INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
国际神经精神药理学报
ISSN: 1461-1457
自引率: 2.7%
发文量: 70
被引量: 6749
影响因子: 5.672
通过率: 暂无数据
出版周期: 月刊
审稿周期: 暂无数据
审稿费用: 0
版面费用: 暂无数据
年文章数: 70
国人发稿量: 21

投稿须知/期刊简介:

Published by Cambridge University Press. ISSN: 1461-1457.<br /><br />The official scientific journal of the Collegium Internationale Neuro-Psychopharmacologicum The International Journal of Neuropsychopharmacology (IJNP) serves as a major forum for the rapid publication and wide dissemination of high quality influential research in neuropsychopharmacology in the basic and clinical domains. The central focus of the journal is on research which advances understanding of existing and new neuropsychopharmacological agents including their mode of action and clinical application or which provides insights into the biological basis of neuropsychiatric disorders and thereby advances their pharmacological treatment. Such research may derive from the full spectrum of biological and psychological fields of inquiry encompassing classical and novel techniques in neuro-psychopharmacology as well as strategies such as neuroimaging genetics psycho-neuroendocrinology and neuropsychology. Emphasis is given to original research which is of wide interest and clearly advances the field.

期刊描述简介:

The official scientific journal of the Collegium Internationale Neuro-Psychopharmacologicum The International Journal of Neuropsychopharmacology (IJNP) serves as a major forum for the rapid publication and wide dissemination of high quality influential research in neuropsychopharmacology in the basic and clinical domains. The central focus of the journal is on research which advances understanding of existing and new neuropsychopharmacological agents including their mode of action and clinical application or which provides insights into the biological basis of neuropsychiatric disorders and thereby advances their pharmacological treatment. Such research may derive from the full spectrum of biological and psychological fields of inquiry encompassing classical and novel techniques in neuro-psychopharmacology as well as strategies such as neuroimaging genetics psycho-neuroendocrinology and neuropsychology. Emphasis is given to original research which is of wide interest and clearly advances the field.

最新论文
  • Metabotropic Glutamate Receptor 5 as a Potential Biomarker of the Intersection of Trauma and Cannabis Use.

    被引量:- 发表:2024

  • Distinct Effects of Major Affective Disorder Diagnoses and Suicidal Symptom Severity on Inhibitory Control Function and Proinflammatory Cytokines: Single-Site Analysis of 800 Adolescents and Adults.

    被引量:- 发表:2024

  • Upregulation of Phosphodiesterase 7A Contributes to Concurrent Pain and Depression via Inhibition of cAMP-PKA-CREB-BDNF Signaling and Neuroinflammation in the Hippocampus of Mice.

    被引量:- 发表:2024

  • GluN2B on Adult-Born Granule Cells Modulates (R,S)-Ketamine's Rapid-Acting Effects in Mice.

    Standard antidepressant treatments often take weeks to reach efficacy and are ineffective for many patients. (R,S)-ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, has been shown to be a rapid-acting antidepressant and to decrease depressive symptoms within hours of administration. While previous studies have shown the importance of the GluN2B subunit of the NMDA receptor on interneurons in the medial prefrontal cortex, no study to our knowledge has investigated the influence of GluN2B-expressing adult-born granule cells. Here, we examined whether (R,S)-ketamine's efficacy depends on adult-born hippocampal neurons using a genetic strategy to selectively ablate the GluN2B subunit of the NMDA receptor from Nestin+ cells in male and female mice, tested across an array of standard behavioral assays. We report that in male mice, GluN2B expression on 6-week-old adult-born neurons is necessary for (R,S)-ketamine's effects on behavioral despair in the forced swim test and on hyponeophagia in the novelty suppressed feeding paradigm, as well on fear behavior following contextual fear conditioning. In female mice, GluN2B expression is necessary for effects on hyponeophagia in novelty suppressed feeding. These effects were not replicated when ablating GluN2B from 2-week-old adult-born neurons. We also find that ablating neurogenesis increases fear expression in contextual fear conditioning, which is buffered by (R,S)-ketamine administration. In line with previous studies, these results suggest that 6-week-old adult-born hippocampal neurons expressing GluN2B partially modulate (R,S)-ketamine's rapid-acting effects. Future work targeting these 6-week-old adult-born neurons may prove beneficial for increasing the efficacy of (R,S)-ketamine.

    被引量:- 发表:2024

  • Investigating the Impact of IL-6 and CXCL8 on Neurodegeneration and Cognitive Decline in Alzheimer's Disease.

    Alzheimer's disease (AD) is a progressive neurodegenerative disorder primarily affecting the elderly, characterized by severe cognitive impairment and memory loss. Emerging evidence suggests that neuroinflammation plays a significant role in AD pathogenesis, with cytokines like interleukin-6 (IL-6) and C-X-C motif chemokine ligand 8 (CXCL8) contributing to the disease progression. We utilized GEO datasets to identify IL-6 and CXCL8 as pivotal inflammatory markers in AD. In vitro experiments were conducted using SK-N-BE(2)-M17 and THP-1 cell lines treated with IL-6 and CXCL8 to model AD. Additionally, in vivo tests on Amyloid Precursor Protein/Presenilin 1 (APP/PS1) AD mouse models were performed to assess the impact of these cytokines on cognitive functions and brain pathology. The results indicated a significant decrease in cell viability, increased apoptosis, and elevated inflammatory factor secretion following IL-6 and CXCL8 treatment in vitro. In vivo, AD mouse models treated with these cytokines exhibited exacerbated emotional distress, decreased social interaction, impaired cognitive functions, and increased amyloid protein deposition in neural tissues. The study highlights the detrimental effects of IL-6 and CXCL8 on neuronal health and cognitive functions in AD. These findings suggest that targeting these cytokines could offer potential therapeutic interventions for improving patient outcomes in Alzheimer's disease.

    被引量:- 发表:1970

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