Fluvoxamine (0.1–10 µM, 5 days) increased neurite outgrowth in PC12 cells exposed to NGF (2.5 ng/ml). NE-100 (1.0 µM) blocked the effect of 10 µM fluvoxamine. Paroxetine and sertraline did not potentiate outgrowth and reduced the response at 10 µM; this model does not establish clinical neuroprotection. [2]
Competitive inhibition of serotonin uptake in rat brain synaptosomes
Biochemical assay · Crude P2 brain synaptosomal fraction from male adult Wistar rats (240–300 g) [1]
Fluvoxamine competitively inhibited serotonin uptake. Lineweaver–Burk plots shared the ordinate intercept, consistent with unchanged Vmax. The reported Ki was lower than those for imipramine and desmethylimipramine in this assay.
Literature-Reported Treatment Conditions
- Treatment concentration
- Inhibitor: 10^-6 M; [3H]-5-HT: 10^-6, 2 × 10^-7 and 6.7 × 10^-8 M
- Exposure duration
- 4 min preincubation at 37°C followed by 5 min uptake
- Method
- Radiolabeled uptake, filtration and liquid scintillation counting; uptake corrected for uptake at 0°C; comparison with inhibitor-free control.
- Reported limits
- Vehicle and replicate count for Table 2 are not specified in the read assay description/table.
Methods and source locations
Compound reported in the paper: Fluvoxamine maleate; Compound label in the paper: Fluvoxamine
Results for the reported maleate material; doses and assay concentrations retained as reported, without salt/base conversion or Adooq lot equivalence.
pp. 505–506, identity and shared methods; p. 508, Table 2 and adjacent Results
Inhibition of radiolabeled serotonin uptake: Lineweaver–Burk uptake analysis; Table 2 also reports imipramine 0.23 and desmethylimipramine 1.2 on the same scale. No uncertainty or n supplied in this table. — p. 506, rat brain synaptosome uptake method; p. 508, Results and Table 2
NGF-dependent neurite outgrowth and sigma-1 antagonist sensitivity
Cell-based study · Rat PC12 cells from RIKEN Cell Bank; NGF-induced differentiation [2]
Fluvoxamine increased NGF-induced neurite outgrowth over 0.1–10 µM. NE-100 blocked potentiation by 10 µM fluvoxamine, while NE-100 alone did not alter the NGF response. These controls support sigma-1 receptor involvement in this functional model.
Literature-Reported Treatment Conditions
- Treatment concentration
- Fluvoxamine 0.1, 1.0 or 10 µM; antagonist control NE-100 1.0 µM
- Exposure duration
- 5 days
- Method
- NGF-induced differentiation followed by blinded live-cell morphometry; representative MAP-2 immunocytochemistry in Figure 4.
- Co-treatment
- NGF 2.5 ng/ml in all selected response groups; additional fluvoxamine 10 µM + NE-100 1.0 µM group. NGF-alone and NGF + NE-100 controls.
- Reported limits
- Drug solvent/vehicle is not specified in the read methods. Figure 2 n = 6 is not further defined as independent biological preparations.
Methods and source locations
Compound reported in the paper: Fluvoxamine maleate; Compound label in the paper: Fluvoxamine
Reported fluvoxamine maleate in PC12 cells with NGF; functional antagonist sensitivity does not supply a binding Ki or establish clinical neuroprotection.
Drugs; Cell culture; Quantification of neurite sprouting; Statistical analysis; Figures 2 and 4 and related Results
Cells with at least one neurite at least as long as the cell-body diameter: Blinded morphometric counting after 5 days; three fields per well, approximately 100 cells/field. Figure 2: mean ± S.E.M., n = 6; one-way ANOVA with Bonferroni/Dunn post hoc testing. No exact bar percentages transcribed. — Figure 2; Results, Effects of SSRIs and Role of sigma-1 receptors; Quantification of neurite sprouting; Statistical analysis
