Literature DB >> 8780653

What stops synchronized thalamocortical oscillations?

T Bal1, D A McCormick.   

Abstract

Slow-wave sleep as well as generalized absence seizures are characterized by the occurrence of synchronized oscillations in thalamocortical systems that spontaneously appear and disappear. The spontaneous appearance of synchronized oscillations results from the initiation by one or a small number of cells followed by the progressive recruitment of large numbers of neighboring neurons into the synchronized network activity. Synchronized network oscillations representative of slow-wave sleep, as well as absence seizures, were demonstrated to cease spontaneously at least in part through the persistent activation of a hyperpolarization-activated cation conductance. Block of this conductance resulted in oscillations that, once generalized, occur continuously. These results indicate that the persistent activation of a hyperpolarization-activated cation conductance is a key mechanism through which synchronized oscillations in thalamocortical networks normally terminate.

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Year:  1996        PMID: 8780653     DOI: 10.1016/s0896-6273(00)80161-0

Source DB:  PubMed          Journal:  Neuron        ISSN: 0896-6273            Impact factor:   17.173


  65 in total

1.  Molecular characterization of a slowly gating human hyperpolarization-activated channel predominantly expressed in thalamus, heart, and testis.

Authors:  R Seifert; A Scholten; R Gauss; A Mincheva; P Lichter; U B Kaupp
Journal:  Proc Natl Acad Sci U S A       Date:  1999-08-03       Impact factor: 11.205

2.  Corticothalamic inputs control the pattern of activity generated in thalamocortical networks.

Authors:  H Blumenfeld; D A McCormick
Journal:  J Neurosci       Date:  2000-07-01       Impact factor: 6.167

Review 3.  Novel neuronal and astrocytic mechanisms in thalamocortical loop dynamics.

Authors:  Vincenzo Crunelli; Kate L Blethyn; David W Cope; Stuart W Hughes; H Rheinallt Parri; Jonathan P Turner; Tibor I Tòth; Stephen R Williams
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2002-12-29       Impact factor: 6.237

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

Authors:  Alain Destexhe; Terrence J Sejnowski
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2002-12-29       Impact factor: 6.237

Review 5.  Regulation of recombinant and native hyperpolarization-activated cation channels.

Authors:  Samuel G A Frère; Mira Kuisle; Anita Lüthi
Journal:  Mol Neurobiol       Date:  2004-12       Impact factor: 5.590

6.  Bursting as an effective relay mode in a minimal thalamic model.

Authors:  Baktash Babadi
Journal:  J Comput Neurosci       Date:  2005 Mar-Apr       Impact factor: 1.621

7.  A computational model of how an interaction between the thalamocortical and thalamic reticular neurons transforms the low-frequency oscillations of the globus pallidus.

Authors:  Arash Hadipour-Niktarash
Journal:  J Comput Neurosci       Date:  2006-04-22       Impact factor: 1.621

8.  Adenylyl cyclases: expression in the developing rat thalamus and their role in absence epilepsy.

Authors:  Petra Ehling; Tatyana Kanyshkova; Arnd Baumann; Peter Landgraf; Sven G Meuth; Hans-Christian Pape; Thomas Budde
Journal:  J Mol Neurosci       Date:  2012-04-25       Impact factor: 3.444

9.  Functional stabilization of weakened thalamic pacemaker channel regulation in rat absence epilepsy.

Authors:  Mira Kuisle; Nicolas Wanaverbecq; Amy L Brewster; Samuel G A Frère; Didier Pinault; Tallie Z Baram; Anita Lüthi
Journal:  J Physiol       Date:  2006-05-25       Impact factor: 5.182

10.  Increased basal synaptic inhibition of hippocampal area CA1 pyramidal neurons by an antiepileptic drug that enhances I(H).

Authors:  Bi-Wen Peng; Jason A Justice; Kun Zhang; Xiao-Hua He; Russell M Sanchez
Journal:  Neuropsychopharmacology       Date:  2010-01       Impact factor: 7.853

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