Title: Coincidence of cholinergic pauses, dopaminergic activation and depolarisation of spiny projection neurons drives synaptic plasticity in the striatum
Journal: Nat Comm, 13(1):1296
Link: https://www.nature.com/articles/s41467-022-28950-0
Comments:
Synaptic plasticity is the physiological basis in learning and memory in the brain. When the center neuron system (CNS) enhances the synaptic activity or generate new synapse, brain will complete this with changes in cellular metabolism. Studies previously showed glutamatergic transmission modulated by dopaminergic inputs in the cerebral cortex and striatum underlay long-term memory. However, we still do not know how dopamine signal triggers formation of the long-term memory in these brain regions. In this paper, the authors reported that when the synapses and spiny neurons generate long-term potentiation (LTP), the dopamine interneurons released dopamine, while the cholinergic interneurons stopped releasing acetylcholine and the spiny neurons will become depolarization at same time. Therefore, the authors hypothesized that the release of dopamine, the pause of cholinergic interneurons and depolarization of spiny neurons enhance the synaptic plasticity.
In their experiments, the authors stimulated the cerebral cortex to inhibit the activity of cholinergic interneurons in the contralateral striatum of mice, while they used the light flash as visual stimulation to make the neostriatum release dopamine. At same time, they recorded the potential change in the striatal neurons and recorded postsynaptic potentials (PSPs) in the striatal spiny neurons. Results showed that long-term potentiation at corticostriatal synapses with striatal spiny neurons was dependent on the coincident pauses in the striatal cholinergic interneurons and phasic dopamine activation. Thus, the pause of activity in the striatal cholinergic neurons seemed to define critical timing of dopamine release essential for induction of synaptic plasticity. This result gave deep insight into understanding the mechanism of synaptic plasticity.
