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5 Publications

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    12/08/05 | Conditional dendritic spike propagation following distal synaptic activation of hippocampal CA1 pyramidal neurons.
    Jarsky T, Roxin A, Kath WL, Spruston N
    Nat Neurosci. 2005 Dec;8(12):1667-76. doi: 10.1038/nn1599

    The perforant-path projection to the hippocampus forms synapses in the apical tuft of CA1 pyramidal neurons. We used computer modeling to examine the function of these distal synaptic inputs, which led to three predictions that we confirmed in experiments using rat hippocampal slices. First, activation of CA1 neurons by the perforant path is limited, a result of the long distance between these inputs and the soma. Second, activation of CA1 neurons by the perforant path depends on the generation of dendritic spikes. Third, the forward propagation of these spikes is unreliable, but can be facilitated by modest activation of Schaffer-collateral synapses in the upper apical dendrites. This 'gating' of dendritic spike propagation may be an important activation mode of CA1 pyramidal neurons, and its modulation by neurotransmitters or long-term, activity-dependent plasticity may be an important feature of dendritic integration during mnemonic processing in the hippocampus.

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    10/01/05 | Factors mediating powerful voltage attenuation along CA1 pyramidal neuron dendrites.
    Golding NL, Mickus TJ, Katz Y, Kath WL, Spruston N
    J Physiol. 2005 Oct 1;568(Pt 1):69-82. doi: 10.1113/jphysiol.2005.086793

    We performed simultaneous patch-electrode recordings from the soma and apical dendrite of CA1 pyramidal neurons in hippocampal slices, in order to determine the degree of voltage attenuation along CA1 dendrites. Fifty per cent attenuation of steady-state somatic voltage changes occurred at a distance of 238 microm from the soma in control and 409 microm after blocking the hyperpolarization-activated (H) conductance. The morphology of three neurons was reconstructed and used to generate computer models, which were adjusted to fit the somatic and dendritic voltage responses. These models identify several factors contributing to the voltage attenuation along CA1 dendrites, including high axial cytoplasmic resistivity, low membrane resistivity, and large H conductance. In most cells the resting membrane conductances, including the H conductances, were larger in the dendrites than the soma. Simulations suggest that synaptic potentials attenuate enormously as they propagate from the dendrite to the soma, with greater than 100-fold attenuation for synapses on many small, distal dendrites. A prediction of this powerful EPSP attenuation is that distal synaptic inputs are likely only to be effective in the presence of conductance scaling, dendritic excitability, or both.

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    07/08/05 | Postsynaptic depolarization requirements for LTP and LTD: a critique of spike timing-dependent plasticity.
    Lisman J, Spruston N
    Nat Neurosci. 2005 Jul;8(7):839-41

    Long-term potentiation and long-term depression require postsynaptic depolarization, which many current models attribute to backpropagating action potentials. New experimental work suggests, however, that other mechanisms can lead to dendritic depolarization, and that backpropagating action potentials may be neither necessary nor sufficient for synaptic plasticity in vivo.

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    06/15/05 | R-type calcium channels contribute to afterdepolarization and bursting in hippocampal CA1 pyramidal neurons.
    Metz AE, Jarsky T, Martina M, Spruston N
    J Neurosci. 2005 Jun 15;25(24):5763-73. doi: 10.1523/JNEUROSCI.0624-05.2005

    Action potentials in pyramidal neurons are typically followed by an afterdepolarization (ADP), which in many cells contributes to intrinsic burst firing. Despite the ubiquity of this common excitable property, the responsible ion channels have not been identified. Using current-clamp recordings in hippocampal slices, we find that the ADP in CA1 pyramidal neurons is mediated by an Ni2+-sensitive calcium tail current. Voltage-clamp experiments indicate that the Ni2+-sensitive current has a pharmacological and biophysical profile consistent with R-type calcium channels. These channels are available at the resting potential, are activated by the action potential, and remain open long enough to drive the ADP. Because the ADP correlates directly with burst firing in CA1 neurons, R-type calcium channels are crucial to this important cellular behavior, which is known to encode hippocampal place fields and enhance synaptic plasticity.

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    06/03/05 | Output-mode transitions are controlled by prolonged inactivation of sodium channels in pyramidal neurons of subiculum.
    Cooper DC, Chung S, Spruston N
    PLoS Biol. 2005 Jun;3(6):e175. doi: 10.1371/journal.pbio.0030175

    Transitions between different behavioral states, such as sleep or wakefulness, quiescence or attentiveness, occur in part through transitions from action potential bursting to single spiking. Cortical activity, for example, is determined in large part by the spike output mode from the thalamus, which is controlled by the gating of low-voltage-activated calcium channels. In the subiculum--the major output of the hippocampus--transitions occur from bursting in the delta-frequency band to single spiking in the theta-frequency band. We show here that these transitions are influenced strongly by the inactivation kinetics of voltage-gated sodium channels. Prolonged inactivation of sodium channels is responsible for an activity-dependent switch from bursting to single spiking, constituting a novel mechanism through which network dynamics are controlled by ion channel gating.

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