Figure 1. How dopamine increases synaptic strength in the hippocampus.

(Left) To test the effects of dopamine on long-term potentiation (LTP), Fuchsberger et al. injected the neurotransmitter into slices of the hippocampus (pink) and recorded the electrical activity of CA1 neurons (white electrode). (Right inset) They found that dopamine triggers the D1/D5 receptor (green) to activate a signaling pathway which includes the enzymes AC1/AC8 (dark blue), cAMP (brown) and PKA (purple). This leads to the production of more proteins that support the strengthening of the synapse and long-term potentiation. At the same time, neurotransmitters released from the pre-synaptic terminal, such as glutamate (dark blue circles), stimulate proteins on the post-synaptic terminal, such as NMDA receptors (light blue), to transmit calcium ions (Ca²⁺; light blue small circles) into the neuron. The calcium ions also activate AC1/AC8, ensuring that dopamine-induced protein synthesis is paired with neural activation. This increases the production of GluA1, a type of subunit that can assemble to form calcium-permeable AMPA receptors (yellow), which Fuchsberger et al. show to be essential for dopamine-induced LTP. AC1/AC8: adenylate cyclase 1/8; cAMP: cyclic adenosine monophosphate; PKA: protein kinase A. Figure 1 was created with BioRender.com.