| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Physiology and Neuroscience, New York University Medical School, 550 1st Avenue, New York, NY 10016, USA
It is well established that the main intrinsic electrophysiological properties of thalamocortical relay cells, production of a low threshold burst upon release from hyperpolarized potential and production of a train of single spikes following stimulation from depolarized potentials, can be readily modelled using a single compartment. There is, however, another less well explored intrinsic electrophysiological characteristic of relay cells for which models have not yet accounted: at somatic potentials near spike threshold, relay cells produce a fast ragged high threshold oscillation in somatic voltage. Optical [Ca2+] imaging and pharmacological tests indicate that this oscillation correlates with a high threshold Ca2+ current in the dendrites. Here we present the development of a new compartment model of the thalamic relay cell guided by the simultaneous constraints that it must produce the familiar regular spiking relay mode and low threshold rebound bursts which characterize these cells, as well as the less-studied fast oscillation occurring at near-threshold somatic potentials. We arrive at a model cell which is capable of the production of isolated high threshold Ca2+ spikes in distal branch segments, driven by a rapidly inactivating intermediate threshold Ca2+ channel. Further, the model produces the low threshold spike behaviour of the relay cell without requiring high T-current density in the distal dendritic segments. The results thus support a new picture of the dendritic tree of relay cells which may have implications for the manner in which thalamic relay cells integrate descending input from the cortex.
(Received 29 June 2004;
accepted after revision 20 December 2004;
first published online 21 December 2004)
Corresponding author P. A. Rhodes: Department of Physiology and Neuroscience, NYU Medical School, 550 1st Avenue, New York, NY 10016, USA. Email: paul{at}rhodesholdings.net
This article has been cited by other articles:
|
|
 |
|
  R. R. Llinas, S. Choi, F. J. Urbano, and H.-S. Shin {gamma}-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice PNAS, November 6, 2007; 104(45): 17819 - 17824. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Pascual, D. Wang, V. Hinton, K. Engelstad, C. M. Saxena, R. L. Van Heertum, and D. C. De Vivo Brain Glucose Supply and the Syndrome of Infantile Neuroglycopenia Arch Neurol, April 1, 2007; 64(4): 507 - 513. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. V. M. Herz, T. Gollisch, C. K. Machens, and D. Jaeger Modeling single-neuron dynamics and computations: a balance of detail and abstraction. Science, October 6, 2006; 314(5796): 80 - 85. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. R. Llinas and M. Steriade Bursting of Thalamic Neurons and States of Vigilance J Neurophysiol, June 1, 2006; 95(6): 3297 - 3308. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
