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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Other titles Japanese journal of psychopharmacology
ISSN 1340-2544
OCLC 33813471
Material type Periodical
Document type Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The pathogenesis of neuropathic pain is quite complicated and diverse. Because pre-existing analgesics, such as opioid analgesics and nonsteroidal anti-inflammatory drugs, are not sufficient to treat it, it is a serious task to establish a strategy of remedy for neuropathic pain. Recently, increasing evidence suggests that immune cell-mediated neuroinflammation in the nervous system induces central and peripheral sensitization, resulting in chronic pain. Initially, the immune system plays an important role in host defense. Although intravital homeostasis is kept constant by innate and adaptive immunity, the immune system is activated excessively due to infection, stress and tissue injury. Activated immune cells produce and release several kinds of inflammatory mediators, which act directly on sensory neurons and promote a recruitment of immune cells, developing the feedback loop of inflammatory exacerbation. We've focused on the role of crosstalk between immune cells and neurons in peripheral neuroinflammation, and explored a novel candidate for a remedy of neuropathic pain. In this review, we will introduce recent reports and our research work that suggest the functional significance of neuroinflammation in neuropathic pain, and survey possibilities of new strategies for chronic pain from the point of view of basic research.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 06/2015; 35(3):65-72.
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    ABSTRACT: Schizophrenia and bipolar disorder show high comorbidity with smoking dependence. Several previous studies reported that glycogen synthase kinase 3β (GSK3β), which is widely expressed in the brain including the dopamine projection areas such as the amygdala, nucleus accumbens and hippocampus, may play a role in neuropsychiatric disorders and dopamine- and serotonin-mediated behavior. In this study, we have analyzed the association of three single nucleotide polymorphisms (SNPs) within GSK3β gene (rs3755557, rs334558, rs6438552) with the smoking habits and age at smoking initiation in a sample of 384 young adult Japanese, which included 172 smokers and 212 non-smokers. As a result, rs334558 was significantly associated with smoking habits in genotype frequency and allelic frequency (P < 0.05). Furthermore, higher haplotype 3 (T-T-T) and haplotype 5 (A-T-C) frequencies were observed in non-smokers than smokers (P < 0.05). Three functional polymorphisms examined in this study reportedly increase transcriptional activity when they have a high-activation allele such as the A allele of -1727A/T (rs3755557), the T allele of -50T/C (rs334558) or T allele of -157T/C (rs6438552). Thus, it was suggested in this study that changes in GSK3β activity may have an impact on smoking habits.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 06/2015; 35(3):73-7.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):53-4.
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    ABSTRACT: A number of behavioral, neurochemical and electrophysiological studies have emphasized the importance of the serotonergic neurons in the pathophysiology of psychiatric disorders and the therapeutic actions of psychotropics. However, no in vitro serotonergic culture systems have successfully analyzed the long-term effects of psychotropics or the neural interaction between serotonergic and excitatory/inhibitory neurons. Recently, we have established rat organotypic raphe slice cultures, which have functional serotonergic neurons with the ability to release 5-HT in response to stimulation and to reuptake 5-HT through serotonin transporter and retain neural and synaptic functions. Here, we show the following results in the raphe slice cultures: 1) acute and sustained treatments with 3,4-methylenedioxymethamphetamine induce the 5-HT efflux via serotonin transporter and AMPA receptor-mediated exocytotic 5-HT release, respectively; 2) sustained treatment with antidepressants enhances the exocytotic 5-HT release, which is dependent on AMPA receptor stimulation, but not on desensitization of 5-HT(1A/1B) autoreceptors; 3) the augmentation therapy of an atypical antipsychotic, olanzapine, with antidepressants is caused by the decrease in the raphe inhibitory GABAergic tone through 5-HT6 receptor antagonism. Our findings suggest that the raphe slice cultures are suitable for analyzing the neural and molecular mechanisms underlying the efficacy of psychotropics in vitro.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):39-44.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):47-8.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):61-2.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):45-6.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):51-2.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):55-6.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):49-50.
  • Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 04/2015; 35(2):57-8.
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    ABSTRACT: We sometimes make decisions relying not necessarily on deliberative thoughts but on intuitive and emotional processes in uncertain situations. The somatic marker hypothesis proposed by Damasio argued that interoception, which means bodily responses such as sympathetic activity, can be represented in the insula and anterior cingulate cortex and can play critical roles in decision-making. Though this hypothesis has been criticized in its theoretical and empirical aspects, recent studies are expanding the hypothesis to elucidate multiple bodily responses including autonomic, endocrine, and immune activities that affect decision-making. In addition, cumulative findings suggest that the anterior insula where the inner model of interoception is represented can act as an interface between the brain and body in decision-making. This article aims to survey recent findings on the brain-body interplays underlying decision-making, and to propose hypotheses on the significance of the body in decision-making.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 02/2015; 35(1):11-8.
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    ABSTRACT: Injury to the nervous system results in debilitating chronic pain states (called neuropathic pain) whose mechanisms remain unclear. Emerging lines of evidence indicate the pivotal role of spinal glial cells in neuropathic pain. Spinal microglia rapidly respond to peripheral nerve injury (PNI) and become activated with changing expression of a variety of genes. The best known example is purinergic P2X4 receptors, an ATP-gated cation channel. The expression of P2X4 receptors is upregulated in spinal microglia after PNI, and inhibition of P2X4 activity suppresses neuropathic pain. Furthermore, interferon regulatory factor-8 (IRF8) and IRF5 are identified as microglial transcription factors whose expression is upregulated in spinal microglia after PNI, and the IRF8-IRF5 transcriptional cascade is the core process for shifting spinal microglia toward a state with high expression of P2X4 receptors. Astrocytes in the spinal cord show a delayed onset of activation and play an important role in the maintenance of neuropathic pain via the transcription factor STAT3 and the intracellular kinase JNK. These results obtained from glial cell research will advance our understanding of the development and maintenance of neuropathic pain and provide a new target for treating this pain.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 02/2015; 35(1):1-4.
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    ABSTRACT: Glial cells receive neurotransmitters, respond to them, and then release so-called gliotransmitters such as ATP, glutamate or D-serine. Astrocytes in particular have received much attention because synaptic structures are surrounded by astrocytic fine processes, by which astrocytes communicate with neurons via gliotransmitters. Here, we introduce recent progress concerning glia-neuron interaction, especially focusing on the major gliotransmitter ATP and astrocytes in parallel with the latest progress in glia-imaging techniques.
    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology 02/2015; 35(1):5-9.
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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: 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: 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. DOI:10.1016/j.bbr.2012.08.010
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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: 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.