@article {47017, title = {Optogenetics: 10 years after ChR2 in neurons-views from the community.}, journal = {Nature Neuroscience}, volume = {18}, year = {2015}, month = {2015 Aug 26}, pages = {1202-12}, issn = {1546-1726}, doi = {10.1038/nn.4106}, author = {Adamantidis, Antoine and Arber, Silvia and Bains, Jaideep S and Bamberg, Ernst and Bonci, Antonello and Buzs{\'a}ki, Gy{\"o}rgy and Cardin, Jessica A and Costa, Rui M and Dan, Yang and Goda, Yukiko and Graybiel, Ann M and H{\"a}usser, Michael and Hegemann, Peter and Huguenard, John R and Insel, Thomas R and Janak, Patricia H and Johnston, Daniel and Josselyn, Sheena A and Koch, Christof and Kreitzer, Anatol C and L{\"u}scher, Christian and Malenka, Robert C and Miesenb{\"o}ck, Gero and Nagel, Georg and Roska, Botond and Schnitzer, Mark J and Shenoy, Krishna V and Soltesz, Ivan and Sternson, Scott M and Tsien, Richard W and Tsien, Roger Y and Turrigiano, Gina G and Tye, Kay M and Wilson, Rachel I} } @article {2126, title = {Associative pairing enhances action potential back-propagation in radial oblique branches of CA1 pyramidal neurons.}, journal = {The Journal of Physiology}, volume = {580}, year = {2007}, month = {2007 May 1}, pages = {787-800}, abstract = {

Back-propagating action potentials (bAPs) are involved in associative synaptic plasticity and the modulation of dendritic excitability. We have used high-speed confocal and two-photon imaging to measure calcium and voltage signals associated with action potential propagation into oblique branches of CA1 pyramidal neurons in adult hippocampal slices. The spatial profile of the bAP-associated Ca(2+) influx was biphasic, with an initial increase in the proximity of the branch point followed by a progressive decrease. Voltage imaging in the branches showed that bAP amplitude was initially constant and then steadily declined with distance from the soma. To determine the role of transient K(+) channels in this profile, we used external Ba(2+) (150 microm) as a channel blocker, after characterizing its effect on A-type K(+) channels in the apical trunk. Bath application of Ba(2+) significantly reduced the A-type K(+) current in outside-out patches and nearly eliminated the distance-dependent decrease in bAP amplitude and its associated Ca(2+) signal. Finally, small amplitude bAPs at more distal oblique branch locations could be boosted by simultaneous branch depolarization, such that the paired Ca(2+) signal became nearly the same for proximal and distal oblique dendrites. These data suggest that dendritic K(+) channels regulate the amplitude of bAPs to create a dendritic Ca(2+) signal whose magnitude is inversely related to the electrotonic distance from the soma when bAPs are not associated with a significant amount of localized synaptic input. This distance-dependent Ca(2+) signal from bAPs, however, can be amplified and a strong associative signal is produced once the proper correlation between synaptic activation and AP output is achieved. We hypothesize that these two signals may be involved in the regulation of the expression and activity of dendritic voltage- and ligand-gated ion channels.

}, keywords = {Action Potentials, Animals, Barium, Calcium, Dendrites, Hippocampus, Knockout, Male, Mice, Neuronal Plasticity, Potassium Channel Blockers, Potassium Channels, Pyramidal Cells, Rats, Sprague-Dawley, Synapses}, issn = {0022-3751}, doi = {10.1002/cbic.201000254}, author = {Gasparini, Sonia and Losonczy, Attila and Chen, Xixi and Johnston, Daniel and Magee, Jeffrey C} } @article {2132, title = {Plasticity of dendritic function.}, journal = {Current Opinion in Neurobiology}, volume = {15}, year = {2005}, month = {2005 Jun}, pages = {334-42}, abstract = {

The various properties of neuronal dendrites{\textendash}their morphology, active membrane and synaptic properties{\textendash}all play important roles in determining the functional capabilities of central nervous system neurons. Because of their fundamental involvement in both synaptic integration and synaptic plasticity, the active dendritic properties are important for both neuronal information processing and storage. The active properties of dendrites are determined by the densities of voltage-gated ion channels located within the dendrites in addition to the biophysical characteristics of those channels. The real power of this system resides in the level of plasticity that is provided by the many forms of channel modulation known to exist in neurons. Indeed, voltage gated ion channel modulation shapes the active properties of neuronal dendrites to specific conditions, thus tailoring the functional role of the single neuron within its circuit.

}, keywords = {Action Potentials, Brain, Dendrites, Ion Channel Gating, Ion Channels, Neuronal Plasticity}, issn = {0959-4388}, doi = {10.1002/cbic.201000254}, author = {Magee, Jeffrey C and Johnston, Daniel} } @article {2135, title = {LTP is accompanied by an enhanced local excitability of pyramidal neuron dendrites.}, journal = {Nature Neuroscience}, volume = {7}, year = {2004}, month = {2004 Feb}, pages = {126-35}, abstract = {

The propagation and integration of signals in the dendrites of pyramidal neurons is regulated, in part, by the distribution and biophysical properties of voltage-gated ion channels. It is thus possible that any modification of these channels in a specific part of the dendritic tree might locally alter these signaling processes. Using dendritic and somatic whole-cell recordings, combined with calcium imaging in rat hippocampal slices, we found that the induction of long-term potentiation (LTP) was accompanied by a local increase in dendritic excitability that was dependent on the activation of NMDA receptors. These changes favored the back-propagation of action potentials into this dendritic region with a subsequent boost in the Ca(2+) influx. Dendritic cell-attached patch recordings revealed a hyperpolarized shift in the inactivation curve of transient, A-type K(+) currents that can account for the enhanced excitability. These results suggest an important mechanism associated with LTP for shaping signal processing and controlling dendritic function.

}, keywords = {Action Potentials, Animals, Calcium, Dendrites, Excitatory Postsynaptic Potentials, Hippocampus, Ion Channels, Long-Term Potentiation, Memory, N-Methyl-D-Aspartate, Neuronal Plasticity, Organ Culture Techniques, Patch-Clamp Techniques, Rats, Receptors}, issn = {1097-6256}, doi = {10.1002/cbic.201000254}, author = {Frick, Andreas and Magee, Jeffrey and Johnston, Daniel} } @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 = {

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.

}, 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} }