@article {46918, title = {Conjunctive input processing drives feature selectivity in hippocampal CA1 neurons.}, journal = {Nature Neuroscience}, year = {2015}, month = {2015 Jul 13}, abstract = {

Feature-selective firing allows networks to produce representations of the external and internal environments. Despite its importance, the mechanisms generating neuronal feature selectivity are incompletely understood. In many cortical microcircuits the integration of two functionally distinct inputs occurs nonlinearly through generation of active dendritic signals that drive burst firing and robust plasticity. To examine the role of this processing in feature selectivity, we recorded CA1 pyramidal neuron membrane potential and local field potential in mice running on a linear treadmill. We found that dendritic plateau potentials were produced by an interaction between properly timed input from entorhinal cortex and hippocampal CA3. These conjunctive signals positively modulated the firing of previously established place fields and rapidly induced new place field formation to produce feature selectivity in CA1 that is a function of both entorhinal cortex and CA3 input. Such selectivity could allow mixed network level representations that support context-dependent spatial maps.

}, issn = {1546-1726}, doi = {10.1038/nn.4062}, author = {Bittner, Katie C and Grienberger, Christine and Vaidya, Sachin P and Milstein, Aaron D and Macklin, John J and Suh, Junghyup and Tonegawa, Susumu and Magee, Jeffrey C} } @article {5924, title = {Control of timing, rate and bursts of hippocampal place cells by dendritic and somatic inhibition.}, journal = {Nature neuroscience}, volume = {15}, year = {2012}, month = {2012 May}, pages = {769-75}, abstract = {A consortium of inhibitory neurons control the firing patterns of pyramidal cells, but their specific roles in the behaving animal are largely unknown. We performed simultaneous physiological recordings and optogenetic silencing of either perisomatic (parvalbumin (PV) expressing) or dendrite-targeting (somatostatin (SOM) expressing) interneurons in hippocampal area CA1 of head-fixed mice actively moving a treadmill belt rich with visual-tactile stimuli. Silencing of either PV or SOM interneurons increased the firing rates of pyramidal cells selectively in their place fields, with PV and SOM interneurons having their largest effect during the rising and decaying parts of the place field, respectively. SOM interneuron silencing powerfully increased burst firing without altering the theta phase of spikes. In contrast, PV interneuron silencing had no effect on burst firing, but instead shifted the spikes{\textquoteright} theta phase toward the trough of theta. These findings indicate that perisomatic and dendritic inhibition have distinct roles in controlling the rate, burst and timing of hippocampal pyramidal cells.}, keywords = {Action Potentials, Animal, Animals, Behavior, Biophysics, Dendrites, Electric Stimulation, Exercise Test, Green Fluorescent Proteins, Halorhodopsins, Hippocampus, Humans, Inbred C57BL, Light, Mice, Movement, Neural Inhibition, Neurons, Optics and Photonics, Parvalbumins, Patch-Clamp Techniques, Photic Stimulation, Probability, Somatostatin, Spectrum Analysis, Time Factors, Time Perception, Touch, Transgenic}, issn = {1546-1726}, doi = {10.1038/nn.3077}, author = {Royer, S{\'e}bastien and Zemelman, Boris V and Losonczy, Attila and Kim, Jinhyun and Chance, Frances and Magee, Jeffrey C and Buzs{\'a}ki, Gy{\"o}rgy} } @article {3915, title = {Compartmentalized dendritic plasticity and input feature storage in neurons.}, journal = {Nature}, volume = {452}, year = {2008}, month = {2008 Mar 27}, pages = {436-41}, abstract = {

Although information storage in the central nervous system is thought to be primarily mediated by various forms of synaptic plasticity, other mechanisms, such as modifications in membrane excitability, are available. Local dendritic spikes are nonlinear voltage events that are initiated within dendritic branches by spatially clustered and temporally synchronous synaptic input. That local spikes selectively respond only to appropriately correlated input allows them to function as input feature detectors and potentially as powerful information storage mechanisms. However, it is currently unknown whether any effective form of local dendritic spike plasticity exists. Here we show that the coupling between local dendritic spikes and the soma of rat hippocampal CA1 pyramidal neurons can be modified in a branch-specific manner through an N-methyl-d-aspartate receptor (NMDAR)-dependent regulation of dendritic Kv4.2 potassium channels. These data suggest that compartmentalized changes in branch excitability could store multiple complex features of synaptic input, such as their spatio-temporal correlation. We propose that this {\textquoteright}branch strength potentiation{\textquoteright} represents a previously unknown form of information storage that is distinct from that produced by changes in synaptic efficacy both at the mechanistic level and in the type of information stored.

}, keywords = {Action Potentials, Animals, Cell Shape, Dendrites, Ion Channel Gating, Male, Mice, Models, N-Methyl-D-Aspartate, Neurological, Neuronal Plasticity, Pyramidal Cells, Rats, Receptors, Shal Potassium Channels, Sprague-Dawley}, issn = {1476-4687}, doi = {10.1038/nature06725}, author = {Losonczy, Attila and Makara, Judit K and Magee, Jeffrey C} } @article {2134, title = {Changes in AMPA receptor currents following LTP induction on rat CA1 pyramidal neurones.}, journal = {The Journal of Physiology}, volume = {559}, year = {2004}, month = {2004 Sep 1}, pages = {543-54}, abstract = {

In the CA1 region of the hippocampus, LTP is thought to be initiated by a transient activation of NMDA receptors and is expressed as a persistent increase in synaptic transmission through AMPA receptors. To investigate the postsynaptic modifications of AMPA receptors involved in this enhanced synaptic transmission, the channel density and single-channel properties of extrasynaptic AMPA receptors located in synaptically active dendritic regions were examined following the induction of LTP. Following tetanic stimulation an outside-out patch was excised from the apical dendrite near the point of stimulation and saturating concentrations of glutamate were rapidly applied to the patch. AMPA current amplitude and duration were increased significantly in patches pulled from dendrites that expressed LTP. Non-stationary fluctuation analysis of AMPA currents indicated that AMPA channel number was nearly twofold larger than in controls, while single channel conductance and maximum open-probability were unchanged. Furthermore, while subtle changes in AMPA channel kinetics could also be observed, we did not find any evidence that receptor affinity or rectification properties were altered by LTP induction. Very similar results were found when CaMK-II activity was increased through the intracellular application of Ca/CaM. Together, we interpret our data to indicate that the stimuli used here produce an increased delivery of AMPA receptors to synaptically active regions of the apical dendrite without inducing any significant changes in their basic biophysical properties and that such delivery is a key element in this form of synaptic plasticity.

}, keywords = {AMPA, Animals, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Calcium-Calmodulin-Dependent Protein Kinases, Glutamic Acid, Long-Term Potentiation, Pyramidal Cells, Rats, Receptors, Sprague-Dawley}, issn = {0022-3751}, doi = {10.1002/cbic.201000254}, author = {Andrasfalvy, Bertalan K and Magee, Jeffrey C} }