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Fluvoxamineis is an antidepressant which pharmacologically functions as a selective serotonin reuptake inhibitor. Serotonin, also known as 5-HT, is amonoamine neurotransmitter with various physiological functions such as mood, appetite, and sleep[1].

In vitro: Fluvoxamine effectively inhibited 5-HT uptake by blood platelets and brain synaptosomes [1].Fluvoxamine (10 mg/kg) increased [5-HT]ex levels in all brain areas and increased [DA]ex levels in the striatum. Fluvoxamine (10 mg/kg) in combination with of quetiapine (10 mg/kg) increased [DA]ex and [5-HT]ex levels in all brain areas when compared with baseline. The combination produced a significant increase of [DA]ex levels in the prefrontal cortex and thalamus whereas neither quetiapine nor fluvoxamine in monotherapy affected [DA]ex levels [2]. Fluvoxamine induced antiallodynic effects on neuropathic pain via descending 5-HT fibers and spinal 5-HT2A or 5-HT2C receptors, and the antinociception on acute mechanical pain via 5-HT3 receptors [3].

In vivo: Single administration of fluvoxamine (10 and 30 mg/kg, i.p.) dose-dependently enhanced synaptic efficacy in the hippocampo-mPFC pathway [4]. Fluvoxamine (10 and 30 mg/kg, i.p.) treatment suppressed long-term potentiation (LTP) in the hippocampal CA1 field of anesthetized rats. NAN-190 (0.5 mg/kg, i.p), the 5-HT(1A) receptor antagonist, completely reversed the fluvoxamine (30 mg/kg, i.p.) suppression of LTP [5].

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