Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology (Nihon Shinkei Seishin Yakurigaku Zasshi Jpn J Psychopharmacol )

Publisher: Nihon Shinkei Seishin Yakuri Gakkai


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    Japanese journal of psychopharmacology
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    ABSTRACT: Obesity is the most critical factor in the pathology of metabolic syndrome (MetS), and is associated with an increased risk of depression. The imbalance of hormones and neural peptides which are involved in energy regulation are observed in obesity. It becomes evident that these hormones and neural peptides also affect mood. Leptin plays a pivotal role in energy regulation mainly acting in the hypothalamus of the brain. Although obese humans and rodents usually have high circulating levels of leptin, leptin neither reduces food intake nor increases energy expenditure. This paradoxical situation in obesity has been termed "leptin resistance", which is considered to be a central dogma for obesity. Based on these observations, we examined the functional significance of leptin in the regulation of the depressive state in diet-induced obese (DIO) mice. Our recent study demonstrated that DIO mice showed severe depressive behavior without response to the antidepressant effect of leptin, which is, in part, due to the impairment of leptin action in the hippocampus (Yamada, et al., Endocrinology, 2011). MetS and CNS dysfunction might have common pathological bases vulnerable to these disorders. Our future direction is to investigate a new treatment strategy of MetS by analyzing CNS dysfunction associated with obesity.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):245-50.
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    ABSTRACT: The incidence of dementia and diabetes mellitus is increasing at an alarming rate, and has become a major public health concern all over the world. Recent epidemiological studies suggest that the risk of Alzheimer's disease is increased in individuals with diabetes mellitus, although the underlying mechanisms remain largely unknown. To analyze underlying mechanisms linking Alzheimer's disease and diabetes mellitus, we established unique animal models that show pathological manifestations of both diseases. Our findings suggest that impaired brain insulin signaling and cerebrovascular changes could be potential underlying mechanisms for this relationship. On the other hand, interestingly, Alzheimer's amyloid pathology aggravated diabetes mellitus in these mouse models, suggesting the presence of mutual interaction between these diseases. In addition, we also found that plasma Abeta levels rapidly and strikingly increased after glucose loading in Alzheimer's disease mouse models, which could be a novel diagnostic marker of Alzheimer's disease. The current review summarizes the results of our recent studies on the pathological relationship between these diseases, which could provide novel insights into this intensely debated association.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):239-44.
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    ABSTRACT: Amyotrophic lateral sclerosis (ALS) is an adult onset neurodegenerative disorder characterized by the death of upper and lower motor neurons. About 10% of all ALS cases are familial; approximately 20% of familial ALS cases are caused by mutations in the superoxide dismutase 1 (SOD1) gene. We developed rats that express a human SOD1 transgene with ALS-associated mutations, developing striking motor neuron degeneration and paralysis. The larger size of this rat model as compared with the ALS mice, will facilitate studies involving manipulations of spinal fluid and the spinal cord. Hepatocyte growth factor (HGF) is one of the most potent survival-promoting factors for motor neurons. We administered human recombinant HGF (hrHGF) by continuous intrathecal delivery to the transgenic rats at the onset of paralysis for 4 weeks. Intrathecal administration of hrHGF attenuated motor neuron degeneration and prolonged the duration of the disease by 63%. To translate this strategy to human treatment, we induced a contusive cervical spinal cord injury in the common marmoset, a primate, and then administered hrHGF intrathecally. The intrathecal administration of hrHGF promoted functional recovery. These results prompted further clinical trials in ALS using continuous intrathecal administration of hrHGF.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):287-92.
