The initiation of bursts in thalamic neurons and the cortical control of thalamic sensitivity

Philos Trans R Soc Lond B Biol Sci. 2002 Dec 29;357(1428):1649-57. doi: 10.1098/rstb.2002.1154.

Abstract

Thalamic neurons generate high-frequency bursts of action potentials when a low-threshold (T-type) calcium current, located in soma and dendrites, becomes activated. Computational models were used to investigate the bursting properties of thalamic relay and reticular neurons. These two types of thalamic cells differ fundamentally in their ability to generate bursts following either excitatory or inhibitory events. Bursts generated with excitatory inputs in relay cells required a high degree of convergence from excitatory inputs, whereas moderate excitation drove burst discharges in reticular neurons from hyperpolarized levels. The opposite holds for inhibitory rebound bursts, which are more difficult to evoke in reticular neurons than in relay cells. The differences between the reticular neurons and thalamocortical neurons were due to different kinetics of the T-current, different electrotonic properties and different distribution patterns of the T-current in the two cell types. These properties enable the cortex to control the sensitivity of the thalamus to inputs and are also important for understanding states such as absence seizures.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials
  • Animals
  • Cerebral Cortex / physiology
  • Epilepsy, Absence / physiopathology
  • Glutamic Acid / physiology
  • Humans
  • In Vitro Techniques
  • Models, Neurological
  • Neural Pathways / physiology
  • Neurons / physiology
  • Rats
  • Receptors, AMPA / physiology
  • Receptors, GABA-A / physiology
  • Thalamus / cytology
  • Thalamus / physiology*
  • gamma-Aminobutyric Acid / physiology

Substances

  • Receptors, AMPA
  • Receptors, GABA-A
  • Glutamic Acid
  • gamma-Aminobutyric Acid