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Objectives: To establish the structural confirmation methods of three suspected new psychoactive substances (NPSs), and explore a more general qualitative testing method.

Methods: Infrared absorption spectroscopy (IR), gas chromatography-mass spectrometry (GC-MS), H-nuclear magnetic resonance spectroscopy (H-NMR), C-nuclear magnetic resonance spectroscopy (C-NMR), F-nuclear magnetic resonance spectroscopy (F-NMR) and other techniques were used to identify the composition and structure of 5 samples containing suspected NPS submitted by public security bureaus.

Results: NPSs were found in the above 5 samples, and 3 were confirmed as NPS included in the newly listed controlled substances on July 1, 2024, namely 2-(methylamino)-2-(2-methylphenyl)cyclohexan-1-one (2-MDCK), 2-(ethylamino)-2-(2-fluorophenyl)cyclohexan-l-one (2-FXE), 1-(3,4-methylenedioxyphenyl)-2-(dimethylamino)pentan-1-one (dipentylone), respectively.

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Nicotine's Effects on Schizophrenia-like Symptoms in a Mice Model: Time Matters.

Brain Sci

August 2024

Laboratório de Neurofisiologia, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro UERJ, Rio de Janeiro 20550-170, RJ, Brazil.

Article Synopsis
  • Tobacco use is common among patients with schizophrenia (SCHZ), and the study explores how the order of tobacco and SCHZ onset affects their relationship.
  • Using a mouse model, researchers tested the effects of either tobacco exposure before or after inducing SCHZ symptoms with phencyclidine (PCP), measuring behaviors linked to schizophrenia.
  • Results revealed that the sequence of exposure alters the impact on behaviors, suggesting that the order of tobacco use and SCHZ plays a crucial role in understanding their interaction and potential neurobiological mechanisms.*
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Dysfunction of the NMDA Receptor in the Pathophysiology of Schizophrenia and/or the Pathomechanisms of Treatment-Resistant Schizophrenia.

Biomolecules

September 2024

Department of Neuropsychiatry, Division of Neuroscience, Graduate School of Medicine, Mie University, Tsu 514-8507, Japan.

For several decades, the dopamine hypothesis contributed to the discovery of numerous typical and atypical antipsychotics and was the sole hypothesis for the pathophysiology of schizophrenia. However, neither typical nor atypical antipsychotics, other than clozapine, have been effective in addressing negative symptoms and cognitive impairments, which are indices for the prognostic and disability outcomes of schizophrenia. Following the development of atypical antipsychotics, the therapeutic targets for antipsychotics expanded beyond the blockade of dopamine D2 and serotonin 5-HT2A receptors to explore the partial agonism of the D2 receptor and the modulation of new targets, such as D3, 5-HT1A, 5-HT7, and metabotropic glutamate receptors.

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Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits.

Nat Commun

September 2024

Neurobiology Department, School of Biological Sciences and Center for Neural Circuits and Behavior, University of California San Diego, La Jolla, CA, 92093-0955, USA.

Cognitive deficits are long-lasting consequences of drug use, yet the convergent mechanism by which classes of drugs with different pharmacological properties cause similar deficits is unclear. We find that both phencyclidine and methamphetamine, despite differing in their targets in the brain, cause the same glutamatergic neurons in the medial prefrontal cortex of male mice to gain a GABAergic phenotype and decrease expression of their glutamatergic phenotype. Suppressing drug-induced gain of GABA with RNA-interference prevents appearance of memory deficits.

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Schizophrenia (SCH) is a mental disorder that requires long-term antipsychotic treatment. SCH patients are thought to have an increased sensitivity to stress. The dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, observed in SCH, could include altered levels of glucocorticoids, glucocorticoid receptors (GRs), and associated proteins.

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