Journal: The Journal of Biological Chemistry

Article Title: A myelin basic protein fragment induces sexually dimorphic transcriptome signatures of neuropathic pain in mice

doi: 10.1074/jbc.RA120.013696

Figure Lengend Snippet: IS MBP(84-104) causes striking sexual dimorphism in spinal nociceptive signaling. a, neuropathic pain network of PLC/IP3R/VGCC axis and ESR1/p300/CBP axis after IS MBP(84-104) in females (left panel) and males (right panel). Pathway components (molecules and complexes) are displayed as circles, arrows indicate molecular interactions according to Ingenuity IPA (Qiagen). Downstream biological processes are highlighted in blue. Red and green colors correspond to up- and down-regulated DE genes according to the color scale (log2FC). Gradient colors indicate regulation of individual components of protein complexes. Threshold FC ≥ 2, p ≤ 0.05. IP3R is a site of xestospongin C action in females (orange line). b, von Frey testing in female mice ipsilateral (left panel) and contralateral (right panel) to IS MBP(84-104) (30 μg in 3 μl). At day 10 after IS MBP(84-104), IT administered IP3R inhibitor, xestospongin C (X2628, 1 nmol/5 µl, n = 5), but not vehicle 10% DMSO (5 µl, n = 4), attenuated the established allodynia. Control i.p. gabapentin (100 mg/kg, n = 3) also attenuated IS MBP(84-104) allodynia. The mean withdrawal tactile thresholds are in gram force (g) ± S.E.; two-way ANOVA (b, left: treatment × time f = 3.220, p = 0.0162, time f = 9.681, p = 0.0002, treatment f = 15.94, p = 0.0011, subject f = 1.125, p = 0.3797; b, right: treatment × time f = 1.407, p = 0.2482, time f = 1.346, p = 0.2803, treatment f = 0.2114, p = 0.8134, subject f = 3.109, p = 0.0107) with Dunnett's post hoc test: *, p ≤ 0.05; **, p ≤ 0.01; ****, p ≤ 0.0001 relative to the DMSO control. Not all groups were tested at the 15- and 45-min time points; these time points are shown in the graph, but were not included in the data analysis. Red arrows indicate drug administration.

Article Snippet: Gabapentin was from Toronto Research Chemicals (Ontario, Canada), and xestospongin C (X2628) was from Sigma-Aldrich.

Techniques:

Journal: Molecules

Article Title: Design, Synthesis and Biological Activity Study of γ-Aminobutyric Acid (GABA) Derivatives Containing Bridged Bicyclic Skeletons as BCAT1 Inhibitors

doi: 10.3390/molecules30040904

Figure Lengend Snippet: BCAT1 inhibitory activity of synthesized compounds 1 – 8 , WQQ-345 and gabapentin.

Article Snippet: Gabapentin (#T0702) was purchased from TargetMol (Boston, MA, USA).

Techniques: Activity Assay, Synthesized

Journal: Molecules

Article Title: Design, Synthesis and Biological Activity Study of γ-Aminobutyric Acid (GABA) Derivatives Containing Bridged Bicyclic Skeletons as BCAT1 Inhibitors

doi: 10.3390/molecules30040904

Figure Lengend Snippet: Dose–inhibition curves of proliferation inhibition of BCAT1 inhibitors 1 , 2 , 4 , 7 and gabapentin in 67R cells and NCI-H1975 cells for 120 h (n = 3; data are expressed as mean ± SD).

Article Snippet: Gabapentin (#T0702) was purchased from TargetMol (Boston, MA, USA).

Techniques: Inhibition

Journal: Molecules

Article Title: Design, Synthesis and Biological Activity Study of γ-Aminobutyric Acid (GABA) Derivatives Containing Bridged Bicyclic Skeletons as BCAT1 Inhibitors

doi: 10.3390/molecules30040904

Figure Lengend Snippet: Summary of IC 50 values of proliferation inhibition of BCAT1 inhibitors 1 , 2 , 4 , 7 and gabapentin in 67R cells and NCI-H1975 cells for 120 h (n = 3).

Article Snippet: Gabapentin (#T0702) was purchased from TargetMol (Boston, MA, USA).

Techniques: Inhibition

Journal: Neural Regeneration Research

Article Title: Enduring alterations in hippocampal astrocyte-synaptic proximity following adolescent alcohol exposure: reversal by gabapentin

doi: 10.4103/1673-5374.274339

Figure Lengend Snippet: AIE-induced reduction of astrocyte-synapse proximity in hippocampal area CA1 is reversed by gabapentin. (A) Left to right: Raw z-series astrocytes (green) and synaptic puncta (red), rendered astrocytes (purple), and points of colocalization of the astrocyte and synaptic maker (white), from control animals that received AIW, those exposed to AIE, and AIE animals that received gabapentin in adulthood (AIE + gabapentin). Scale bars: 15 μm. (B) Left Column: Astrocytes (green) and synaptic puncta (red) from each of the treatment groups described under A. Inset boxes represent regions for expanded magnification. Scale bars: 15 μm. Right column: Expanded magnification of areas inset in left column. Yellow asterisks indicate identified points of astrocyte-synaptic colocalization. Scale bars: 15 μm. (C) Mean (± SEM) ratio of astrocyte surface area (SA) to volume (V) was unchanged by AIE or Gabapentin treatment. (D) Mean (± SEM) percent of colocalization of astrocyte viral labeling and synaptic puncta was reduced in hippocampal area CA1 in adulthood following AIE ( P < 0.05, vs . AIW), and this decrease was reversed by treatment with gabapentin ( P < 0.05, vs . AIE and P > 0.05, vs . AIW + gabapentin). The number of animals used for each treatment group was: AIW – n = 6, AIE – n = 6, AIW + gabapentin – n = 8, AIE + gabapentin – n = 7. An average of five cells per animal were included in the mixed linear modeling analysis. AIE: Adolescent intermittent ethanol; AIW: adolescent intermittent water.

Article Snippet: Approximately 2 weeks after virus surgery (described below), gabapentin (100 mg/kg in sterile 0.9% NaCl, i.p.; Chem-Impex International, Inc., Wood Dale, IL, USA) or isovolumetric saline injections were initiated.

Techniques: Labeling

Journal: Aging Cell

Article Title: Astrocyte Senescence Impairs Synaptogenesis due to Thrombospondin‐1 Loss

doi: 10.1111/acel.70382

Figure Lengend Snippet: The competitive TSP‐1 receptor antagonist gabapentin (GBP) blocks the synaptogenic effect of SAMR1 ACMs. (A and C) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACMs from Diff‐Ast SAMR1 and SAMP8 with or without GBP 32 μM. (B and D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) colocalization vesicles in hippocampal neurons treated with ACMs from ACSA‐2 + SAMR1 and SAMP8 of 6‐m mice with or without GBP 32 μM. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05, ** p < 0.01, and *** p < 0.001. Scale bar: 50 μm.

Article Snippet: At 11 DIV, neuron medium was totally replaced by ACM from Ast‐Diff or half replaced by ACSA‐2 + ACM during 3 h. Gabapentin (GBP, MedChemExpress, HY‐A0057) and TSP‐1 (MedChemExpress, HY‐P701325) dosages were based on Cheng et al. ( ) procedures.

Techniques: Immunostaining