Skip to main content

Main menu

  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE

User menu

  • Log out
  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • Log out
  • Log in
  • My Cart
Journal of Neuroscience

Advanced Search

Submit a Manuscript
  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE
PreviousNext
Cover ArticleArticles, Cellular/Molecular

NMDA Spike/Plateau Potentials in Dendrites of Thalamocortical Neurons

Sigita Augustinaite, Bernd Kuhn, Paul Johannes Helm and Paul Heggelund
Journal of Neuroscience 13 August 2014, 34 (33) 10892-10905; https://doi.org/10.1523/JNEUROSCI.1205-13.2014
Sigita Augustinaite
1Institute of Basic Medical Sciences, University of Oslo, N-0317 Oslo, Norway,
2Okinawa Institute of Science and Technology Graduate University, Onna-son, Okinawa, 904-0495 Japan, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Bernd Kuhn
2Okinawa Institute of Science and Technology Graduate University, Onna-son, Okinawa, 904-0495 Japan, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Paul Johannes Helm
3Centre for Molecular Biology and Neuroscience and the Letten Centre–Laboratory for Molecular Neuroscience, Institute of Basic Medical Sciences, University of Oslo, N-0317 Oslo, Norway
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Paul Heggelund
1Institute of Basic Medical Sciences, University of Oslo, N-0317 Oslo, Norway,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Article Figures & Data

Figures

  • Figure 1.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 1.

    Local dendritic glutamate application elicited spike/plateau potentials in TC neurons. A, Scheme of experiment: simultaneous two-photon imaging of dendritic activity and somatic whole-cell recording was made from TC neurons in dLGN in vitro. Responses were elicited by local dendritic glutamate application. vLGN, ventral lateral geniculate nucleus; LP, lateral posterior nucleus. B, Image of a TC neuron. The neuron was filled with Alexa Fluor 594 (50 μm in pipette) via the recording electrode. Glutamate stimulation was applied at a dendritic site (marked by an asterisk) via a high-resistance (0.5–0.6 GΩ) theta electrode with glutamate (300 mm) in one chamber and Alexa Fluor 594 (100 μm) in the other. In this example the glutamate application site was 126 μm from the soma and 5 μm from the selected dendrite. Notice the lack of prominent spines. C, Somatically recorded potentials elicited by the local glutamate stimulation. The strength of the stimulation current, indicated by the color code, reflects the amount of the released glutamate. The responses, elicited by a particular current strength, were quite stable (amplitudes varied only by 0.4 ± 0.6 mV). Here, and in all the other figures, each trace in color is an average of three trials obtained with at least 10 s intertrial intervals. The start of the glutamate application is indicated by an arrowhead below the traces. In all experiments GABAergic synaptic inputs were blocked by gabazine and CGP52432 or CGP55845. D, The peak response amplitude of this neuron plotted against stimulation strength. Color of the dots corresponds to the color scale in C. E, The duration of the potential, measured at half-maximum amplitude, plotted against stimulation strength. Dots colored according to color scale in C.

  • Figure 2.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 2.

    Changes of the amplitude of the potential by increasing strength of glutamate stimulation. A, Individual curves showing the peak amplitude with increasing strength of glutamate stimulation for all neurons. To the left of each curve the baseline (0 mV) is indicated together with a curve identifier (color and line type) for the specific curve. B, Normalized response amplitudes plotted against the glutamate stimulation strength for all neurons (mean ± SD; n = 34). Dotted lines: linear regression line fitted to the mean values below the spike threshold and to the mean values above the spike threshold.

  • Figure 3.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 3.

    Changes of the duration of the potential by increasing intensity of glutamate stimulation. A, The duration of the potential at the half-maximum amplitude plotted against stimulus strength for each of the studied neurons. To the left of each curve the baseline (0 ms) is indicated together with a curve identifier (color and line type). For a given neuron the color and line style is the same as in Figure 2A. B, Values of normalized half-amplitude duration plotted against stimulus strength for all neurons (mean ± SD; n = 34). Dotted lines: linear regression line fitted to the values below spike threshold and to the values above the threshold.

