Dendritic spikes induced in fast pyramidal tract neurons by thalamic stimulation

Deschênes, Martin

doi:10.1007/bf00238371

Cited by 63 publications

(7 citation statements)

References 13 publications

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“…14C). This is in agreement with previous intracellular studies of neocortical pyramidal cells in vivo and in vitro 5,9,30,52 where it was observed that synaptic stimuli can elicit dendritic spikes (reviewed in Ref. 66).…”

Section: Synaptically-evoked Spikessupporting

confidence: 93%

“…However, the applicability of this model to other cell types was questioned when the first intradendritic recordings revealed that dendrites can sustain active electrogenesis. 33,34,63 In neocortical and hippocampal pyramidal neurons for instance, intracellular recordings revealed that dendritic spikes can be elicited by synaptic inputs 5,9,30,52 and that they can amplify synaptic inputs electrotonically distant from the soma to initiate APs. 5 Moreover, the proximal apical dendrites of pyramidal neurons were found to contain voltage-gated Ca 2+ and Na + conductances capable of generating current densities similar to those observed at the soma.…”

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confidence: 99%

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Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

Paré¹,

Lang²,

Destexhe³

1998

Neuroscience

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Abstract--The effect of synaptic inputs on somatodendritic interactions during action potentials was investigated, in the cat, using in vivo intracellular recording and computational models of neocortical pyramidal cells. An array of 10 microelectrodes, each ending at a different cortical depth, was used to preferentially evoke synaptic inputs to different somatodendritic regions. Relative to action potentials evoked by current injection, spikes elicited by cortical microstimuli were reduced in amplitude and duration, with stimuli delivered at proximal (somatic) and distal (dendritic) levels evoking the largest and smallest decrements, respectively. When the inhibitory postsynaptic potential reversal was shifted to around 50 mV by recording with KCl pipettes, synaptically-evoked spikes were significantly less reduced than with potassium acetate or cesium acetate pipettes, suggesting that spike decrements are not only due to a shunt, but also to voltage-dependent effects. Computational models of neocortical pyramidal cells were built based on available data on the distribution of active currents and synaptic inputs in the soma and dendrites. The distribution of synapses activated by extracellular stimulation was estimated by matching the model to experimental recordings of postsynaptic potentials evoked at different depths. The model successfully reproduced the progressive spike amplitude reduction as a function of stimulation depth, as well as the effects of chloride and cesium. The model revealed that somatic spikes contain an important contribution from proximal dendritic sodium currents up to ]100 µm and ]300 µm from the soma under control and cesium conditions, respectively. Proximal inhibitory postsynaptic potentials can prevent this dendritic participation thus reducing the spike amplitude at the soma. The model suggests that the somatic spike amplitude and shape can be used as a ''window'' to infer the electrical participation of proximal dendrites.Thus, our results suggest that inhibitory postsynaptic potentials can control the participation of proximal dendrites in somatic sodium spikes.1998 IBRO. Published by Elsevier Science Ltd.Key words: multicompartment models, intrinsic electrophysiological properties, in vivo intracellular recordings, action potentials, dendritic integration.By comparing the shape of antidromic, orthodromic and current-evoked action potentials (APs) in motoneurons, Coombs et al. 7 provided compelling evidence for the idea that APs are initiated at the initial segment (IS) and then invade the somatodendritic compartment. However, the applicability of this model to other cell types was questioned when the first intradendritic recordings revealed that dendrites can sustain active electrogenesis. 33,34,63 In neocortical and hippocampal pyramidal neurons for instance, intracellular recordings revealed that dendritic spikes can be elicited by synaptic inputs 5,9,30,52 and that they can amplify synaptic inputs electrotonically distant from the soma to initiate APs. 5 Moreover, the prox...

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Section: Synaptically-evoked Spikessupporting

confidence: 93%

mentioning

confidence: 99%

Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

Paré¹,

Lang²,

Destexhe³

1998

Neuroscience

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“…These events are likely to be dendritic spikes that did not reach action potential threshold in the soma/axon region, similar to the fast prepotentials described by Spencer and Kandel (1961). Similar events were reported in intracellular recordings of neocortical pyramidal cells in vivo (Deschênes 1981).…”

Section: Firing Properties During Active Periodssupporting

confidence: 74%

Impact of Network Activity on the Integrative Properties of Neocortical Pyramidal Neurons In Vivo

