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. 2022 Jan 5;15:822614. doi: 10.3389/fncel.2021.822614

Figure 1.

Figure 1

Schematic diagram of the antidepressant, fluoxetine, and astrocytes. Fluoxetine (FLX) increases vesicular nucleotide transporter (VNUT)-dependent ATP exocytosis from astrocytes and causes elevation of extracellular ATP (ATPo). Kir4.1 may be an important target molecule of FLX in astrocytes. Extracellular ATP and its metabolite, adenosine, act on P2Y11 and A1b receptors to increase cAMP levels and enhance Bdnf transcription in astrocytes via CREB phosphorylation. The BDNF produced and released by astrocytes is thought to cause synapse and network remodeling and to exhibit antidepressant effects. cAMP may also enhance VNUT expression via protein kinase A, which further strengthens ATP/adenosine signaling.