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Distinct kinetics of inhibitory currents in thalamocortical neurons that arise from dendritic or axonal origin

Sunggu Yang*, Gubbi Govindaiah, Sang-Hun Lee, Sungchil Yang, Charles L Cox*

*Corresponding author for this work

Research output: Journal Publications and ReviewsRGC 21 - Publication in refereed journalpeer-review

65 Downloads (CityUHK Scholars)

Abstract

Thalamocortical neurons in the dorsal lateral geniculate nucleus (dLGN) transfer visual information from retina to primary visual cortex. This information is modulated by inhibitory input arising from local interneurons and thalamic reticular nucleus (TRN) neurons, leading to alterations of receptive field properties of thalamocortical neurons. Local GABAergic interneurons provide two distinct synaptic outputs: axonal (F1 terminals) and dendritic (F2 terminals) onto dLGN thalamocortical neurons. By contrast, TRN neurons provide only axonal output (F1 terminals) onto dLGN thalamocortical neurons. It is unclear if GABAA receptor-mediated currents originating from F1 and F2 terminals have different characteristics. In the present study, we examined multiple characteristics (rise time, slope, halfwidth and decay τ) of GABAA receptor-mediated miniature inhibitory postsynaptic synaptic currents (mIPSCs) originating from F1 and F2 terminals. The mIPSCs arising from F2 terminals showed slower kinetics relative to those from F1 terminals. Such differential kinetics of GABAAR-mediated responses could be an important role in temporal coding of visual signals.
Original languageEnglish
Article numbere0189690
JournalPLoS ONE
Volume12
Issue number12
DOIs
Publication statusPublished - 18 Dec 2017

Research Keywords

  • Animals
  • Axons
  • Cerebral Cortex
  • Dendrites
  • Electrophysiology
  • Female
  • GABAergic Neurons
  • Geniculate Bodies
  • Inhibitory Postsynaptic Potentials
  • Kinetics
  • Male
  • Neural Inhibition
  • Neurons
  • Presynaptic Terminals
  • Protein Domains
  • Rats
  • Rats, Sprague-Dawley
  • Thalamic Nuclei
  • Thalamus
  • Journal Article

Publisher's Copyright Statement

  • The work is made available under the Creative Commons CC0 public domain dedication. https://creativecommons.org/publicdomain/zero/1.0/

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