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  1 / 20041 MEDLINE  
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PMID:28468634
Autor:Ito N; Hirose E; Ishida T; Hori A; Nagai T; Kobayashi Y; Kiyohara H; Oikawa T; Hanawa T; Odaguchi H
Endereço:Department of Clinical Research, Oriental Medicine Research Center, Kitasato University, Tokyo, Japan. ito-n@insti.kitasato-u.ac.jp.
Título:Kososan, a Kampo medicine, prevents a social avoidance behavior and attenuates neuroinflammation in socially defeated mice.
Fonte:J Neuroinflammation; 14(1):98, 2017 May 03.
ISSN:1742-2094
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Kososan, a Kampo (traditional Japanese herbal) medicine, has been used for the therapy of depressive mood in humans. However, evidence for the antidepressant efficacy of kososan and potential mechanisms are lacking. Recently, it has been recognized that stress triggers neuroinflammation and suppresses adult neurogenesis, leading to depression and anxiety. Here, we examined whether kososan extract affected social behavior in mice exposed to chronic social defeat stress (CSDS), an animal model of prolonged psychosocial stress, and neuroinflammation induced by CSDS. METHODS: In the CSDS paradigm, C57BL/6J mice were exposed to 10 min of social defeat stress from an aggressive CD-1 mouse for 10 consecutive days (days 1-10). Kososan extract (1.0 g/kg) was administered orally once daily for 12 days (days 1-12). On day 11, the social avoidance test was performed to examine depressive- and anxious-like behaviors. To characterize the impacts of kososan on neuroinflammation and adult neurogenesis, immunochemical analyses and ex vivo microglial stimulation assay with lipopolysaccharide (LPS) were performed on days 13-15. RESULTS: Oral administration of kososan extract alleviated social avoidance, depression- and anxiety-like behaviors, caused by CSDS exposure. CSDS exposure resulted in neuroinflammation, as indicated by the increased accumulation of microglia, the resident immune cells of the brain, and their activation in the hippocampus, which was reversed to normal levels by treatment with kososan extract. Additionally, in ex vivo studies, CSDS exposure potentiated the microglial pro-inflammatory response to a subsequent LPS challenge, an effect that was also blunted by kososan extract treatment. Indeed, the modulatory effect of kososan extract on neuroinflammation appears to be due to a hippocampal increase in an anti-inflammatory phenotype of microglia while sparing an increased pro-inflammatory phenotype of microglia caused by CSDS. Moreover, reduced adult hippocampal neurogenesis in defeated mice was recovered by kososan extract treatment. CONCLUSIONS: Our findings suggest that kososan extract prevents a social avoidant behavior in socially defeated mice that is partially mediated by the downregulation of hippocampal neuroinflammation, presumably by the relative increased anti-inflammatory microglia and regulation of adult hippocampal neurogenesis. Our present study also provides novel evidence for the beneficial effects of kososan on depression/anxiety and the possible underlying mechanisms.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Drugs, Chinese Herbal); 0 (Inflammation Mediators); 0 (Plant Extracts); 0 (koso-san)