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    ABSTRACT: Alpha-synuclein (SNCA) gene expression is an important factor in the pathogenesis of Parkinson's disease (PD). Gene multiplication can cause inherited PD, and promoter polymorphisms that increase SNCA expression are associated with sporadic PD. CpG methylation in the promoter region may also influence SNCA expression. By using cultured cells, we identified a region of the SNCA CpG island in which the methylation status altered along with increased SNCA expression. Postmortem brain analysis revealed regional non-specific methylation differences in this CpG region in the anterior cingulate and putamen among controls and PD; however, in the substantia nigra of PD, methylation was significantly decreased. This CpG region may function as an intronic regulatory element for the SNCA gene. Our findings suggest that a novel epigenetic regulatory mechanism controlling SNCA expression influences PD pathogenesis.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):269-73.
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    ABSTRACT: Metabolic disorders, such as diabetes and obesity, have been indicated to disturb the function of the central nervous system (CNS) as well as several peripheral organs. Clinically, it is well recognized that the prevalence of anxiety and depression is higher in diabetic and obesity patients than in the general population. We have recently indicated that streptozotocin-induced diabetic and diet-induced obesity mice have enhanced fear memory and higher anxiety-like behavior in several tests such as the conditioned fear, tail-suspension, hole-board and elevated open-platform tests. The changes in fear memory and anxiety-like behavior of diabetic and obese mice are due to the dysfunction of central glutamatergic and monoaminergic systems, which is mediated by the changes of intracellular signaling. These results suggest that metabolic disorders strongly affect the function of the CNS and disturb the higher brain functions. These dysfunctions of the CNS in diabetes and obesity are involved in the increased prevalence of anxiety disorders and depression. Normalization of these dysfunctions in the CNS will be a new attractive target to treat the metabolic disorders and their complications.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):251-5.
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    ABSTRACT: Epigenetic mechanisms typically involve heritable alterations in chromatin structure, which, in turn, regulate gene expression. Fundamental insights about epigenetic heritability have come from studies of cell division and development. However, there is increasing evidence that the regulation of chromatin structure through histone modifications and DNA methylation might mediate the expression of key genes involved in acquired chronic disorders. This idea is fascinating because similar mechanisms are used for triggering and storing long-term memories at the cellular level during, for example, higher-brain dysfunction, stress disease, drug dependence, aging, and chronic pain. This review will explore the most current issues in the field of epigenetics, with a focus on next levels of transcriptional mechanisms underlying aging, enriched environment and drug addiction. Epigenetic mechanisms, which are key cellular and molecular processes that integrate diverse environmental stimuli to exert potent and often long-lasting changes in gene expression through the regulation of chromatin structure, contribute to transcriptional and behavioral changes.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):275-80.
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    ABSTRACT: Social cognition is defined as the capacity to engage in information processing with the aim of accurate cognition of other persons' character or intentions. Development of social cognition can be observed in behavioral patterns. However, their neural basis remains largely unknown. A functional neuroimaging technique has enabled us to observe neural activities in the human brain noninvasively. First the principle and history of functional magnetic resonance imaging (fMRI), and its future perspective are introduced. As an example, presented is our attempt to apply simultaneous fMRI measurements of two individuals to elucidate the neural basis of joint attention, one of the most important behavioral milestones in the development of social cognition. Second, neural substrates of pro-social behavior are discussed. Specifically, it was found that social acceptance or praise is important for human altruistic behavior, and has a neural basis similar to that of basic reward or monetary reward. Lastly, I stress the importance of combining current and ongoing progress in neuroscience, from the 'micro' through 'macro' levels, with scholarship within the humanities. As a connecting node for the different research fields, functional neuroimaging techniques will play a critical for the ultimate goal of comprehensive understanding of human social cognition.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):299-303.
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    ABSTRACT: Neurological injuries are widely known to promote neurogenesis in the adult hippocampal dentate gyrus. Our previous studies demonstrated that the granule cells in the hippocampal dentate gyrus are injured and eradicated by treatment with trimethyltin (TMT), with being regenerated in the dentate granule cell layer (GCL) after neuronal loss. Recent collective reports indicate that during brain injury and in neurodegenerative disorders, neurogenesis is controlled by cytokines, chemokines, neurotransmitters, and reactive oxygen/nitrogen species, which are released by dying neurons as well as by activated macrophages, micro-glia, and astrocytes. To elucidate the role of activated microglia in the neuroregeneration following the dentate granule cell loss, in this study, we evaluated the involvement of activated microglial cells and a related factor in the generation of newly-generated cells of the hippocampal dentate gyrus following neuronal loss induced by TMT. Our results support the possibility that pro-inflammatory cytokines released from activated microglial cells may be involved in promotion of the neurogenesis mechanism through activation of the NF-kappaB signaling pathway following the dentate neuronal loss induced by TMT treatment.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):281-5.
