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Action potentials are generally thought to originate near the neuronal soma and then to propagate along axons into synaptic terminals, where they trigger neurotransmitter release. However, a

recent paper in Science indicates that midbrain dopamine (DA) neurons and their terminals in the striatum may be an exception. Using the DA sensor GRABDA2m, Liu et al. detected spontaneous

DA release in striatal slices, which do not contain DA neuron cell bodies. It is known that the axons of cholinergic (ACh) interneurons intermingle with DA axons in the striatum and can

stimulate DA release, and indeed the authors found that spontaneous DA release in striatal slices was blocked when they inhibited nicotinic acetylcholine receptors (nAChRs). By directly

recording from individual DA axons, Liu et al. observed action potentials in individual axons in response to current injection or application of an nAChR agonist. These action potentials

could also be triggered by optogenetic stimulation of ACh neurons. Finally, they found evidence that this mechanism is engaged in vivo during movement and when mice are presented with

flashes of light. Liu et al. speculate that that these local action potentials may spread through the DA axon network, allowing ACh to ‘broadcast’ DA release, and they think that this may

allow a mode of DA signaling with greater spatial control than soma-initiated firing.

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