治療学会  

J-GLOBAL

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Language：Japanese  

J-GLOBAL

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Language：Japanese   Publisher：日本神経治療学会  

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Language：Japanese   Publisher：(一社)日本小児神経学会  

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Language：Japanese   Publisher：(株)中外医学社  

J-GLOBAL

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Language：English  

DOI： 10.1172/JCI76901

Web of Science

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Language：Japanese   Publisher：(一社)日本生理学会  

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Language：Japanese   Publisher：(一社)日本生理学会  

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Language：Japanese   Publisher：(一社)日本生理学会  

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Language：Japanese   Publisher：京都大学霊長類研究所  

CiNii Books

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Language：Japanese   Publisher：(公社)日本理学療法士協会  

DOI： 10.14900/cjpt.2012.0.48100735.0

J-GLOBAL

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：Japanese   Publisher：(公社)日本薬理学会  

CiNii Books

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Language：Japanese  

CiNii Books

J-GLOBAL

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Publisher：6  

PubMed

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Language：English  

CiNii Books

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Publisher：4  

DOI： 10.4161/cib.4.4.15470

PubMed

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Language：Japanese  

J-GLOBAL

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Language：Japanese   Publisher：(株)先端医学社  

CiNii Books

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Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2011.07.1413

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2011.07.242

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2011.07.897

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2011.07.270

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2011.07.1416

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2011.07.1651

Web of Science

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Language：Japanese   Publisher：第一三共生命科学研究振興財団  

CiNii Books

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Language：English   Publisher：(公社)日本生化学会  

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Language：English   Publisher：(一社)日本神経化学会  

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Language：English   Publisher：日本神経化学会  

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Language：English   Publisher：(一社)日本神経化学会  

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Language：English   Publisher：(一社)日本神経化学会  

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Language：English   Publisher：(一社)日本神経化学会  

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Language：English   Publisher：(一社)日本神経化学会  

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Language：Japanese  

DOI： 10.11477/mf.2425100958

J-GLOBAL

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Language：Japanese   Publisher：横浜市立大学医学会  

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Language：Japanese   Publisher：金原一郎記念医学医療振興財団  

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2010.07.1776

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2010.07.1230

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2010.07.155

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2010.07.2537

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2010.07.1522

Web of Science

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Language：Japanese  

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Language：English   Publisher：(一社)日本神経化学会  

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Language：Japanese  

J-GLOBAL

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Language：Japanese   Publisher：(公財)ライフサイエンス振興財団  

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2009.09.1235

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2009.09.051

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2009.09.219

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2009.09.216

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.neures.2009.09.156

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：Japanese   Publisher：(公財)上原記念生命科学財団  

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Language：Japanese   Publisher：(株)羊土社  

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Web of Science

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Publisher：PHYSIOLOGICAL SOCIETY OF JAPAN  

Sex differences in the response to nociceptive stimuli have long been recognized in many species. For example, in rats, females are more sensitive to formalin-induced nociceptive stimuli than males, as revealed by behavioral test. However, the neural mechanism for sex differences in the response to nociceptive stimuli was still unclear. In the previous study, we showed that females were more sensitive to formalin-induced nociceptive stimuli than males, as revealed by behavioral test. We looked for a possible sex difference in the response of the brain to formalin-induced nociceptive stimuli by checking the expression of phosphorylated cAMP response element-binding protein (pCREB) as a marker of neural activity. We found that, in the bed nucleus of the stria terminalis lateral subdivision (BSTL), the number of cells expressing pCREB was increased 5-10 min after formalin injection in female rats but not in male rats. In the present study, we examined the function of CREB in the BSTL. We found that the expression of a dominant negative form of CREB (mCREB) using adenovirus vector, significantly attenuated the response to formalin only in females but not in males, suggesting that CREB in the BSTL play a role for controlling pain-related behavior only in females. &lt;b&gt;[J Physiol Sci. 2008;58 Suppl:S165]&lt;/b&gt;

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Publisher：PHYSIOLOGICAL SOCIETY OF JAPAN  

The brain initiates activation of the gonadotropin-releasing hormone (GnRH) system at puberty onset. Since GnRH neurons are suggested to show a plasticity during postnatal development, remodeling of GnRH neurons may be involved in the onset of puberty. The present study was done by attempting to block plasticity in the GnRH neuronal network, by interfering with the synaptic delivery of GluR1 whose trafficking is critical in synaptic plasticity and thus necessary for memory. To this end, GluR1-C-tail, a dominant negative mutant of GluR1, was expressed in the POA of female rats at day 21 using lentivirus. GluR1-C-tail has been shown to act by competing with GluR1 for synaptic delivery during synaptic plasticity. As the result, the onset of puberty, by checking viginal opening, was significantly delayed. After that, the estrous cyclicity was checked by viginal smear and found that the rat injected with GluR1-C-tail exhibited a regular estrous cycle. However, the surge of luteinizing hormone (LH) secretion in the rat injected with GluR1-C-tail was significantly attenuated, compared to the control rat. Injection with GluR1-C-tail in mature rats had no effect on the surge of LH secretion. The present study suggests that GluR1-mediated plasticity occurs at the time of puberty and is important to maintain surge of LH secretion in adults. &lt;b&gt;[J Physiol Sci. 2008;58 Suppl:S140]&lt;/b&gt;

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Language：Japanese   Publisher：(一社)日本肥満学会  

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Language：Japanese   Publisher：東京生化学研究会  

CiNii Books

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Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

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Language：Japanese   Publisher：(株)学研メディカル秀潤社  

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Language：Japanese   Publisher：秀潤社  

CiNii Books

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CiNii Books

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Other Link： http://search.jamas.or.jp/link/ui/2000267642

Language：Japanese  

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Language：Japanese   Publisher：(株)学研メディカル秀潤社  

CiNii Books

CiNii Research

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Language：Japanese   Publisher：(株)学研メディカル秀潤社  

CiNii Books

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Language：Japanese   Publisher：(株)学研メディカル秀潤社  

CiNii Books

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Language：Japanese   Publisher：(株)羊土社  

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Language：Japanese   Publisher：(株)メディカルレビュー社  

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