Neuronal basis of the slow ( <1 Hz) oscillation in neurons of the nucleus reticularis thalami in vitro

J Neurosci. 2006 Mar 1;26(9):2474-86. doi: 10.1523/JNEUROSCI.3607-05.2006.

Abstract

During deep sleep and anesthesia, the EEG of humans and animals exhibits a distinctive slow (<1 Hz) rhythm. In inhibitory neurons of the nucleus reticularis thalami (NRT), this rhythm is reflected as a slow (<1 Hz) oscillation of the membrane potential comprising stereotypical, recurring "up" and "down" states. Here we show that reducing the leak current through the activation of group I metabotropic glutamate receptors (mGluRs) with either trans-ACPD [(+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid] (50-100 microM) or DHPG [(S)-3,5-dihydroxyphenylglycine] (100 microM) instates an intrinsic slow oscillation in NRT neurons in vitro that is qualitatively equivalent to that observed in vivo. A slow oscillation could also be evoked by synaptically activating mGluRs on NRT neurons via the tetanic stimulation of corticothalamic fibers. Through a combination of experiments and computational modeling we show that the up state of the slow oscillation is predominantly generated by the "window" component of the T-type Ca2+ current, with an additional supportive role for a Ca2+-activated nonselective cation current. The slow oscillation is also fundamentally reliant on an Ih current and is extensively shaped by both Ca2+- and Na+-activated K+ currents. In combination with previous work in thalamocortical neurons, this study suggests that the thalamus plays an important and active role in shaping the slow (<1 Hz) rhythm during deep sleep.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / radiation effects
  • Animals
  • Apamin / pharmacology
  • Cadmium / pharmacology
  • Cats
  • Computer Simulation
  • Cycloleucine / analogs & derivatives
  • Cycloleucine / pharmacology
  • Dose-Response Relationship, Radiation
  • Drug Interactions
  • Electric Capacitance
  • Electric Stimulation / methods
  • Excitatory Amino Acid Antagonists / pharmacology
  • GABA Antagonists / pharmacology
  • In Vitro Techniques
  • Intralaminar Thalamic Nuclei / cytology*
  • Models, Neurological
  • Neural Pathways / drug effects
  • Neural Pathways / radiation effects
  • Neurons / drug effects
  • Neurons / physiology*
  • Neurons / radiation effects
  • Neuroprotective Agents / pharmacology
  • Nickel / pharmacology
  • Organophosphorus Compounds / pharmacology
  • Periodicity*
  • Pyridazines / pharmacology
  • Pyrimidines / pharmacology
  • Sodium Channel Blockers / pharmacology
  • Tetrodotoxin / pharmacology
  • Time Factors

Substances

  • Excitatory Amino Acid Antagonists
  • GABA Antagonists
  • Neuroprotective Agents
  • Organophosphorus Compounds
  • Pyridazines
  • Pyrimidines
  • Sodium Channel Blockers
  • Cadmium
  • Cycloleucine
  • 1-amino-1,3-dicarboxycyclopentane
  • ICI D2788
  • CGP 54626
  • Apamin
  • Tetrodotoxin
  • Nickel
  • gabazine