  2 / 20041 MEDLINE  
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PMID:29278699
Autor:Yamashita A; Kondo K; Kunishima Y; Iseki S; Kondo T; Ota MS
Endereço:Laboratory of Anatomy, Physiology and Food Biological Science, Department of Food and Nutrition, Japan Women's University, Bunkyo-ku, Tokyo, Japan.
Título:Postnatal development of bitter taste avoidance behavior in mice is associated with ACTIN-dependent localization of bitter taste receptors to the microvilli of taste cells.
Fonte:Biochem Biophys Res Commun; 495(4):2579-2583, 2018 01 22.
ISSN:1090-2104
País de publicação:United States
Idioma:eng
Resumo:Bitter taste avoidance behavior (BAB) plays a fundamental role in the avoidance of toxic substances with a bitter taste. However, the molecular basis underlying the development of BAB is unknown. To study critical developmental events by which taste buds turn into functional organs with BAB, we investigated the early phase development of BAB in postnatal mice in response to bitter-tasting compounds, such as quinine and thiamine. Postnatal mice started to exhibit BAB for thiamine and quinine at postnatal day 5 (PD5) and PD7, respectively. Histological analyses of taste buds revealed the formation of microvilli in the taste pores starting at PD5 and the localization of type 2 taste receptor 119 (TAS2R119) at the microvilli at PD6. Treatment of the tongue epithelium with cytochalasin D (CytD), which disturbs ACTIN polymerization in the microvilli, resulted in the loss of TAS2R119 localization at the microvilli and the loss of BAB for quinine and thiamine. The release of ATP from the circumvallate papillae tissue due to taste stimuli was also declined following CytD treatment. These results suggest that the localization of TAS2R119 at the microvilli of taste pores is critical for the initiation of BAB.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Actins)


  3 / 20041 MEDLINE  
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PMID:29260547
Autor:Hong SM; Soe KH; Lee TH; Kim IS; Lee YM; Lim BO
Endereço:BK21PLUS Glocal Education Program of Nutraceuticals Development, Konkuk University , Chungju-si, Chungcheongbuk-do 27478, Republic of Korea.
Título:Cognitive Improving Effects by Highbush Blueberry (Vaccinium crymbosum L.) Vinegar on Scopolamine-Induced Amnesia Mice Model.
Fonte:J Agric Food Chem; 66(1):99-107, 2018 Jan 10.
ISSN:1520-5118
País de publicação:United States
Idioma:eng
Resumo:The present study aimed to evaluate the preventive effects of highbush blueberry (Vaccinium corymbosum L.) vinegar (BV) on cognitive functions in a scopolamine (Sco)-induced amnesia model in mice. In this study, Sco (1 mg/kg, intraperitoneal injection) was used to induce amnesia. ICR mice were orally administered donepezil (5 mg/kg), blueberry extract (120 mg/kg), and BV (120 mg/kg) for 7 days. After inducing cognitive impairment by Sco, a behavioral assessment using behavior tests (i.e., Y-maze and passive avoidance tests) was performed. The BV group showed significantly restored cognitive function in the behavioral tests. BV facilitated cholinergic activity by inhibiting acetylcholinesterase activity, and enhanced antioxidant enzyme activity. Furthermore, BV was found to be rehabilitated in the cornu ammonis 1 neurons of hippocampus. In our study, we demonstrated that the memory protection conferred by BV was linked to activation of brain-derived neurotrophic factor (BDNF)/cAMP response element binding protein (CREB)/serine-threonine kinase (AKT) signaling.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Neuroprotective Agents); 0 (Plant Extracts); 451IFR0GXB (Scopolamine Hydrobromide); EC 3.1.1.7 (Acetylcholinesterase); N9YNS0M02X (Acetylcholine)


  4 / 20041 MEDLINE  
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PMID:27159044
Autor:Levendowski D; Cunnington D; Swieca J; Westbrook P
Endereço:a Advanced Brain Monitoring, Inc ., Carlsbad , California , USA.
Título:User Compliance and Behavioral Adaptation Associated With Supine Avoidance Therapy.
Fonte:Behav Sleep Med; 16(1):27-37, 2018 Jan-Feb.
ISSN:1540-2010
País de publicação:England
Idioma:eng
Resumo:This study investigates behavioral adaptation to vibrotactile position-avoidance therapy during sleep in patients with obstructive sleep apnea (n =135) across 15 to 52 weeks. The overall compliance, based on nights used ≥ 4 hr, was 71%. Overall regular use, that is, ≥ 4 hr/night over 70% of nights, was 88%. Poor early compliance strongly predicted poor long-term treatment adherence, with 92% of those noncompliant across the first 12 weeks of therapy remaining noncompliant. Conversely, 21% of those with compliant utilization in the short term became noncompliant in the long term. It appears that patients do not habituate to the stimulus during sleep, nor was there a training effect associated with long-term use.
Tipo de publicação: JOURNAL ARTICLE


