[Serial review No.8. Dental embryology: microstructural formation of teeth].
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Animals↗
Biomedical subjects
Tsuneyuki Yamamoto
Publications and source records attributed to Tsuneyuki Yamamoto.
Hippocampal serotonergic system is involved in anxiety-like behavior induced by corticotropin-releasing factor.
To clarify the interaction between anxiety-like behavior produced by corticotropin-releasing factor (CRF) and the 5-HT system, we investigated the effects of intracerebroventricular (i.c.v.) administration of CRF on an elevated plus-maze performance as indices of anxiety, measuring extracellular levels of 5-HT in the ventral hippocampus using an in vivo brain dialysis method in rats. The time spent in the open arms of the maze and the number of open arm entries were decreased in a dose-dependent manner by the administration of CRF (0.3-1.0 microg/rat). These effects of CRF were prevented by pretreatment with a 5-HT(1A) receptor agonist, 8-OH-DPAT (0.5 mg/kg, s.c.). In biochemical studies, CRF increased 5-HT release about 150-250% above baseline in the ventral hippocampus and this elevation was significantly inhibited by a CRF receptor antagonist, alpha-Helical CRF(9-41) (50 mug/rat), and 5-HT(1A) receptor agonist, 8-OH-DPAT (0.5 mg/kg, s.c.). These results suggested that the anxiety-like effect produced by CRF may have involved increased 5-HT transmission in the ventral hippocampus. Taken with the evidence for hypersecretion of CRF in patients with depression and anxiety-related disorders, our findings lead to the intriguing hypothesis that interaction between CRF and 5-HT, especially in the ventral hippocampus, plays a role in the etiology of affective and anxiety disorders.
8-Hydroxy-2-(di-n-propylamino)tetralin↗
Prostaglandin E2 attenuates SR141716A-precipitated withdrawal in tetrahydrocannabinol-dependent mice.
The present study aimed to clarify the role of the arachidonic acid cascade in mediating the expression of withdrawal signs in cannabinoid-dependent mice. Mice were injected with Delta(8)-tetrahydrocannabinol (THC) at 20 mg/kg (i.p.) every 12 h, 11 times. When SR141716A, a specific cannabinoid CB1 receptor antagonist, at 10 mg/kg (i.p.) was given 4 h after the last THC injection, withdrawal signs such as forepaw licking, facial preening, grooming, forepaw tremor, head shakes and weight loss were clearly observed. PGE(2) at 0.1, 1.0 and 3.2 microg (per animal; i.c.v.) given prior to SR141716A (10 mg/kg, i.p.) dose-dependently decreased the number of forepaw licking, facial preening, grooming and forepaw tremor episodes. Instead of SR141716A, a cyclooxygenase inhibitor diclofenac at 10 mg/kg (i.p.) also precipitated these withdrawal signs. The results suggest that the expression of THC withdrawal is due to a decrease in prostaglandin levels through inactivation of the arachidonic acid cascade in the brain.
Animals↗
Necrotising fasciitis and myositis that originated from gastrointestinal bacterial infection: two fatal cases.
We present two cases of aggressive myofasciitis after gastrointestinal infections. The first patient developed necrosis of the legs over 5 days and he died on the 20th day. Vibrio vulnificus was cultured. The second patient developed bullae on his thigh and he died the next day. Streptococcus pyogenes was cultured.
Aged↗
Role of the PLC-related, catalytically inactive protein p130 in GABA(A) receptor function.
The protein p130 was isolated from rat brain as an inositol 1,4,5-trisphosphate-binding protein with a domain organization similar to that of phospholipase C-delta1 but lacking PLC activity. We show that p130 plays an important role in signaling by the type A receptor for gamma-aminobutyric acid (GABA). Yeast twohybrid screening identified GABARAP (GABA(A) receptor-associated protein), which is proposed to contribute to the sorting, targeting or clustering of GABA(A) receptors, as a protein that interacts with p130. Furthermore, p130 competitively inhibited the binding of the gamma2 subunit of the GABA(A) receptor to GABARAP in vitro. Electrophysiological analysis revealed that the modulation of GABA-induced Cl- current by Zn2+ or diazepam, both of which act at GABA(A) receptors containing gamma subunits, is impaired in hippocampal neurons of p130 knockout mice. Moreover, behavioral analysis revealed that motor coordination was impaired and the intraperitoneal injection of diazepam induced markedly reduced sedative and antianxiety effects in the mutant mice. These results indicate that p130 is essential for the function of GABA(A) receptors, especially in response to the agents acting on a gamma2 subunit.
Adaptor Proteins, Signal Transducing↗
Ultrastructural study of cell-cell interaction between osteoclasts and osteoblasts/stroma cells in vitro.