  • Figure 4.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 4.

    CPP eliminated the calcium signal as well as the somatic spike/plateau potential. A, Image of the recorded TC neuron. The glutamate application site (indicated by asterisk) was 106 μm from the soma and 8 μm from the selected dendrite. The green arrowhead marks the dendritic site where the calcium signal was recorded during the line scans. B, The somatically recorded spike/plateau potential. Notice the marked reduction of the response during CPP. C, The corresponding Ca2+ transient. Notice that the Ca2+ transient was nearly eliminated by CPP (15 μm). D, In the presence of CPP, the response could not be recovered by stronger stimulation current.

  • Figure 5.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 5.

    Conductances mediated by NMDA receptors are necessary for the generation of the spike/plateau potentials, whereas Ca2+ and Na+ conductances have only minor contributions. A, Image of the recorded TC neuron in B–D. The glutamate application site (indicated by asterisk) was 79 μm from the soma and 13 μm from the selected dendrite. B, Application of Cd2+ (100 μm) and TTX (1 μm) reduced the glutamate elicited spike/plateau potential by about 20%. C, The spike/plateau potential could be re-initiated by means of stronger glutamate stimulation in the presence of Cd2+ and TTX. D, The re-initiated spike/plateau was almost eliminated by 15 μm CPP. E, The application of nimodipine (50 μm) reduced the potential by about 9%, while the addition of CPP removed about 80% of the response obtained in the control condition. F, The application of Ni2+ (0.4 mm) reduced the response by about 16%, while the addition of CPP removed about 74% of the response obtained in the control condition. G, At −65 mV, the application of Ni2+ (0.4 mm) removed the T-type Ca2+ burst without affecting the plateau part of the glutamate elicited response. The data in A–D and in E–G are from different neurons.

  • Figure 6.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 6.

    Glutamate-elicited Ca2+ transients were restricted to a small dendritic region near the stimulation site. A, Image of the recorded TC neuron in B and C. Glutamate was applied at 110 μm from the soma and 7 μm from the dendrite. The green arrowheads mark the dendritic sites where the line scans of the Ca2+ transients were recorded. B, Single line scans, which demonstrate that the signal of the Ca2-insensitive Alexa 594 was constant, while the fluorescence intensity of the calcium indicator Fluo-5F, changed after the stimulation. In this case, calcium signals were recorded by line scans with identical scanning parameters at three dendritic locations. C, The uppermost row of traces shows somatically recorded potentials elicited at three different glutamate stimulation strengths. The remaining three rows of traces show the corresponding Ca2+ transients (ΔG/R), measured at three different positions indicated in A. D, Half-amplitude duration of the Ca2+ signals plotted as a function of distance from the glutamate application site. These data were collected from the neurons (n = 15) where the Ca2+ transients were recorded at different sites along the same dendritic arbor. Points from the same dendrite have the same color. The calcium signals were elicited by the plateau potentials. E, Population data (n = 28) showing the decay of the Ca2+ signal duration as a function of increasing distance from the glutamate application site. Dataset in D included. The dashed line shows a Gaussian function fitted to the data.

  • Figure 7.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 7.

    Attenuation of the potential along the dendrite. Comparisons of response amplitudes at the soma elicited by glutamate stimulation at two different distances from soma along the same dendrite. A, Image of the TC neuron recorded in B. Two stimulation sites along the same dendrite are marked by asterisks in red. Glutamate application Site 1 was 76 μm from the soma and 7 μm from the dendrite; Site 2 was 102 μm from the soma and 9 μm from the dendrite. B, Traces recorded by different stimulus strength at two distances from soma. Stimulation strength is indicated by the color scale. C, Amplitudes of initial spikes elicited at two glutamate stimulation sites (n = 7).

  • Figure 8.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 8.

