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4 Janelia Publications

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    12/03/07 | Coincidence detection of place and temporal context in a network model of spiking hippocampal neurons.
    Katz Y, Kath WL, Spruston N, Hasselmo ME
    PLoS Computational Biology. 2007 Dec;3(12):e234. doi: 10.1371/journal.pcbi.0030234

    Recent advances in single-neuron biophysics have enhanced our understanding of information processing on the cellular level, but how the detailed properties of individual neurons give rise to large-scale behavior remains unclear. Here, we present a model of the hippocampal network based on observed biophysical properties of hippocampal and entorhinal cortical neurons. We assembled our model to simulate spatial alternation, a task that requires memory of the previous path through the environment for correct selection of the current path to a reward site. The convergence of inputs from entorhinal cortex and hippocampal region CA3 onto CA1 pyramidal cells make them potentially important for integrating information about place and temporal context on the network level. Our model shows how place and temporal context information might be combined in CA1 pyramidal neurons to give rise to splitter cells, which fire selectively based on a combination of place and temporal context. The model leads to a number of experimentally testable predictions that may lead to a better understanding of the biophysical basis of information processing in the hippocampus.

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    10/23/07 | Dendritic spikes induce single-burst long-term potentiation.
    Remy S, Spruston N
    Proceedings of the National Academy of Sciences of the United States of America. 2007 Oct 23;104(43):17192-7. doi: 10.1073/pnas.0707919104

    The hippocampus is essential for episodic memory, which requires single-trial learning. Although long-term potentiation (LTP) of synaptic strength is a candidate mechanism for learning, it is typically induced by using repeated synaptic activation to produce precisely timed, high-frequency, or rhythmic firing. Here we show that hippocampal synapses potentiate robustly in response to strong activation by a single burst. The induction mechanism of this single-burst LTP requires activation of NMDA receptors, L-type voltage-gated calcium channels, and dendritic spikes. Thus, dendritic spikes are a critical trigger for a form of LTP that is consistent with the function of the hippocampus in episodic memory.

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    05/15/07 | Dendritic D-type potassium currents inhibit the spike afterdepolarization in rat hippocampal CA1 pyramidal neurons.
    Metz AE, Spruston N, Martina M
    The Journal of Physiology. 2007 May 15;581(Pt 1):175-87. doi: 10.1113/jphysiol.2006.127068

    In CA1 pyramidal neurons, burst firing is correlated with hippocampally dependent behaviours and modulation of synaptic strength. One of the mechanisms underlying burst firing in these cells is the afterdepolarization (ADP) that follows each action potential. Previous work has shown that the ADP results from the interaction of several depolarizing and hyperpolarizing conductances located in the soma and the dendrites. By using patch-clamp recordings from acute rat hippocampal slices we show that D-type potassium current modulates the size of the ADP and the bursting of CA1 pyramidal neurons. Sensitivity to alpha-dendrotoxin suggests that Kv1-containing potassium channels mediate this current. Dual somato-dendritic recording, outside-out dendritic recordings, and focal application of dendrotoxin together indicate that the channels mediating this current are located in the apical dendrites. Thus, our data present evidence for a dendritic segregation of Kv1-like channels in CA1 pyramidal neurons and identify a novel action for these channels, showing that they inhibit action potential bursting by restricting the size of the ADP.

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    02/01/07 | Stability and plasticity of intrinsic membrane properties in hippocampal CA1 pyramidal neurons: effects of internal anions.
    Kaczorowski CC, Disterhoft J, Spruston N
    The Journal of Physiology. 2007 Feb 1;578(Pt 3):799-818. doi: 10.1113/jphysiol.2006.124586

    CA1 pyramidal neurons from animals that have acquired hippocampal tasks show increased neuronal excitability, as evidenced by a reduction in the postburst afterhyperpolarization (AHP). Studies of AHP plasticity require stable long-term recordings, which are affected by the intracellular solutions potassium methylsulphate (KMeth) or potassium gluconate (KGluc). Here we show immediate and gradual effects of these intracellular solutions on measurement of the AHP and basic membrane properties, and on the induction of AHP plasticity in CA1 pyramidal neurons from rat hippocampal slices. The AHP measured immediately after establishing whole-cell recordings was larger with KMeth than with KGluc. In general, the AHP in KMeth was comparable to the AHP measured in the perforated-patch configuration. However, KMeth induced time-dependent changes in the intrinsic membrane properties of CA1 pyramidal neurons. Specifically, input resistance progressively increased by 70% after 50 min; correspondingly, the current required to trigger an action potential and the fast afterdepolarization following action potentials gradually decreased by about 50%. Conversely, these measures were stable in KGluc. We also demonstrate that activity-dependent plasticity of the AHP occurs with physiologically relevant stimuli in KGluc. AHPs triggered with theta-burst firing every 30 s were progressively reduced, whereas AHPs elicited every 150 s were stable. Blockade of the apamin-sensitive AHP current (I(AHP)) was insufficient to block AHP plasticity, suggesting that plasticity is manifested through changes in the apamin-insensitive slow AHP current (sI(AHP)). These changes were observed in the presence of synaptic blockers, and therefore reflect changes in the intrinsic properties of the neurons. However, no AHP plasticity was observed using KMeth. In summary, these data show that KMeth produces time-dependent changes in basic membrane properties and prevents or obscures activity-dependent reduction of the AHP. In whole-cell recordings using KGluc, repetitive theta-burst firing induced AHP plasticity that mimics learning-related reduction in the AHP.

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