  5 / 20041 MEDLINE  
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PMID:29184202
Autor:Yu K; Ahrens S; Zhang X; Schiff H; Ramakrishnan C; Fenno L; Deisseroth K; Zhao F; Luo MH; Gong L; He M; Zhou P; Paninski L; Li B
Endereço:Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Título:The central amygdala controls learning in the lateral amygdala.
Fonte:Nat Neurosci; 20(12):1680-1685, 2017 Dec.
ISSN:1546-1726
País de publicação:United States
Idioma:eng
Resumo:Experience-driven synaptic plasticity in the lateral amygdala is thought to underlie the formation of associations between sensory stimuli and an ensuing threat. However, how the central amygdala participates in such a learning process remains unclear. Here we show that PKC-δ-expressing central amygdala neurons are essential for the synaptic plasticity underlying learning in the lateral amygdala, as they convey information about the unconditioned stimulus to lateral amygdala neurons during fear conditioning.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:EC 2.7.1.- (Prkcd protein, mouse); EC 2.7.11.13 (Protein Kinase C-delta)


  6 / 20041 MEDLINE  
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PMID:29037662
Autor:Ward M; Norman H; D'Souza MS
Endereço:Department of Pharmaceutical and Biomedical Sciences, The Raabe College of Pharmacy, Ohio Northern University, 525 S Main Street, Ada, OH 45810, United States.
Título:Effects of pharmacological manipulation of the kappa opioid receptors on the aversive effects of nicotine.
Fonte:Behav Brain Res; 338:56-65, 2018 Feb 15.
ISSN:1872-7549
País de publicação:Netherlands
Idioma:eng
Resumo:Nicotine, an addictive component of tobacco smoke, produces both rewarding and aversive effects. Increasing the aversive effects of nicotine may help in promoting smoking cessation. However, neural targets mediating the aversive effects of nicotine have not been fully identified. In this study, we evaluated the role of kappa opioid receptors (KORs) in the aversive effects of nicotine (0.4 mg/kg, base; s.c.) using the nicotine-induced conditioned taste aversion (CTA) model in Wistar rats. The KORs were activated using the selective KOR agonist (±)U-50,488H (0, 0.03, 0.15 & 0.3mg/kg; s.c.) and inhibited using the KOR antagonist nor-binaltorphimine (nor-BNI; 0, 15 & 30mg/kg; s.c.) in separate groups of rats using a between-subjects design. Pretreatment with the KOR agonist (±)U-50,488H (0.3mg/kg) significantly increased aversion for the nicotine-associated solution. Additionally, (±)U-50,488H (0.3mg/kg) on its own induced aversion to the flavored solution associated with it even in the absence of nicotine, suggesting that the KOR agonist induced increase in nicotine-induced aversion was an additive effect. Interestingly, administration of the KOR antagonist nor-BNI (30mg/kg) prior to conditioning with nicotine/saline, but not after conditioning with nicotine/saline, attenuated nicotine-induced aversive effects compared to saline controls. Taken together, these data suggest a role for KORs in the aversive effects of nicotine.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Narcotic Antagonists); 0 (Receptors, Opioid, kappa); 36OOQ86QM1 (norbinaltorphimine); 5S6W795CQM (Naltrexone); 67198-13-4 (3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer); 6M3C89ZY6R (Nicotine)