    Spike/plateaus at different membrane potentials. A, Image of the recorded TC neuron in B. The glutamate application site (indicated by an asterisk) was 99 μm from the soma and 7 μm from the dendrite. B, Somatically recorded potentials elicited by local dendritic application of glutamate at different membrane potentials: −65 (left), −58 (middle), and −55 mV (right). The color code indicates the strength of the stimulation current. Notice that the T-type Ca2+ potential (indicated by an arrow) was reduced or disappeared at more depolarized membrane potentials. C, Superimposed spike/plateau potentials recorded at different membrane potentials. The stimulation strength (3 μA) was the same in all cases. The action potentials are truncated. The color code indicates the holding membrane potential. The neuron in C is different from the one in A and B. D, The average amplitude of the spike/plateau potential plotted as a function of the membrane potential (n = 8).

  • Figure 9.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 9.

    A spike/plateau potential elicited at a single distal dendrite can inactivate T-type Ca2+ conductance in TC neurons thereby preventing burst firing. A, Image of the recorded TC neuron. The glutamate application site (indicated by an asterisk) was 67 μm from the soma and 5 μm from the dendrite. B, Scheme of experiment: simultaneous two-photon imaging and somatic whole-cell recording. vLGN, ventral lateral geniculate nucleus; LP, lateral posterior nucleus. C, T-type Ca2+ bursts were elicited by two depolarizing pulses (each 10 ms, 150 pA) to the soma of a hyperpolarized (−65 mV) TC neuron. The timing of the pulses is indicated by the current trace (gray) below the trace of the response. D, Responses, elicited by local dendritic glutamate stimulation (left, 3 μA; right, 4 μA). The time of the application of the glutamate pulse is indicated by the arrowhead below each trace. E, Responses elicited by combined somatic depolarizing pulses and dendritic glutamate stimulation. Due to the NMDA spike/plateau, a T-type calcium burst in response to the second somatic pulse was not elicited. The glutamate stimulation started 50 ms (top), 100 ms (middle), or 150 ms (bottom) after the first depolarizing pulse. Action potentials are truncated at 0 mV.

  • Figure 10.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 10.

    A depolarizing current injection to the soma of a TC neuron can inactivate T-type Ca2+ conductance (A) and facilitate the retinogeniculate signal transmission (B). A1, Scheme of experiment: somatic whole-cell recording and depolarizing current injection through the recording electrode. A2, T-type Ca2+ bursts were elicited by two depolarizing pulses (each 10 ms, 200 pA) to the soma of a hyperpolarized (−65 mV) TC neuron. The timing of the pulses is indicated by the current trace (gray) below the response trace. A3, Response elicited by a 300 ms depolarizing current injection (50 pA). A4, Responses elicited by combined somatic depolarizing current injection and somatic depolarizing pulses. Due to the long somatic depolarization step, the second somatic pulse did not elicit a T-type calcium burst. The current injection (300 ms) started 150 ms after the first 10 ms pulse. B1, Scheme of experiment: somatic whole-cell recording and depolarizing current injection through the recording electrode; optic tract (OT) fibers were stimulated electrically. B2, Response to OT stimulation (20 pulses at 40 Hz) elicited at −55 mV membrane potential. The timing of each pulse is indicated by a marker below the trace. B3, Response elicited by a depolarizing current injection (300 ms, 25 pA). B4, Response to the combined OT stimulation and a 300 ms somatic depolarizing current injection. Due to the long somatic depolarization step, more action potentials were generated by the EPSPs, which were elicited through the retinal input. The depolarizing current injection started 100 ms after the beginning of the electrical train stimulation.

  • Figure 11.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 11.

    NMDA spike/plateaus potentials facilitate the retinogeniculate signal transmission. A, Scheme of experiment: simultaneous two-photon imaging and somatic whole-cell recording from a TC neuron in vitro. Responses were elicited by electric stimulation of optic tract (OT) fibers, combined with local dendritic glutamate application. vLGN, ventral lateral geniculate nucleus; LP, lateral posterior nucleus. B, Image of the recorded neuron. The glutamate application site (indicated by an asterisk) was 123 μm from the soma and 7 μm from the dendrite. C, Responses elicited at three different membrane potentials. Left column, Responses to OT stimulation (20 pulses at 40 Hz). The timing of each pulse is indicated by a marker below each trace. Center column, NMDA spike/plateau potentials elicited by local dendritic glutamate stimulation (stimulation site marked by the asterisk in B). The timing of the glutamate pulse is indicated by the arrowhead below each trace. Right column, Responses to the combined OT and dendritic glutamate stimulation. Due to the long-lasting NMDA spike/plateau, more action potentials were elicited by the EPSPs generated through the retinal input. Notice that the electrical train stimulation started 100 ms before the glutamate application. Response period used for comparison of the transfer ratio (see Results) is indicated by the thick gray line.

