Somatodendritic neuropeptide release potentiates GABAergic synapses in the VTA

Dr. Julie Kauer is a Professor of Psychiatry & Behavioral Sciences at Stanford University.

Neuropeptides are contained in nearly every neuron in the central nervous system and can be released not only from nerve terminals but also from somatodendritic sites. Cholecystokinin (CCK), among the most abundant neuropeptides in the brain, is expressed in the majority of midbrain dopamine neurons. Despite this high
expression, CCK function within the ventral tegmental area (VTA) is not well understood. We found that VTA dopamine neurons release CCK from somatodendritic regions, where it triggers long-term potentiation of GABAergic  synapses. The somatodendritic release occurs during trains of optogenetic stimuli or prolonged but modest depolarization. Paired-recording experiments demonstrated that CCK released from a single dopamine neuron is sufficient to induce LTP in synapses on neighboring neurons, suggesting that somatodendritic CCK release may influence a substantial fraction of nearby dopamine neurons and coordinate plasticity across local ensembles rather than acting in a strict cell- or synapse-autonomous manner.  In vivo, intra-VTA–infused CCK reduced dopamine cell Ca2+ signals during food consumption and was correlated with reduced food intake. Our experiments introduce somatodendritic neuropeptide release as a previously unknown feedback regulator of VTA dopamine cell excitability and support the idea that peptide signaling adds complexity and richness to neural circuits.

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