  7 / 20041 MEDLINE  
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PMID:29195794
Autor:Piplani P; Jain A; Devi D; Anjali; Sharma A; Silakari P
Endereço:University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India. Electronic address: ppvohra28in@pu.ac.in.
Título:Design, synthesis and pharmacological evaluation of some novel indanone derivatives as acetylcholinesterase inhibitors for the management of cognitive dysfunction.
Fonte:Bioorg Med Chem; 26(1):215-224, 2018 01 01.
ISSN:1464-3391
País de publicação:England
Idioma:eng
Resumo:The present study reports the effect of indanone derivatives on scopolamine induced deficit cholinergic neurotransmission serving as promising leads for the therapeutics of cognitive dysfunction. Eleven compounds 54-64 have been designed, synthesised and evaluated against behavioural alterations using step down passive avoidance protocol at a dose of 0.5 mg/kg with Donepezil (1) as the reference standard. All the synthesised compounds were evaluated for their in vitro acetylcholinesterase (AChE) inhibition at five different concentrations using mice brain homogenate as the source of the enzyme. Compounds 54, 56, 59 and 64 displayed appreciable activity with an IC value of 14.06 µM, 12.30 µM, 14.06 µM and 12.01 µM, respectively towards acetylcholinesterase inhibition. The molecular docking study performed to predict the binding mode of the compounds suggested that these compounds could bind appreciably to the amino acids present at the active site of recombinant human acetylcholinesterase (rhAChE). The behavioural, biochemical and in silico pharmacokinetic studies were in concordance with each other.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Cholinesterase Inhibitors); 0 (Indans); 451IFR0GXB (Scopolamine Hydrobromide); B926Y9U4QN (indacrinone); EC 3.1.1.7 (Acetylcholinesterase)


  8 / 20041 MEDLINE  
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PMID:29184203
Autor:Jung EM; Moffat JJ; Liu J; Dravid SM; Gurumurthy CB; Kim WY
Endereço:Department of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Título:Arid1b haploinsufficiency disrupts cortical interneuron development and mouse behavior.
Fonte:Nat Neurosci; 20(12):1694-1707, 2017 Dec.
ISSN:1546-1726
País de publicação:United States
Idioma:eng
Resumo:Haploinsufficiency of the AT-rich interactive domain 1B (ARID1B) gene causes autism spectrum disorder and intellectual disability; however, the neurobiological basis for this is unknown. Here we generated Arid1b-knockout mice and examined heterozygotes to model human patients. Arid1b-heterozygous mice showed a decreased number of cortical GABAergic interneurons and reduced proliferation of interneuron progenitors in the ganglionic eminence. Arid1b haploinsufficiency also led to an imbalance between excitatory and inhibitory synapses in the cerebral cortex. Furthermore, we found that Arid1b haploinsufficiency suppressed histone H3 lysine 9 acetylation (H3K9ac) overall and particularly reduced H3K9ac of the Pvalb promoter, resulting in decreased transcription. Arid1b-heterozygous mice exhibited abnormal cognitive and social behaviors, which were rescued by treatment with a positive allosteric GABA receptor modulator. Our results demonstrate a critical role for Arid1b in interneuron development and behavior and provide insight into the pathogenesis of autism spectrum disorder and intellectual disability.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Arid1b protein, mouse); 0 (Transcription Factors); 56-12-2 (gamma-Aminobutyric Acid)


