Dendritic Ca2+ plays an important role not only in synaptic integration and synaptic plasticity, but also in dendritic excitability in midbrain dopamine neurons. However, the functional organization of dendritic Ca2+ signals in the dopamine neurons remains largely unknown. We therefore investigated dendritic Ca2+ signals by measuring glutamate-induced Ca2+ increases along the dendrites of acutely isolated midbrain dopamine neurons. Maximal doses of glutamate induced a [Ca2+]c rise with similar amplitudes in proximal and distal dendritic regions of a dopamine neuron. Glutamate receptors contributed incrementally to the [Ca2+]c rise according to their distance from the soma, with a reciprocal decrement in the contribution of voltage-operated Ca2+ channels (VOCCs). The contribution of AMPA and NMDA receptors increased with dendritic length, but that of metabotropic glutamate receptors decreased. At low doses of glutamate at which spontaneous firing was sustained, the [Ca2+]c rise was higher in the distal than the proximal regions of a dendrite, possibly due to the increased spontaneous firing rate. These results indicate that functional organization of Ca2+ signals in the dendrites of dopamine neurons requires different combination of VOCCs and glutamate receptors according to dendritic length, and that regional Ca2+ rises in dendrites respond differently to applied glutamate concentration.
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