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Dendritic calcium encodes striatal neuron output during up-states
Jason N D Kerr1, Dietmar Plenz
1Unit of Neural Network Physiology, Laboratory of Systems Neuroscience, National Institute of Mental Health, Bethesda, Maryland 20892, USA.
Summary
Striatal spiny projection neurons
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Computational Neuroscience
Background:
- Striatal spiny projection neurons are critical for basal ganglia function, mediating outputs to the globus pallidus and substantia nigra.
- Activity bursts in these neurons are essential for normal basal ganglia function and implicated in dysfunction.
- Corticostriatal inputs drive these bursts by depolarizing neurons from a resting down-state to an up-state.
Purpose of the Study:
- To investigate how dendritic calcium signals encode action potential bursts in striatal spiny projection neurons during different cellular states.
- To elucidate the role of active dendritic signal propagation in shaping calcium transients during burst firing.
Main Methods:
- Utilized organotypic cortex-striatum-substantia nigra cultures (5-6 weeks in vitro).
- Employed somatic whole-cell patch-clamp recordings combined with Fura-2 imaging to measure intracellular calcium concentration ([Ca2+]i).
- Applied somatic current pulses and voltage commands to evoke action potentials and bursts.
Main Results:
- Dendritic [Ca2+]i transients during up-state bursts strongly correlated with burst strength.
- Action potentials evoked during down-states also produced dendritic [Ca2+]i transients correlated with burst strength.
- Up-state bursts induced supralinear increases (>200%) in dendritic [Ca2+]i compared to down-state activity.
- Tetrodotoxin blocked burst-evoked dendritic [Ca2+]i transients, indicating reliance on active action potential propagation.
Conclusions:
- Dendritic calcium transients in spiny projection neurons encode somatic bursts supralinearly during up-states via active action potential propagation.
- This mechanism allows for precise encoding of neuronal output contributing to basal ganglia function.
- Findings suggest a feedback mechanism where dendritic activity informs corticostriatal synapses about neuronal output.