Short-term facilitation and depression of transmitter release at amphibian sympathetic ganglionic cells - Mathematical/computational modeling.

There have been few investigations of the short-term plasticity of synaptic transmission at amphibian sympathetic ganglionic cells where the frequency of miniature excitatory postsynaptic potentials is too low to measure an accurate quantum size. This has made it difficult to investigate the mechanism of synaptic transmission at the ganglionic cells by quantal analysis. A theoretical equation, therefore, is proposed.

Association study of polymorphisms in the group III metabotropic glutamate receptor genes, GRM4 and GRM7, with schizophrenia.

Based on the hypothesis that a glutamatergic dysfunction is involved in the pathophysiology of schizophrenia, we have been conducting systematic studies on the association between glutamate receptor genes and schizophrenia. Here we report association studies of schizophrenia with polymorphisms in group III metabotropic glutamate receptor genes, GRM4 and GRM7. We selected 8 and 43 common SNPs distributed in the entire gene regions of GRM4 (>111 kb) and GRM7 (>900 kb), respectively.

Genetic structure of the dopamine receptor D4 gene (DRD4) and lack of association with schizophrenia in Japanese patients.

In order to investigate the contribution of genetic variation in the human dopamine receptor D4 gene (DRD4) to the risk of developing schizophrenia, we carried out a genetic analysis of 27 polymorphisms in 216 schizophrenic patients and 243 healthy controls from the Kyushu region of Japan. Twenty-two single nucleotide polymorphisms (SNPs) and five insertion/deletion polymorphisms were analyzed in this study, including four novel SNPs and a novel mononucleotide repeat. Linkage disequilibrium (LD) and haplotype analyses reveal weak LD across the DRD4 gene.

Association study of polymorphisms in the GluR7, KA1 and KA2 kainate receptor genes (GRIK3, GRIK4, GRIK5) with schizophrenia.

On the basis of the glutamatergic dysfunction hypothesis of schizophrenia, we have been conducting a systematic study of the association of glutamate receptor genes with schizophrenia. Here we report association studies of schizophrenia with polymorphisms in three kainate receptor genes: GRIK3, GRIK4 and GRIK5. We selected 16, 24 and 5 common single nucleotide polymorphisms (SNPs) distributed in the entire gene regions of GRIK3 (>240 kb), GRIK4 (>430 kb) and GRIK5 (>90 kb), respectively.

Identification of single-nucleotide polymorphisms in the human N-methyl-D-aspartate receptor subunit NR2D gene, GRIN2D, and association study with schizophrenia.

Objectives: The glutamatergic dysfunction is one of the main hypotheses for the pathophysiology of schizophrenia. N-methyl-D-aspartate receptors are of major interest because phencyclidine, a non-competitive antagonist of N-methyl-D-aspartate receptors, produces a schizophrenia-like psychosis. Therefore, the genes encoding N-methyl-D-aspartate receptor subunits are strong candidates for schizophrenia susceptibility genes.

Association study of polymorphisms in the excitatory amino acid transporter 2 gene (SLC1A2) with schizophrenia.

Background: The glutamatergic dysfunction hypothesis of schizophrenia suggests that genes involved in glutametergic transmission are candidates for schizophrenic susceptibility genes. We have been performing systematic association studies of schizophrenia with the glutamate receptor and transporter genes. In this study we report an association study of the excitatory amino acid transporter 2 gene, SLC1A2 with schizophrenia.

Positive associations of polymorphisms in the metabotropic glutamate receptor type 8 gene (GRM8) with schizophrenia.

The glutamatergic dysfunction has been implicated in pathophysiology of schizophrenia. The Group III metabotropic glutamate receptor 4 (mGluR4), 6, 7, and 8 are thought to modulate glutamatergic transmission in the brain by inhibiting glutamate release at the synapse. We tested association of schizophrenia with GRM8 using 22 single nucleofide polymorphisms (SNPs) with the average intervals of 40.

The effects of a switch-off response accompanied by hypothalamically induced restlessness on immunoendocrinological changes in cats.

Electrical stimulation of the anterior hypothalamus in cats elicits a behavior called restlessness. When a switch is available for the cats to shut off the electrical stimulation, the cats learn to turn off the stimulation (switch-off response; SOR). In this study, we examined the relationship between the SOR and immunoendocrinological alterations.

Differential characteristics of the middle latency auditory evoked magnetic responses to interstimulus intervals.

Objective: The human middle latency auditory evoked magnetic fields were recorded with different interstimulus intervals (ISI) to investigate the differential natures of P30m and the P50m, including whether the P50m source was spatially different or not from the P30m source.

Methods: Twenty right-handed healthy subjects participated in the experiment. Auditory magnetic responses were recorded in the 0.