  9 / 20041 MEDLINE  
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PMID:27776994
Autor:Kokhan VS; Matveeva MI; Bazyan AS; Kudrin VS; Mukhametov A; Shtemberg AS
Endereço:Laboratory of Extreme Physiology, Institute of Medico-Biological Problems RAS, Moscow, Russia. Electronic address: viktor_kohan@hotmail.com.
Título:Combined effects of antiorthostatic suspension and ionizing radiation on the behaviour and neurotransmitters changes in different brain structures of rats.
Fonte:Behav Brain Res; 320:473-483, 2017 03 01.
ISSN:1872-7549
País de publicação:Netherlands
Idioma:eng
Resumo:Space flight factors (SFF) significantly affect the operating activity of astronauts during deep space missions. In contrast to an orbital flight, leaving the Earth's magnetic field is fraught with the dangers of exposure to ionizing radiation and more specifically, the high-energy nuclei component of galactic cosmic rays. Microgravity, just another critical non-radiation factor, significantly affects the normal functioning of the CNS. Some morphological structures of the brain, such as the prefrontal cortex and the hippocampus, that are rich in monoaminergic and acetylcholinergic neurones, are the most sensitive to the effects of ionizing radiation and non-radiation spaceflight factors (SFF). In this work we have studied the combined effects of microgravity (in antiorthostatic suspension model, AS) and irradiation (γ-ray and protons in spread-out Bragg peak) on the behaviour, cognitive abilities, and metabolism of monoamines and acetylcholine in the key structures of the rat's brain. Irradiation (as independently as combined with AS) resulted in the decrease of thigmotaxis in rats. Learning problems, caused by the malfunctioning of the working memory but not the spatial memory, were observed in response to AS as well as to the SFF in combination. Analysis of monoamines metabolism showed that the serotoninergic system was the most affected by the SFF. Concentration of acetylcholine in the hippocampus significantly increased in the groups of irradiated rats, and in the groups which were exposed to the SFF in combination, compared to the rats exposed only to AS.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Neurotransmitter Agents)


  10 / 20041 MEDLINE  
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PMID:28458424
Autor:Pattanashetti LA; Taranalli AD; Parvatrao V; Malabade RH; Kumar D
Endereço:Department of Pharmacology, K.L.E. University's, College of Pharmacy, Belgaum, Karnataka, India.
Título:Evaluation of neuroprotective effect of quercetin with donepezil in scopolamine-induced amnesia in rats.
Fonte:Indian J Pharmacol; 49(1):60-64, 2017 Jan-Feb.
ISSN:1998-3751
País de publicação:India
Idioma:eng
Resumo:OBJECTIVE: The objective of this study was to evaluate the neuroprotective effect of quercetin with donepezil in scopolamine-induced amnesia in rats. MATERIALS AND METHODS: Five groups of adult male Wistar rats (12 months old) weighing 180-200 g ( = 6) were used. The normal control group received normal saline and test group animals were pretreated orally with quercetin (25 mg/kg), donepezil (3 mg/kg), and a combination of quercetin (25 mg/kg) with donepezil (3 mg/kg), respectively, dosed at every 24 h interval for 14 consecutive days, afterward amnesia was induced by scopolamine (3 mg/kg) on the 14 day through intraperitoneal route. Cognitive performance was assessed by the Morris water maze, elevated plus maze, and passive avoidance paradigm. Acetylcholinesterase enzyme (AchE) level, biochemical markers such as lipid peroxidase (LPO), glutathione (GSH), ß amyloid level, and histopathological study of rat brain were estimated. Statistical analysis was done by one-way analysis of variance, followed by Dunnett's test. ≥ 0.05 was considered statistically significant. RESULTS: Pretreatment with quercetin, donepezil, and their combination showed a significant increase in escape latency, step-through latency, and decreased transfer latency in respective cognitive models of the Morris water maze, passive avoidance test, and elevated plus maze. Further coadministration significantly decreased AchE level, ß amyloid level as compared to individual therapy. Biochemical markers such as elevated GSH, decreased LPO were observed, and histopathological studies revealed the reversal of neuronal damage in the treatment group ( < 0.05) as compared to scopolamine-treated control group. CONCLUSION: Pretreatment with quercetin potentiates the action of donepezil in scopolamine-induced amnesia in rats. The improved cognitive memory could be due to the synergistic effect of the drugs by decreasing AchE level, ß amyloid level, and antioxidant action in rat brain.
Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE
Nome de substância:0 (Antioxidants); 0 (Indans); 0 (Neuroprotective Agents); 0 (Nootropic Agents); 0 (Piperidines); 451IFR0GXB (Scopolamine Hydrobromide); 8SSC91326P (donepezil); 9IKM0I5T1E (Quercetin)



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