Electrical activity of the isolated cerebral hemisphere and isolated thalamus

Kellaway, Peter; Gol, Alexander; Proler, Meyer L.

doi:10.1016/0014-4886(66)90115-4

Cited by 64 publications

(19 citation statements)

References 22 publications

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“…Thus, the slow oscillation and the spontaneous burst discharges in chronically deafferented cortex may share a fundamental underlying mechanism that operates in deafferented cortical networks. This mechanism may critically depend on the strength of recurrent excitatory synaptic connections, such that large intact cortical networks during sleep or acutely isolated cortical gyri or hemispheres may generate slow oscillations (Kellaway et al, 1966;Gloor et al, 1977;Timofeev et al, 2000), but small cortical slabs, which lack long-range corticocortical excitatory connections, may only support slow oscillatory activity after upregulation of recurrent excitation.…”

Section: Discussionmentioning

confidence: 99%

Homeostatic Synaptic Plasticity Can Explain Post-traumatic Epileptogenesis in Chronically Isolated Neocortex

Houweling¹,

Bazhenov²,

Timofeev³

et al. 2004

Cerebral Cortex

155

150

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Chronically isolated neocortex develops chronic hyperexcitability and focal epileptogenesis in a period of days to weeks. The mechanisms operating in this model of post-traumatic epileptogenesis are not well understood. We hypothesized that the spontaneous burst discharges recorded in chronically isolated neocortex result from homeostatic plasticity (a mechanism generally assumed to stabilize neuronal activity) induced by low neuronal activity after deafferentation. To test this hypothesis we constructed computer models of neocortex incorporating a biologically based homeostatic plasticity rule that operates to maintain firing rates. After deafferentation, homeostatic upregulation of excitatory synapses on pyramidal cells, either with or without concurrent downregulation of inhibitory synapses or upregulation of intrinsic excitability, initiated slowly repeating burst discharges that closely resembled the epileptiform burst discharges recorded in chronically isolated neocortex. These burst discharges lasted a few hundred ms, propagated at 1-3 cm/s and consisted of large (10-15 mV) intracellular depolarizations topped by a small number of action potentials. Our results support a role for homeostatic synaptic plasticity as a novel mechanism of post-traumatic epileptogenesis.

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Section: Discussionmentioning

confidence: 99%

Homeostatic Synaptic Plasticity Can Explain Post-traumatic Epileptogenesis in Chronically Isolated Neocortex

Houweling¹,

Bazhenov²,

Timofeev³

et al. 2004

Cerebral Cortex

155

150

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“…Since a proposed general pace-maker, situated in the medial thalamus, is not unconditional for cortical spindle appearance and since virtually all spindle activity disappears after a total thalamectomy (Kristiansen & Courtois, 1949;Jasper, 1949; Kellaway, Gol & Proler, 1966;Andersen et al 1967), we wanted to study the nature of the thalamo-cortical relations during spindle activity. Is the spindle activity of a given cortical area controlled by a specific aggregate of thalamic neurones, and if so, what are the topographical relations of this or these groups?…”

Section: Introductionmentioning

confidence: 99%

Nature of thalamo‐cortical relations during spontaneous barbiturate spindle activity

Andersen¹,

Andersson²,

Lømo³

1967

The Journal of Physiology

103

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SUMMARY1. The relation between thalamic and cortical spontaneous spindles was investigated in cats anaesthetized with barbiturates.2. Simultaneous recordings with multiple electrodes in the thalamus and cortex revealed a high correlation between thalamic and cortical spindle activity, both with regard to the occurrence of the spindles as well as to their individual waves, provided a critical location of the electrodes was secured. The results indicate a point-to-point relation between a group of thalamic cells and a small cortical area to which these cells project. In the spontaneous rhythm, the cortical columns are probably individually controlled by a thalamic rhythmic entity. This point-to-point relation was found in all the major sensory projection systems and in one thalamic 'association' nucleus and its corresponding 'association' cortex.3. Cortical barbiturate spindles appeared either as local spindles in a restricted cortical area or as compound spindles in several areas. Spindles recorded from electrodes separated by 2 mm or more were clearly different with regard to intraspindle wave frequency, duration, and the time of start and stop of the spindle. These differences increased with increasing distance between the electrodes, and were most pronounced when the corticograms of the two hemispheres were compared.4. Spontaneous spindle activity interfered with orthodromic transmission through n. ventralis posterolateralis (VPL) and medial geniculate nucleus (MG), judged by depression of the thalamic and cortical responses to peripheral nerve volleys or clicks. Such inhibition required the afferent volley to be delivered at a particular time of the spontaneous oscillations. Further, orthodromic volleys reset the rhythmic spindle waves in the appropriate thalamic and cortical areas.5. These findings lead to a new concept of the thalamic pace-maker function. During barbiturate anaesthesia, small assemblages of thalamic neurones seem to have the ability to generate independent rhythmic 284 P. ANDERSEN, S. A. ANDERSSON AND T. LOMO discharges, and thereby control the rhythm of the particular cortical column to which this thalamic group projects.6. During barbiturate anaesthesia, many facultative pace-makers seem to be present in the thalamus. The total number may be as large as 25,000-35,000. Usually, many of these rhythmic thalamic units beat in synchrony or near synchrony.

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“…In the best cat isolated cerebral hemisphere preparations, electrocortical activity consists of 300-1,000 [tV, 0 5-4-0 Hz potentials with superimposed 25-70 Hz rhythm (Kellaway, Gol & Proler, 1966). In poorer preparations, this activity was interrupted by brief recurrent isoelectric periods (' flattening '), prolonged and more frequent during hypoxia, and considered an expression of a 'pathological' state.…”

Section: Discussionmentioning

confidence: 99%

Actions of dexamphetamine and amphetamine‐like amines in chickens with brain transections

Marley

Stephenson

1971

British J Pharmacology

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Summary1. A method for preparing the encephale isole preparation in young fowls is described. Certain important differences were found between electrocortical activity of chicken and mammalian encephale isole preparations. Electrocortical effects of excitant sympathomimetic amines and their antagonism were readily quantified because of stable electrocortical activity of the chick encephale isole preparation. 2. Amphetamine-like excitant amines ((+ )-and (-)-amphetamine, a-methyltryptamine, tryptamine, /8-phenethylamine, cyclopentamine, 3-tetrahydronaphthylamine and tuaminoheptane) evoked electrocortical desynchronization in chick encephale isole preparations, confirming the central origin of these effects. Behavioural changes were also observed. 3. The electrocortical response to these amines was antagonized by methysergide, a selective tryptamine antagonist and by a catecholamine, a-methylnoradrenaline. Behavioural changes were also antagonized. 4. Electrocortical desynchronization to dexamphetamine was prevented by an anterior transection of the brain which separated the telencephalon from the diencephalon. More posterior transections reduced the duration of the electrocortical response to dexamphetamine; intensity of response was either increased or decreased.

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Electrical activity of the isolated cerebral hemisphere and isolated thalamus

Cited by 64 publications

References 22 publications

Homeostatic Synaptic Plasticity Can Explain Post-traumatic Epileptogenesis in Chronically Isolated Neocortex

Homeostatic Synaptic Plasticity Can Explain Post-traumatic Epileptogenesis in Chronically Isolated Neocortex

Nature of thalamo‐cortical relations during spontaneous barbiturate spindle activity

Actions of dexamphetamine and amphetamine‐like amines in chickens with brain transections

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