Integrative Properties of Radial Oblique Dendrites in Hippocampal CA1 Pyramidal Neurons

Losonczy, Attila; Magee, Jeffrey C.

doi:10.1016/j.neuron.2006.03.016

Cited by 557 publications

(839 citation statements)

References 41 publications

(92 reference statements)

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“…Basal spiny dendrites of neocortical pyramidal neurons exhibit regenerative Ca 2+ spikes mediated by NMDARs (Schiller et al, 2000), which could contribute to the observed Ca 2+ signals during coincident EPSP-bAP trains described here [in addition to the recently described spikes in radial oblique dendrites of CA1 neurons by Losonczy and Magee (2006), see above]. In addition, BDNF rapidly enhances NMDA-induced currents in cultured hippocampal neurons, primarily through receptors containing NR2B subunits (Levine and Kolb, 2000).…”

Section: Discussionsupporting

confidence: 62%

“…1A shows a montage of fluorescence images of a representative CA1 pyramidal neuron loaded with OGB-1 through the somatic whole-cell electrode. Measurements of Ca 2+ -indicator fluorescence intensity were obtained from secondary spiny dendrites after branching from the main apical primary dendrite, which sometimes included the so-called radial oblique dendrites Losonczy and Magee, 2006). Intracellular Ca 2+ elevations were evoked by one of the following protocols (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…It is important to note that our results do not contradict those of Magee and Johnston (Magee and Johnston, 1997), who found that pairing EPSPs with bAPs evoked larger Ca 2+ elevations than bAP alone, for two reasons. First, Magee and Johnston (1997) imaged the main primary apical dendrite, whereas we have imaged the smaller radial branches off the main primary dendrite, recently dubbed "radial oblique dendrites" by the same authors Losonczy and Magee, 2006). We focused on these secondary branches because they express a higher density of spines and of synaptic contacts than the main apical trunk, and because our prior work on BDNF-induced spine formation focused on these spiny secondary dendritic branches Pozzo-Miller, 2001, 2003;Alonso et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…We focused on these secondary branches because they express a higher density of spines and of synaptic contacts than the main apical trunk, and because our prior work on BDNF-induced spine formation focused on these spiny secondary dendritic branches Pozzo-Miller, 2001, 2003;Alonso et al, 2004). These radial oblique dendrites have been shown to have different properties than the main apical trunk, including the amplitude of Ca 2+ signals evoked by bAPs , and the generation of local dendritic spikes involving Na + , Ca 2+ , and K + channels (Losonczy and Magee, 2006). Another potential reason for the difference with the Magee and Johnston (1997) observations is the fact that those studies were performed in acute hippocampal slices, whereas our measurements were done in organotypic slice cultures, a requirement for the long-term exposure to BDNF.…”

Section: Discussionmentioning

confidence: 99%

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BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Pozzo-Miller

2006

Brain Research

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BDNF, a member of the neurotrophin family, is emerging as a key modulator of synaptic structure and function in the CNS. Due to the critical role of postsynaptic Ca 2+ signals in dendritic development and synaptic plasticity, we tested whether long-term exposure to BDNF affects Ca 2+ elevations evoked by coincident excitatory postsynaptic potentials (EPSPs) and back-propagating action potentials (bAPs) in spiny dendrites of CA1 pyramidal neurons within hippocampal slice cultures. In control neurons, a train of 5 coincident EPSPs and bAPs evoked Ca 2+ elevations in oblique radial branches of the main apical dendrite that were of similar amplitude than those evoked by a train of 5 bAPs alone. On the other hand, dendritic Ca 2+ signals evoked by coincident EPSPs and bAPs were always larger than those triggered by bAPs in CA1 neurons exposed to BDNF for 48 h. This difference was not observed after blockade of NMDA receptors (NMDARs) with D,L-APV, but only in BDNFtreated neurons, suggesting that Ca 2+ signals in oblique radial dendrites include a synaptic NMDARdependent component. Co-treatment with the receptor tyrosine kinase inhibitor k-252a prevented the effect of BDNF on coincident dendritic Ca 2+ signals, suggesting the involvement of neurotrophin Trk receptors. These results indicate that long-term exposure to BDNF enhances Ca 2+ signaling during coincident pre-and postsynaptic activity in small spiny dendrites of CA1 pyramidal neurons, representing a potential functional consequence of neurotrophin-mediated dendritic remodeling in developing neurons.

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Section: Discussionsupporting

confidence: 62%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Pozzo-Miller

2006

Brain Research

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“…When a dendritic action potential (dAP) was generated at the apical trunk it quickly propagated to the soma and elicited a reliable and precise action potential 91 . When the dAP was initiated in the oblique dendrites it propagated to the soma but did not lead to an action potential 92 . Instead, a rapid voltage deflection was observed at the soma, followed by a slower (but still nonlinear) deflection that was due to calcium entry.…”

Section: Decoding Synchronous Inputs In Spatially Extended Neuronsmentioning

confidence: 98%

Regulation of spike timing in visual cortical circuits

2008

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A train of action potentials (a spike train) can carry information in both the average firing rate and the pattern of spikes in the train. But can such a spike-pattern code be supported by cortical circuits? Neurons in vitro produce a spike pattern in response to the injection of a fluctuating current. However, cortical neurons in vivo are modulated by local oscillatory neuronal activity and by top-down inputs. In a cortical circuit, precise spike patterns thus reflect the interaction between internally generated activity and sensory information encoded by input spike trains. We review the evidence for precise and reliable spike timing in the cortex and discuss its computational role.Reliability and precision are two different quantities. When you make an appointment with your friend, she can either keep the appointment or not show up at all. If she does show up, she might or might not be on time. The former uncertainty is related to reliability, whereas the latter is related to precision. When the same stimulus waveform is repeatedly injected at the soma of a neuron in vitro (FIG. 1a), a similar spike train is obtained on each trial 1,2 (FIG. 1b). When approximately the same number of spikes occur on each trial the neuron is said to be reliable, whereas when the spikes occur almost at the same time across trials it is said to be precise (FIG. 1c). For a single neuron, the potential information content of precise and reliable spike times is many times larger than that which is contained in the firing rate, which is averaged across a typical interval of a hundred milliseconds [3][4][5][6] . The information contained in spike timing is available immediately, rather than after an averaging period. Furthermore, the timing of patterns of spikes can potentially transmit even more information than the timing of the individual constituent spikes 3,7 . The potential relevance of spike patterns becomes apparent when we consider neurons at the population level: when a group of similar neurons (a 'pool') produces precise and reliable spike trains, the neurons they project to receive volleys of synchronous spikes 8,9 . This opens up the possibility of communicating between different cortical areas through synchronous spike volleys.In contrast to the in vitro situation described above, in the intact cortex most excitatory synaptic inputs arrive at the dendrites rather than at the soma (FIG. 1d), and synaptic transmission is typically unreliable [10][11][12][13] . Furthermore, most of these dendritic inputs are not directly related to ongoing sensory stimulation; rather, they reflect spatiotemporally structured internal activity. Therefore, when the same stimulus is presented repeatedly, the resulting spike trains are usually neither precise nor reliable when they are aligned to the stimulus onset 6 . Instead, HHMI Author ManuscriptHHMI Author Manuscript HHMI Author Manuscript neural activity in vivo might be dominated by internally generated complex reverberations or rhythmic oscillations, and precise and reliable sp...

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