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The Journal of Neuroscience, June 17, 2009, 29(24):7833-7845; doi:10.1523/JNEUROSCI.0573-09.2009

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Cellular/Molecular
Synaptic Activation and Membrane Potential Changes Modulate the Frequency of Spontaneous Elementary Ca²⁺ Release Events in the Dendrites of Pyramidal Neurons

Satoshi Manita and William N. Ross

Department of Physiology, New York Medical College, Valhalla, New York 10595

Correspondence should be addressed to Dr. William N. Ross, Department of Physiology, New York Medical College, Valhalla, NY 10595. Email: ross{at}nymc.edu

In most neurons postsynaptic [Ca²⁺]_i changes result from synaptic activation opening voltage gated channels, ligand gated channels, or mobilizing Ca²⁺ release from intracellular stores. In addition to these changes that result directly from stimulation we found that in pyramidal cells there are spontaneous, rapid, Ca²⁺ release events, predominantly, but not exclusively localized at dendritic branch points. They are clearest on the main apical dendrite but also have been detected in the finer branches and in the soma. Typically they have a spatial extent at initiation of ~2 µm, a rise time of <15 ms, duration <100 ms, and amplitudes of 10–70% of that generated by a backpropagating action potential at the same location. These events are not caused by background electrical or synaptic activity. However, their rate can be increased by repetitive synaptic stimulation at moderate frequencies, mainly through metabotropic glutamate receptor mobilization of IP₃. In addition, their frequency can be modulated by changes in membrane potential in the subthreshold range, predominantly by affecting Ca²⁺ entry through L-type channels. They resemble the elementary events ("sparks" and "puffs") mediated by IP₃ receptors and ryanodine receptors that have been described primarily in non-neuronal preparations. These spontaneous Ca²⁺ release events may be the fundamental units underlying some postsynaptic signaling cascades in mature neurons.

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Received Feb. 3, 2009; revised April 24, 2009; accepted May 12, 2009.

Correspondence should be addressed to Dr. William N. Ross, Department of Physiology, New York Medical College, Valhalla, NY 10595. Email: ross{at}nymc.edu

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