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    ABSTRACT: Recent research has demonstrated that complex 'epigenetic' mechanisms, which regulate gene transcription without altering the DNA code, could play a critical role in the pathophysiology of psychiatric disorders. We previously reported that pretreatment of mice with 5-HT(1A) receptor agonists 24 hr before testing suppressed the decrease in emotional behaviors induced by exposure to acute restraint stress. In addition, DNA microarray analysis showed that such a pretreatment with 5-HT(1A) receptor agonist produces changes in several gene transcriptions in the hippocampus including the reduction of histone deacetylase 10. Based on these findings, we recently carried out studies focused on the relationship between the development of emotional resistance to stress and histone acetylation induced by a 5-HT(1A) receptor agonist as well as a histone deacetylase inhibitor. The findings suggest that 5-HT(1A) receptor agonists may be useful for preventing mental illnesses that arise due to a decreased resistance and adaptability to stress. Moreover, the notion that chromatin remodeling is an important mechanism in mediating emotionality under stressful situations is further supported.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):263-7.
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    ABSTRACT: Although mammalian neurogenesis is mostly completed by the perinatal period, new neurons are continuously generated throughout adulthood in the restricted regions of the brain. Newly generated neurons are incorporated into the neural networks of both the hippocampal dentate gyrus and the olfactory bulb, and there is growing evidence that adult neurogenesis is important for various brain functions. Continuous neurogenesis is achieved by the coordinated proliferation and differentiation of adult neural stem cells. In this review, we discuss the recent findings concerning the roles of Notch signaling and Hes-family genes in adult neural stem cells. We also discuss the recent findings about the integration mode of new neurons into the existing neural circuits and the potential significance of adult neurogenesis in higher brain functions, such as spatial and olfactory memory.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):293-7.
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    ABSTRACT: The atypical antipsychotic medication olanzapine is a useful agent in acute and maintenance treatment of schizophrenia and related disorders. It has beneficial effects on both positive and negative symptoms, an early onset of antipsychotic action and a favourable side effect profile. On the other hand, olanzapine has many reports of causing weight gain, glucose metabolism disturbances and lipidosis. We carried out blood tests (leptin, adiponectin, remnant-like lipoprotein cholesterol (RLP-C), total cholesterol, HbA1C, 75-OGTT and etc.) on patients with schizophrenia who had taken olanzapine. As a result, leptin, neutral lipid and RLP-C were significantly correlated by BMI. (The average blood test data and BMI revealed a normal range). Most analysis results of the lipoprotein fraction by a polyacrylamide-gel-electrophoresis method were normal patterns. Furthermore, the serum insulin concentrations from 75 g glucose tolerance (75 g-OGTT) 30 minutes later, in one third of patients receiving olanzapine, registered more than 100 microU/ml. The mechanism of the insulin secretion rise by olannzapine is unknown. Olanzapine may impair glucose tolerance due in part to increased insulin resistance. These findings do not necessarily imply that olanzapine is directly associated with a risk of impairment of weight gain, glucose metabolism disturbances and lipidosis. These results suggest that it is useful to promote diet cure and exercise therapy with patients with high BMI levels.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 11/2012; 32(5-6):257-61.
