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This Article Full Text Full Text (PDF) All Versions of this Article: 98/5/2910    most recent 00660.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kloppenburg, P. Articles by Harris-Warrick, R. M. Search for Related Content PubMed PubMed Citation Articles by Kloppenburg, P. Articles by Harris-Warrick, R. M.

Heterogeneous Effects of Dopamine on Highly Localized, Voltage-Induced Ca²⁺ Accumulation in Identified Motoneurons

¹Department of Neurobiology and Behavior, ²Department of Biomedical Engineering, and ³Developmental Resource for Biophysical Imaging and Opto-Electronics, Applied and Engineering Physics, Cornell University, Ithaca, New York; and ⁴Institute of Zoology and Physiology, University of Cologne, Cologne, Germany

Submitted 14 June 2007; accepted in final form 27 August 2007

Modulation of synaptic transmission is a major mechanism for the functional reconfiguration of neuronal circuits. Neurotransmitter release and, consequently, synaptic strength are regulated by intracellular Ca²⁺ levels in presynaptic terminals. In identified neurons of the lobster pyloric network, we studied localized, voltage-induced Ca²⁺ accumulation and its modulation in varicosities on distal neuritic arborizations, which have previously been shown to be sites of synaptic contacts. We previously demonstrated that dopamine (DA) weakens synaptic output from the pyloric dilator (PD) neuron and strengthens synaptic output from the lateral pyloric (LP) and pyloric constrictor (PY) neurons. Here we show that DA modifies voltage-activated Ca²⁺ accumulation in many varicosities in ways that are consistent with DA's effects on synaptic transmission: DA elevates Ca²⁺ accumulation in LP and PY varicosities and reduces Ca²⁺ accumulation in PD varicosities. However, in all three neuron types, we also found varicosities that were unaffected by DA. In the PY neurons, we found that DA can simultaneously increase and decrease voltage-evoked Ca²⁺ accumulation at different varicosities, even within the same neuron. These results suggest that regulation of Ca²⁺ entry is a common mechanism to regulate synaptic strength in the pyloric network. However, voltage-evoked local Ca²⁺ accumulation can be differentially modulated to control Ca²⁺-dependent processes in functionally separate varicosities of a single neuron.