Back to top

In this issue

The Journal of Neuroscience: 34 (33)
Journal of Neuroscience
Vol. 34, Issue 33
13 Aug 2014
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by author
  • Advertising (PDF)
  • Ed Board (PDF)
Email

Thank you for sharing this Journal of Neuroscience article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
NMDA Spike/Plateau Potentials in Dendrites of Thalamocortical Neurons
(Your Name) has forwarded a page to you from Journal of Neuroscience
(Your Name) thought you would be interested in this article in Journal of Neuroscience.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
View Full Page PDF
Citation Tools
NMDA Spike/Plateau Potentials in Dendrites of Thalamocortical Neurons
Sigita Augustinaite, Bernd Kuhn, Paul Johannes Helm, Paul Heggelund
Journal of Neuroscience 13 August 2014, 34 (33) 10892-10905; DOI: 10.1523/JNEUROSCI.1205-13.2014

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Respond to this article
Request Permissions
Share
NMDA Spike/Plateau Potentials in Dendrites of Thalamocortical Neurons
Sigita Augustinaite, Bernd Kuhn, Paul Johannes Helm, Paul Heggelund
Journal of Neuroscience 13 August 2014, 34 (33) 10892-10905; DOI: 10.1523/JNEUROSCI.1205-13.2014
Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Introduction
    • Materials and Methods
    • Results
    • Discussion
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Keywords

  • dendritic integration
  • LGN
  • NMDA spike
  • NMDA spike/plateau potential
  • thalamocortical
  • cortical feedback

Responses to this article

Respond to this article

Jump to comment:

No eLetters have been published for this article.

Related Articles

Cited By...

More in this TOC Section

Articles

  • Memory Retrieval Has a Dynamic Influence on the Maintenance Mechanisms That Are Sensitive to ζ-Inhibitory Peptide (ZIP)
  • Neurophysiological Evidence for a Cortical Contribution to the Wakefulness-Related Drive to Breathe Explaining Hypocapnia-Resistant Ventilation in Humans
  • Monomeric Alpha-Synuclein Exerts a Physiological Role on Brain ATP Synthase
Show more Articles

Cellular/Molecular

  • Atypical Cadherin FAT2 Is Required for Synaptic Integrity and Motor Behaviors
  • Sex Differences in Histamine Regulation of Striatal Dopamine
  • CXCL12 Engages Cortical Inhibitory Neurons to Enhance Dendritic Spine Plasticity and Structured Network Activity
Show more Cellular/Molecular
  • Home
  • Alerts
  • Follow SFN on BlueSky
  • Visit Society for Neuroscience on Facebook
  • Follow Society for Neuroscience on Twitter
  • Follow Society for Neuroscience on LinkedIn
  • Visit Society for Neuroscience on Youtube
  • Follow our RSS feeds

Content

  • Early Release
  • Current Issue
  • Issue Archive
  • Collections

Information

  • For Authors
  • For Advertisers
  • For the Media
  • For Subscribers

About

  • About the Journal
  • Editorial Board
  • Privacy Notice
  • Contact
  • Accessibility
(JNeurosci logo)
(SfN logo)

Copyright © 2025 by the Society for Neuroscience.
JNeurosci Online ISSN: 1529-2401

The ideas and opinions expressed in JNeurosci do not necessarily reflect those of SfN or the JNeurosci Editorial Board. Publication of an advertisement or other product mention in JNeurosci should not be construed as an endorsement of the manufacturer’s claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in JNeurosci.