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    ABSTRACT: Pharmacological agents enhancing fear extinction may be promising tools for the treatment of PTSD. Histone acetylation is involved in memory formation, and histone deacetylase (HDAC) inhibitors increase histone acetylation and subsequently enhance fear extinction. In this study, we examined whether vorinostat, an HDAC inhibitor, facilitated fear extinction, using a contextual fear conditioning (FC) paradigm. We found that vorinostat facilitated fear extinction. Next, the levels of global acetylated histone were measured by Western blotting. We also assessed the effect of vorinostat on the hippocampal levels of NMDA receptor mRNA by real-time quantitative PCR (RT-PCR). The levels of acetylated histone and NR2B mRNA, but not NR1 or NR2A mRNA, were elevated in the hippocampus 2 h after administration of vorinostat. We investigated the levels of acetylated histones and phospho-CREB (p-CREB) binding at the promoter of the NR2B gene using the chromatin immunoprecipitation (ChIP) assay followed by RT-PCR. The levels of acetylated histone and the binding of p-CREB to its binding site at the promoter of the NR2B gene were increased. These findings suggest that vorinostat in conjunction with exposure therapy can be a promising new avenue for the treatment of PTSD.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):195-201.
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    ABSTRACT: Depression is a stress-induced disorder and there is compelling evidence for the involvement of hypothalamic-pituitary-adrenal (HPA) axis abnormalities in the disease. Chronic hyperactivity of the HPA axis and resultant excessive glucocorticoid (hypercortisolism) may be causal to depression. We demonstrated that the dexamethasone (DEX)/CRH test is a sensitive state-dependent marker to monitor HPA axis abnormalities. Restoration from HPA axis abnormalities occurs with clinical responses to treatment. Brain-derived neurotrophic factor (BDNF) has also been implicated in depression. We found that glucocorticoid (DEX) suppresses BDNF-induced dendrite outgrowth and synaptic formation via blocking the MAPK pathway in early-developing cultured hippocampal neurons. Furthermore, we demonstrated that glucocorticoid receptor (GR) and TrkB (a specific receptor of BDNF) interact and that DEX acutely suppresses BDNF-induced glutamate release by affecting the PLC-gamma pathway in cultured cortical neurons, indicating a mechanism underlying the effect of excessive glucocorticoid on BDNF function and resultant damage in cortical neurons. In a macroscopic view using magnetic resonance imaging (MRI), we found that individuals with hypercortisolism detected by the DEX/CRH test demonstrated volume loss in gray matter and reduced neural network assessed with diffusion tensor imaging in several brain regions. Finally, we observed that individuals with hypocortisolism detected by the DEX/CRH test tend to present more distress symptoms, maladaptive coping styles, and schizotypal personality traits than their counterparts, which points to the important role of hypocortisolism as well as hypercortisolism in depression spectrum disorders.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):203-9.
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    ABSTRACT: The relationship between the polymorphisms (SNPs) of the beta-adrenergic receptor (beta-AR) gene and personality assessed by TCI (Temperament and Character Inventory), was studied among 192 healthy Japanese subjects (121 male subjects and 71 female subjects). In this study, the statistical analyses were performed overall and separately for each sex. As a result, it was shown that there were significant relationships between SD (self-directedness) and 49Ser/Gly (rs1801252) in ADRB1, P (persistence) and 389Arg/Gly (rs1801253) in ADRB1, and ST (self-transcendence) and 27Gln/Glu (rs1042714) in ADRB2 overall. Among the male subjects, there were further significant relationships between ST and 49Ser/Gly in ADRB1, NS (novelty-seeking), HA (harm avoidance) and P and 389Arg/Gly in ADRB1, and P and 64Arg/Trp(rsrs4994) in ADRB3. Among the female subjects, there were also significant relationships between SD and 49Ser/Gly in ADRB1, and C (cooperativeness) and 389Arg/Gly in ADRB1. Thus it was shown that there were correlations between beta-AR gene polymorphisms and several subscales of TCI.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):227-31.