Many biochemical reports support cell-cell interaction between osteoclasts and osteoblasts/stroma cells in vitro, however there have been few morphological studies supporting this. Details of cell-cell interaction between osteoclasts and osteoblasts/stroma cells remain unclear. The present study examined cell-cell interaction between osteoclasts and osteoblasts/stroma cells by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Osteoclasts, osteoblasts/stroma cells, and bone marrow cells obtained from 10-day-old ddY mice were cultured on dentin slices for 72 hr. Specimens were fixed, and some were examined by SEM. Specimens were decalcified, embedded in Epon after determination of the tartrate-resistant acid phosphatase activity (TRAP), and TRAP-positive cells for investigation were serially sectioned by alternating semithin and ultrathin sections, and then examined by TEM. By SEM, many cellular contacts were seen between the cells cultured on the dentin, but by TEM there were few special structures on the cell membranes between osteoclasts and osteoblasts/stroma cells, or between osteoclasts and bone marrow cells. A special structure on the cell membranes of osteoclasts was observed between an osteoclast and a cytoplasmic process of osteoblast/stroma cells, and this cell membrane was coated with electron dense or bristle-like structures. These bristle-like structures were very similar to those of coated pits. The present results show that the coated pit-like structure plays an important role in cell-cell interaction between osteoclasts and osteoblasts/stroma cells in vitro, and suggest that macromolecules binding to the osteoclast-surface receptor via ligands, accumulate in the coated pits, and enter the osteoclast as receptor-macromolecule complexes in endocytic vesicles.
Acid Phosphatase↗
Effects of intrahippocampal CT105, a carboxyl terminal fragment of beta-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats.
In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of beta-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-alpha (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1beta (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-alpha, which may occur in the brains of patients with Alzheimer's disease.
Alzheimer Disease↗
Nefiracetam improves the impairment of local cerebral blood flow and glucose utilization after chronic focal cerebral ischemia in rats.
In this study we investigated the effects of nefiracetam (DM-9384) on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCMR(glc)) in the chronic phase after middle cerebral artery (MCA) occlusion in rats. Nefiracetam (10 mg/kg) was administered orally once a day for 2 weeks from day 15 after MCA occlusion. On day 28 after MCA occlusion, LCBF and LCMR(glc) were measured by an autoradiographic image-processing method. In MCA-occluded rats, LCBF and LCMR(glc) in the ischemic side of seven regions including the frontal cortex were significant decreased compared with those of the nonischemic side. Nefiracetam significantly improved the impairment of LCBF in the frontal cortex, parietal cortex, caudate putamen, ventral thalamus, amygdaloid nucleus and hippocampus. It also improved the decrease of LCMR(glc) in the frontal cortex, ventral thalamus and hippocampus. These results suggested that nefiracetam has ameliorating effects on chronic disorders of LCBF and LCMR(glc) induced by MCA occlusion.
Animals↗
[Animal models of psychiatric disorder and their validity--from the perspective of behavioral pharmacology].
Animal models of psychiatric disorders are indispensable tools to gain insights into neural mechanisms underlying these disorders and to assess potential therapeutic actions of novel compounds in preclinical settings. However, it is difficult to establish appropriate animal models for these disorders because there is no proof on whether or not what occurs in the animal brain is comparable to what occurs in the human brain. The initial development of animal models of psychiatric disorders is often based on "face validity" as reflected in the similarity of behavioral signs and symptoms observed in humans and animal and subsequently based on "construct validity" as measured by strong correlation in behaviors and neural events between the animal model and patients of the disorder. The practical value of such animal models is reflected ultimately in their "predictive validity" in predicting the therapeutic efficacy of new treatments for psychiatric disorders. The present review will focus on animal models of schizophrenia and depression by the use of mainly environmental stress and pharmacological treatments, which are expected to induce signs and symptoms analogous to those of patients with such disorders.
Animals↗
A crown reconstructing method for resin-embedded transparent teeth.
OBJECTIVE: Resin-embedded transparent teeth are devoid of the original crown morphology, because enamel is lost by demineralization. This study was designed to reproduce artificial enamel and to reconstruct the original crown morphology for resin-embedded transparent teeth. METHOD AND MATERIALS: The impression of the coronal portion of human permanent teeth was taken with a silicone impression material. After demineralization, drawing ink was injected into the pulp cavities. The ink-infiltrated teeth were made transparent with methyl salicylate and embedded with polyester resin. Urethane prepolymer was injected into the impression, and the resin-embedded teeth were reinserted into the impression. After polymerization of the urethane resin, the specimens and the urethane resin were removed from the impression. RESULTS: The original crown morphology of the resin-embedded transparent teeth could be precisely reconstructed with artificial and removable enamel. The resin-embedded teeth showed morphologic details of the black-stained pulp cavities through the transparent dentin and cementum. CONCLUSION: This study established a crown reconstructing method for resin-embedded transparent teeth. The specimens will be useful for demonstration of morphology of teeth and pulp cavities.
Carbon↗