Literature DB >> 7509269

Cortical and thalamic cellular correlates of electroencephalographic burst-suppression.

M Steriade1, F Amzica, D Contreras.   

Abstract

This experimental study on anesthetized cats used intracellular recordings of cortical, thalamocortical and reticular thalamic neurons (n = 54), as well as multi-site extracellular recordings (n = 36), to investigate the cellular correlates of EEG burst-suppression patterns, defined as alternating wave bursts and periods of electrical silence. Burst-suppression was elicited by the administration of the same or other anesthetic agents upon the background of an already synchronized EEG activity. About 95% of cortical cells entered burst-suppression, in close time-relation with EEG activity, displaying sequences of phasic depolarizing events associated with bursts of EEG waves and an electrical silence of the neuronal membrane during flat EEG epochs. The membrane potential (Vm) hyperpolarized by approximately 10 mV prior to any EEG change and the slow rhythms reflecting deep stages of anesthesia progressively disorganized with transition to burst-suppression. During flat EEG epochs, the apparent input resistance (tested through short hyperpolarizing current pulses) decreased (range 12-60%) and neuronal responsiveness to orthodromic volleys (tested by thalamic and cortical evoked excitatory postsynaptic potentials) was dramatically reduced. It is proposed that the decreased input resistance is mainly due to an increase in K+ conductances. At variance with cortical neurons, only 60-70% of thalamic cells ceased firing before overt EEG burst-suppression and were completely silent during flat periods of EEG activity. The remaining 30-40% of thalamic cells discharged rhythmic (1-4 Hz) spike bursts during periods of EEG silence. This rhythm, within the frequency range of delta waves, is generated in thalamic cells by the interplay between two of their intrinsic currents at critical levels of Vm hyperpolarization. However, with the deepening of burst-suppression, when silent EEG periods became longer than 30 sec, thalamic cells also ceased firing. The assumption that full-blown burst-suppression is achieved through virtually complete disconnection in brain circuits implicated in the genesis of the EEG is corroborated by the revival of normal cellular and EEG activities after volleys setting into action thalamic and cortical networks.

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Year:  1994        PMID: 7509269     DOI: 10.1016/0013-4694(94)90108-2

Source DB:  PubMed          Journal:  Electroencephalogr Clin Neurophysiol        ISSN: 0013-4694


  70 in total

1.  Hyperpolarisation rectification in cat lateral geniculate neurons modulated by intact corticothalamic projections.

Authors:  D A Nita; M Steriade; F Amzica
Journal:  J Physiol       Date:  2003-08-22       Impact factor: 5.182

2.  A neurophysiological-metabolic model for burst suppression.

Authors:  Shinung Ching; Patrick L Purdon; Sujith Vijayan; Nancy J Kopell; Emery N Brown
Journal:  Proc Natl Acad Sci U S A       Date:  2012-02-07       Impact factor: 11.205

3.  Neural origin of spontaneous hemodynamic fluctuations in rats under burst-suppression anesthesia condition.

Authors:  Xiao Liu; Xiao-Hong Zhu; Yi Zhang; Wei Chen
Journal:  Cereb Cortex       Date:  2010-06-07       Impact factor: 5.357

4.  Individual indicators of appropriate hypnotic level during propofol anesthesia: highest alpha power and effect-site concentrations of propofol at loss of response.

Authors:  Hongling Kang; Hassan Mamdouh Hassan Mohamed; Masaki Takashina; Takahiko Mori; Yuji Fujino; Satoshi Hagihira
Journal:  J Anesth       Date:  2017-02-14       Impact factor: 2.078

5.  The human burst suppression electroencephalogram of deep hypothermia.

Authors:  M Brandon Westover; Shinung Ching; Vishakhadatta M Kumaraswamy; Seun Oluwaseun Akeju; Eric Pierce; Sydney S Cash; Ronan Kilbride; Emery N Brown; Patrick L Purdon
Journal:  Clin Neurophysiol       Date:  2015-01-16       Impact factor: 3.708

6.  Interaction of slow cortical rhythm with somatosensory information processing in urethane-anesthetized rats.

Authors:  Attila Toth; Erika Gyengesi; Laszlo Zaborszky; Laszlo Detari
Journal:  Brain Res       Date:  2008-06-05       Impact factor: 3.252

7.  Early Exposure to General Anesthesia with Isoflurane Downregulates Inhibitory Synaptic Neurotransmission in the Rat Thalamus.

Authors:  Pavle M Joksovic; Nadia Lunardi; Vesna Jevtovic-Todorovic; Slobodan M Todorovic
Journal:  Mol Neurobiol       Date:  2015-06-06       Impact factor: 5.590

Review 8.  Modeling the dynamical effects of anesthesia on brain circuits.

Authors:  Shinung Ching; Emery N Brown
Journal:  Curr Opin Neurobiol       Date:  2014-01-21       Impact factor: 6.627

9.  Quantification of neonatal amplitude-integrated EEG patterns.

Authors:  Lauren Thorngate; Shuyuann Wang Foreman; Karen A Thomas
Journal:  Early Hum Dev       Date:  2013-10-09       Impact factor: 2.079

10.  Repertoire of mesoscopic cortical activity is not reduced during anesthesia.

Authors:  Anthony G Hudetz; Jeannette A Vizuete; Siveshigan Pillay; George A Mashour
Journal:  Neuroscience       Date:  2016-10-14       Impact factor: 3.590

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