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Biochemical and biophysical research communications

ISSN 1090-2104

4 papers in the library · 18 citations · publishing 2023-2025

Papers

Adolescent administration of ketamine impairs excitatory synapse formation onto parvalbumin-positive GABAergic interneurons in mouse prefrontal cortex.

Biochemical and biophysical research communications September 17, 2024 Jia-Wei Zhang, Hai-Qian Zhou, Zhen Zhu et al. 7 citations

Adolescent ketamine abuse causes lasting deficits in cognition and social behavior by reducing excitatory synapses on parvalbumin (PV) inhibitory neurons in the medial prefrontal cortex (mPFC), while sparing excitatory pyramidal neurons. In rats given sub-chronic ketamine during early adolescence, the density of these synapses remained lower into adulthood, leading to hyperexcitability, impaired working memory, and reduced social interaction compared to controls. Bioinformatic analysis revealed decreased expression of a gene co-expression module (M1) critical for inhibitory neuron synapse development. The findings suggest that adolescent ketamine exposure irreversibly disrupts synaptic development, pointing to potential therapeutic targets.

S-ketamine ameliorates post-stroke depression in mice via attenuation of neuroinflammation, synaptic restoration, and BDNF pathway activation.

Biochemical and biophysical research communications July 8, 2025 Jiaxin Tian, Yanhong Xie, Sen Ye et al. 6 citations

A single acute dose of S-ketamine (10 mg/kg) given to mice with post-stroke depression (PSD) alleviated depressive-like behaviors for at least five days. The treatment reduced pro-inflammatory cytokines in the medial prefrontal cortex, increased dendritic spine density and synaptic proteins (SYP, PSD-95), and upregulated brain-derived neurotrophic factor (BDNF) along with related signaling molecules (TrkB, p-Akt, p-Erk, p-CaMKII, p-CREB). These findings suggest S-ketamine acts through anti-inflammatory, synaptic enhancing, and BDNF pathway modulating effects, offering promise for PSD treatment.

A mechanistic insight for the biosynthesis of N,N-dimethyltryptamine: An ONIOM theoretical approach.

Biochemical and biophysical research communications October 20, 2023 Lucas Pinheiro Coutinho, Sérgio Ruschi Bergamachi Silva, Pedro de Lima-Neto et al. 3 citations

The biosynthetic pathway of the psychoactive compound N,N-dimethyltryptamine (DMT) involves two methylation steps of tryptamine, but the molecular details of the double methylation were previously unknown. Using computational modeling—molecular dynamics, density functional theory, and ONIOM QM:MM calculations—the authors show that the reaction follows an SN2 mechanism. The second methylation is the rate-limiting step, with an energy barrier 60 kJ·mol⁻¹ higher than the first, due to more repulsive non-covalent interactions in the second transition state. The findings provide geometric details about each reaction step and clarify the energetics of DMT biosynthesis.

Crystal structure of an antibody specifically recognizing 3,4-methyl enedioxy methamphetamine through the epoxide moiety.

Biochemical and biophysical research communications November 12, 2024 Geonho Cheon, Dahyun Hwang, Truc Chi Le et al. 2 citations

Antibodies that detect MDMA (ecstasy) often also recognize its chemical analogue methamphetamine (METH), but two antibodies, 1bB11 and 1bF12, were identified that bind MDMA specifically without binding METH. The crystal structure of 1bB11 bound to MDMA, solved at 3.2 Å resolution, shows that key interactions involve the epoxide moiety of MDMA with residues S34 and Y36 of the antibody's light chain, and an additional interaction with E33 of the heavy chain. Mutagenesis confirmed these residues are important for binding. Comparing this structure to another antibody that binds both drugs revealed opposite binding orientations, providing a structural basis for developing a highly specific antibody for MDMA diagnosis.