@article {2133,
	title = {On the initiation and propagation of dendritic spikes in CA1 pyramidal neurons.},
	journal = {The Journal of Neuroscience: The Official Journal of the Society for Neuroscience},
	volume = {24},
	year = {2004},
	month = {2004 Dec 8},
	pages = {11046-56},
	abstract = {<p>Under certain conditions, regenerative voltage spikes can be initiated locally in the dendrites of CA1 pyramidal neurons. These are interesting events that could potentially provide neurons with additional computational abilities. Using whole-cell dendritic recordings from the distal apical trunk and proximal tuft regions and realistic computer modeling, we have determined that highly synchronized and moderately clustered inputs are required for dendritic spike initiation: approximately 50 synaptic inputs spread over 100 mum of the apical trunk/tuft need to be activated within 3 msec. Dendritic spikes are characterized by a more depolarized voltage threshold than at the soma [-48 +/- 1 mV (n = 30) vs -56 +/- 1 mV (n = 7), respectively] and are mainly generated and shaped by dendritic Na+ and K+ currents. The relative contribution of AMPA and NMDA currents is also important in determining the actual spatiotemporal requirements for dendritic spike initiation. Once initiated, dendritic spikes can easily reach the soma, but their propagation is only moderately strong, so that it can be modulated by physiologically relevant factors such as changes in the V(m) and the ionic composition of the extracellular solution. With effective spike propagation, an extremely short-latency neuronal output is produced for greatly reduced input levels. Therefore, dendritic spikes function as efficient detectors of specific input patterns, ensuring that the neuronal response to high levels of input synchrony is a precisely timed action potential output.</p>
},
	keywords = {Action Potentials, AMPA, Animals, Dendrites, Electrodes, Excitatory Postsynaptic Potentials, Ion Channels, Models, N-Methyl-D-Aspartate, Neurological, Pyramidal Cells, Rats, Receptors, Sprague-Dawley},
	issn = {1529-2401},
	doi = {10.1002/cbic.201000254},
	author = {Gasparini, Sonia and Migliore, Michele and Magee, Jeffrey C}
}
@article {2138,
	title = {Normalization of Ca2+ signals by small oblique dendrites of CA1 pyramidal neurons.},
	journal = {The Journal of Neuroscience: The Official Journal of the Society for Neuroscience},
	volume = {23},
	year = {2003},
	month = {2003 Apr 15},
	pages = {3243-50},
	abstract = {<p>Oblique dendrites of CA1 pyramidal neurons predominate in stratum radiatum and receive approximately 80\% of the synaptic input from Schaffer collaterals. Despite this fact, most of our understanding of dendritic signal processing in these neurons comes from studies of the main apical dendrite. Using a combination of Ca2+ imaging and whole-cell recording techniques in rat hippocampal slices, we found that the properties of the oblique dendrites differ markedly from those of the main dendrites. These different properties tend to equalize the Ca2+ rise from single action potentials as they backpropagate into the oblique dendrites from the main trunk. Evidence suggests that this normalization of Ca2+ signals results from a higher density of a transient, A-type K+ current [I(K(A))] in the oblique versus the main dendrites. The higher density of I(K(A)) may have important implications for our understanding of synaptic integration and plasticity in these structures.</p>
},
	keywords = {4-Aminopyridine, Action Potentials, Animals, Calcium, Calcium Channel Blockers, Calcium Signaling, Dendrites, Electric Stimulation, Fluorescent Dyes, Hippocampus, Patch-Clamp Techniques, Potassium Channel Blockers, Potassium Channels, Pyramidal Cells, Rats, Sodium Channels, Sprague-Dawley, Tetrodotoxin},
	issn = {1529-2401},
	doi = {10.1002/cbic.201000254},
	author = {Frick, Andreas and Magee, Jeffrey and Koester, Helmut J and Migliore, Michele and Johnston, Daniel}
}