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    ABSTRACT: Collegium Internationale Neuropsychopharmacologicum (CINP) is an international society which was established to facilitate academic exchange of basic and clinical studies related to psychotropic drugs. The CINP has been devoted to the problems of methodology and to the analysis of the pharmacological and therapeutic results with psychotropic drugs under normal and pathological conditions as well to the medico-social implications of neuropsychopharmacology. The CINP was organized by Prof. Trabucchi (Milan) in collaboration with an international team of neuropsychopharmacologists from 15 countries. The first International CINP Congress was held on September of 1958 in Rome. Thereafter, CINP world congresses were held every two years until 2012. The number of Japanese neuropsycho-pharmacologists who are members has been increasing since the 1970s. The 17th CINP Congress was held in Kyoto in 1990, and the CINP Hiroshima regional meeting was held, combined the annual meeting of the Japanese Society of Neuropsychopharmacology and Korean Society of Psychopharmacology in 2001. The early history of CINP between 1958 and 2000 is briefly described with special reference to the participation of the Japanese Society of Neuropsychopharmacology.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):173-80.
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    ABSTRACT: Recent research has raised the notion that epigenetic mechanisms (e.g., DNA methylation and histone modifications), which exert lasting control over gene expression without altering the genetic code, could mediate stable changes in brain function. However, the role of environmental factors along with genetic factors in the epigenetic regulation of the pathogenesis of depression is largely unknown. Two genetically distinct mice strains, BALB/c (BALB) and C57BL/6 (B6), exhibit different behavioral responses to chronic stress. With chronic stress, BALB mice showed depressive-like behaviors, but not B6 mice, and glial cell-derived neurotrophic factor (GDNF) expression level was decreased in the ventral striatum of BALB mice but increased in B6 mice. In BALB mice, depressive-like behaviors and decreased GDNF expression were recovered by chronic antidepressant treatment. Therefore, we used these two mice strains to investigate how the epigenetic status of the GDNF gene in the ventral striatum modulates stress vulnerability. Both mice strains showed increased DNA methylation levels and MeCP2 recruitment in the GDNF promoter region. However, histone H3 acetylation level was decreased in BALB mice, but increased in B6 mice. Furthermore, BALB mice showed increased histone deacetylase2 (HDAC2) expression level and Re-ChIP assay revealed HDAC2-MeCP2 complex in BALB mice. Our results indicate the crucial role of histone modification by HDAC2 and MeCP2 complex for the control of GDNF expression and subsequent behavioral responses to chronic stress, in other words, the susceptibility to stress. In addition, we investigated the effect of antidepressants on the epigenetic regulation of GDNF expression. We found a reduced level of HDAC4 recruitment at the GDNF promoter region with antidepressants. Thus, our data suggest that antidepressants increase transcriptional activity of the GDNF gene through the modulation of histone acetylation by HDAC4. Finally, we examined the expressions of GDNF and epigenetic-related molecules mRNAs with major depressive and bipolar disorder patients by using quantitative real-time PCR. We found the aberrant expression of GDNF and epigenetic-related genes including HDAC2 and HDAC4 in mood disorder patients. Thus, our data provide novel insights suggesting that epigenetic mechanisms of GDNF expression are involved in the pathogenesis or pathophysiology of depression.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):181-6.
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    ABSTRACT: The neuropathology of psychiatric disorders has long been of interest in psychiatry. Several abnormalities in the prefrontal cortex have been demonstrated in major depressive disorders; however, only a small number of quantitative studies have been conducted, partly because the stereological techniques often used for such investigations are hampered by intrinsically low throughput, typically requiring long periods of time to complete. Recently, we developed a quantitative cell-counting method for frozen unfixed postmortem brains using a flow cytometer. Anisotropic frozen brain tissue was transformed into an isotropic suspension of nuclei; the numbers and fluorescent intensities of 7-AAD(+), a DNA marker, were quantified; and the nuclei were immunolabeled for the neuronal and oligodendroglial nuclear markers, NeuN and olig2, respectively. Using this method, the frontopolar and inferior temporal cortical gray matter of major depressive disorder patients, as well as that of normal controls, was analyzed. We found that the densities of 7-AAD(+) and olig2(+) nuclei in the gray matter tissue of the frontopolar cortex from major depressive disorder subjects were significantly reduced when compared to those from controls, but not in the inferior temporal cortex. Our findings suggest that the pathogenesis of major depressive disorders may involve some abnormalities in cortical myelination in the adult frontopolar cortex.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):211-8.