Positive associations of polymorphisms in the metabotropic glutamate receptor type 3 gene (GRM3) with schizophrenia.

Objectives: Glutamatergic dysfunction is one of the major hypotheses of schizophrenia pathophysiology. We have been conducting systematic studies on the association between glutamate receptors and schizophrenia. We focused on the metabotropic glutamate receptor type 3 gene (GRM3) as a candidate for schizophrenia susceptibility.

Positive association of the AMPA receptor subunit GluR4 gene (GRIA4) haplotype with schizophrenia: linkage disequilibrium mapping using SNPs evenly distributed across the gene region.

The glutamatergic dysfunction hypothesis suggests that genes involved in the glutamate neurotransmitter system are candidates for schizophrenia-susceptibility genes. We have been conducting systematic studies of the association between glutamate receptors and schizophrenia. We report on a positive association of some haplotypes of the AMPA receptor subunit GluR4 gene (GRIA4) with schizophrenia.

Association study of polymorphisms in the GluR6 kainate receptor gene (GRIK2) with schizophrenia.

The glutamatergic dysfunction hypothesis of schizophrenia suggests genes involved in glutamatergic transmission as candidates for schizophrenia-susceptibility genes. The GluR6 kainate receptor gene GRIK2 is located on chromosome 6q16.3-q21, a schizophrenia susceptibility region, as suggested by multiple linkage studies.

A patient with Cotard syndrome who showed an improvement in single photon emission computed tomography findings after successful treatment with antidepressants.

We report the case of a presenile woman with Cotard syndrome, in the context of major depression, who showed an improvement in bilateral frontal hypoperfusion in a SPECT study using 99mTc-HMPAO after undergoing successful treatment with antidepressant therapy. We also retrospectively evaluated her clinical course based on the clinical stages. The symptoms of Cotard syndrome have been reported to change dramatically according to the stages.

Polymorphism analysis of the upstream region of the human N-methyl-D-aspartate receptor subunit NR1 gene (GRIN1): implications for schizophrenia.

Dysfunction of the gene for the NR1 subunit of the N-methyl-D-aspartate (NMDA) receptor (GRIN1) has been implicated in the pathogenesis of schizophrenia. In support of this hypothesis are behavioral abnormalities reminiscent of schizophrenia in mice with an attenuated expression of the NR1 subunit receptor and the reduced level of NR1 mRNA in postmortem brains of patients with schizophrenia. We screened single nucleotide polymorphisms (SNPs) in the upstream region between +51 and -941 from the translation initiation codon of GRIN1 and identified 17 SNPs, 10 of which were located within the region containing the Sp1 motif and the GSG motifs.

Frustration and fulfillment of needs in dissociative and conversion disorders.

We reviewed all patients with dissociative disorders (nine patients with dissociative amnesia or dissociative fugue) and conversion disorders (10 patients) who were admitted and treated during the past 15 years. Needs frustrated at the appearance of the symptoms and those fulfilled at discharge were studied in both groups using Maslow's hierarchy of needs. The patients of both groups who encountered troubles in their life events were found to have frustrated needs.

Effect of sucrose on formation of the beta-amyloid fibrils and D-aspartic acids in Abeta 1-42.

Beta-amyloid peptide 1-42 is a major peptide constituent of beta-amyloid fibrils. We investigated the role of sucrose on the deposition and the D-aspartic acid formation in an amyloidogenic peptide 1-42 under physiological conditions. From analyses using thioflavine-T fluorometric assay and electronmicroscopic spectroscopy after 60 h incubation at 37 degrees C, it was found that sucrose retarded the fibril formation in the amyloidogenic peptide.

The effects of neuroleptics on the GABA-induced Cl- current in rat dorsal root ganglion neurons: differences between some neuroleptics.

1. Several neuroleptics inhibited the 3 microM gamma-aminobutyric acid induced-chloride current (GABA-current) on dissociated rat dorsal root ganglion neurons in whole-cell patch-clamp investigations. 2.

Amyloid-beta-protein (A beta) (25-35)-associated free radical generation is strongly influenced by the aggregational state of the peptides.

We investigated whether or not the Amyloid-beta-protein (A beta) itself spontaneously generates free radicals using electron spin resonance (ESR) spectroscopy while also monitoring the aggregational state of A beta and A beta-induced cytotoxicity. The present results demonstrated a four-line spectrum in the presence of A beta25-35 with N-tert-butyl-alpha-phenylnitrone (PBN) but not in the presence of PBN alone in phosphate-buffered saline (PBS). The fact that the four-line spectrum obtained for the A beta25-35/PBN in PBS was completely abolished in the presence of the iron-chelating agent Desferal demonstrated the observed four-line spectrum to be iron-dependent.