Destexhe

Paré

1999

Journal of Neurophysiology

571

585

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Destexhe, Alain and Denis Paré. Impact of network activity on the integrative properties of neocortical pyramidal neurons in vivo. J. Neurophysiol. 81: 1531Neurophysiol. 81: -1547Neurophysiol. 81: , 1999. During wakefulness, neocortical neurons are subjected to an intense synaptic bombardment. To assess the consequences of this background activity for the integrative properties of pyramidal neurons, we constrained biophysical models with in vivo intracellular data obtained in anesthetized cats during periods of intense network activity similar to that observed in the waking state. In pyramidal cells of the parietal cortex (area 5-7), synaptic activity was responsible for an approximately fivefold decrease in input resistance (R in ), a more depolarized membrane potential (V m ), and a marked increase in the amplitude of V m fluctuations, as determined by comparing the same cells before and after microperfusion of tetrodotoxin (TTX). The model was constrained by measurements of R in , by the average value and standard deviation of the V m measured from epochs of intense synaptic activity recorded with KAc or KClfilled pipettes as well as the values measured in the same cells after TTX. To reproduce all experimental results, the simulated synaptic activity had to be of relatively high frequency (1-5 Hz) at excitatory and inhibitory synapses. In addition, synaptic inputs had to be significantly correlated (correlation coefficient ϳ0.1) to reproduce the amplitude of V m fluctuations recorded experimentally. The presence of voltage-dependent K ϩ currents, estimated from current-voltage relations after TTX, affected these parameters by Ͻ10%. The model predicts that the conductance due to synaptic activity is 7-30 times larger than the somatic leak conductance to be consistent with the approximately fivefold change in R in . The impact of this massive increase in conductance on dendritic attenuation was investigated for passive neurons and neurons with voltage-dependent Na ϩ /K ϩ currents in soma and dendrites. In passive neurons, correlated synaptic bombardment had a major influence on dendritic attenuation. The electrotonic attenuation of simulated synaptic inputs was enhanced greatly in the presence of synaptic bombardment, with distal synapses having minimal effects at the soma. Similarly, in the presence of dendritic voltage-dependent currents, the convergence of hundreds of synaptic inputs was required to evoke action potentials reliably. In this case, however, dendritic voltage-dependent currents minimized the variability due to input location, with distal apical synapses being as effective as synapses on basal dendrites. In conclusion, this combination of intracellular and computational data suggests that, during low-amplitude fast electroencephalographic activity, neocortical neurons are bombarded continuously by correlated synaptic inputs at high frequency, which significantly affect their integrative properties. A series of predictions are suggested to test this model.

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“…Despite their differences in connectivity and function, the neurons in each of the regions of the thalamus examined appear to exhibit similar electrophysiological properties, including similarities in input resistance, time constant, and level of spontaneous activity. Furthermore, in several cases neurons exhibited fast spikelike events somewhat similar to the FPPs described in other preparations (Eccles et al, 1958;Deschenes, 1981; Kuno and Llinas, 1970;Llinas and Nicholson, 1971;Spencer and Kandel, 1961). These events do not appear to be synaptically mediated, since the rapid falling phase of the spike suggests that the event is active in nature; furthermore, their frequency of occurrence can be altered by direct polarization of the soma.…”

Section: Electrophysiological Propertiessupporting

confidence: 61%

Modulation of dorsal thalamic cell activity by the ventral pallidum: Its role in the regulation of thalamocortical activity by the basal ganglia

Lavín

Grace

1994

Synapse

127

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The actions mediated by limbic system output projections of the basal ganglia were investigated by studying the effects of ventral pallidum (VP) stimulation on the activity of neurons in thalamic target nuclei, including several of the dorsal thalamic nuclei and the nucleus reticularis, using in vivo intracellular recordings in rats. Intracellular injection of Lucifer yellow was used in a subset of experiments to identify the neurons recorded and to confirm their location with respect to the specific thalamic nuclei targeted. Stimulation of the VP evoked ipsps in 79% of the mediodorsal cells recorded. In the reticular nucleus, 73% of the neurons tested responded with evoked ipsps. In contrast, in other dorsal thalamic nuclei VP stimulation evoked depolarizations in 58% of the cells recorded. The latency to onset of the ipsps in the mediodorsal nucleus and in the reticular nucleus were not substantially different (1.7 +/- 1.1 msec vs. 2.7 +/- 1.1 msec), whereas the depolarizing response evoked in dorsal thalamic nucleus neurons typically occurred at longer and more variable latencies (3.5 +/- 2.7 msec). These experiments support a dual functional role for limbic system output from the basal ganglia in the regulation of thalamocortical activity: a) a direct inhibitory projection from the VP to the mediodorsal nucleus and b) an indirect disinhibition of neurons in other dorsal thalamic nuclei that occurs via a direct inhibitory projection to the reticular nucleus of the thalamus. Such an anatomical arrangement may be relevant to the presence of hypofrontality and the breakdown of cognitive filtering observed in schizophrenics.

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Dendritic spikes induced in fast pyramidal tract neurons by thalamic stimulation

Cited by 63 publications

References 13 publications

Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

Impact of Network Activity on the Integrative Properties of Neocortical Pyramidal Neurons In Vivo

Modulation of dorsal thalamic cell activity by the ventral pallidum: Its role in the regulation of thalamocortical activity by the basal ganglia

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