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    ABSTRACT: Recently, abnormalities of glutamatergic transmission have been implicated in the pathophysiology of depression. Moreover, both ketamine, an NMDA receptor antagonist, and riluzole, a modulator of glutamatergic, transmission have been reported to be effective for the treatment of patients with treatment-refractory depression. Based on these findings, extensive studies to develop agents acting on glutamatergic transmission have been conducted. Glutamate receptors are divided into two main subtypes, ionotropic glutamate receptors and metabotropic glutamate (mGlu) receptors, both of which have subtypes. Of these, much attention has been paid to mGlu2/3 receptors. mGlu2/3 receptor antagonists such as MGS0039 and LY341495 have been reported to exert antidepressant effects in animal models of depression including the forced swim test, tail suspension test, learned helplessness paradigm, olfactory bulmectomy model and isolation rearing model, and to enhance serotonin release in the prefrontal cortex and dopamine release in the nucleus accumbens. Moreover, activation of AMPA receptor and mTOR signaling have been suggested to be involved in the antidepressant effects of mGlu2/3 receptor antagonists, as demonstrated in the actions of ketamine. Thus, mGlu2/3 receptor antagonists may share some neural networks with ketamine in exerting their antidepressant effects. In addition, the potential of other agents targeting glutamatergic transmission for novel antidepressants is being investigated.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):219-26.
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    ABSTRACT: The important functional role of fatty acids in both onset and suppression of pain has become increasingly apparent in recent years. Recently, we have also demonstrated that the release of an endogenous opioid peptide, beta-endorphin, plays an important role in the induction of docosahexaenoic acid (DHA)-induced antinociception. It is well known that fatty acids affect intracellular and intercellular signaling as well as the membrane fluidity of neurons. In addition to intracellular actions, unbound free fatty acids (FFAs) can also carry out extracellular signaling by stimulating the G-protein-coupled receptor (GPCR). Among these receptors, GPR40 has been reported to be activated by long-chain fatty acids such as DHA, eicosapentaenoic acid (EPA) and arachidonic acid. In a peripheral area, GPR40 is preferentially expressed in pancreatic beta-cells and is known to be related to the secretion of hormone and peptides. On the other hand, even though this receptor is widely distributed in the central nervous system, reports studying the role and functions of GPR40 in the brain are not found. In this review, we summarize the findings of our recent study about the long-chain fatty acid receptor GPR40 as a novel pain regulatory system.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):233-7.
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    ABSTRACT: A growing body of evidence suggests that the brain serotonin (5-HT) nervous system is an important component related to the etiology as well as the treatment of stress-related psychiatric disorders. Molecular cloning studies have revealed the existence of 14 different genes, each encoding a distinct 5-HT receptor subtype. The 5-HT7 receptor is the most recently identified member of the 5-HT receptor subtypes, and the physiological role of this receptor is still unknown. Recently, either selective agonists or antagonists for 5-HT7 receptors, as well as 5-HT7 receptor knockout mice, have been developed, and these have recently been used as the experimental tools for determining the actual function of 5-HT7 receptors. The first half of the present article introduces the reports that have examined the role of the 5-HT7 receptor on emotional regulation. On the other hand, it has been indicated that the ability to adapt to stress is an important defensive function of a living body, and impairment of this ability may contribute to some stress-related disorders. Thus, the examination of brain mechanisms involved in stress adaptation could help to pave the way for new therapeutic strategies for stress-related psychiatric disorders. The second half of the present article introduces our recent studies focusing on the relationship between brain 5-HT7 receptors and the mechanisms of stress adaptation.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 08/2012; 32(4):187-93.