Delayed ischemic electrocortical suppression during rapid repeated cerebral ischemia and kainate-induced seizures in rat

Andrei Ilie; Stefan Spulber; Sinziana Avramescu; Dragos Alexandru Nita; Ana-Maria Zagrean; Leon Zagrean; Mihai Moldovan

doi:10.1111/j.1460-9568.2006.04747.x

Delayed ischemic electrocortical suppression during rapid repeated cerebral ischemia and kainate-induced seizures in rat

Andrei Ilie, Stefan Spulber, Sinziana Avramescu, Dragos Alexandru Nita, Ana-Maria Zagrean, Leon Zagrean, Mihai Moldovan

Motor Control

9 Citations (Scopus)

Abstract

Global cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression (T(ES)) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate-induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a 'four-vessel occlusion' model. We devised an automatic method of T(ES) estimation based on the decay of the root mean square of two-channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared T(ES) with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, T(ES) was approximately 15 s and remained unchanged when five ischemic episodes were separated by 10-min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion T(ES) progressively increased, reaching a plateau value of approximately 24 s. A similar plateau was reached during kainate-induced seizures. The T(ES) plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro.

Original language	English
Journal	European Journal of Neuroscience
Volume	23
Issue number	8
Pages (from-to)	2135-2144
Number of pages	9
ISSN	0953-816X
DOIs	https://doi.org/10.1111/j.1460-9568.2006.04747.x
Publication status	Published - 2006

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10.1111/j.1460-9568.2006.04747.x

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@article{68c658f06c3811dcbee902004c4f4f50,

title = "Delayed ischemic electrocortical suppression during rapid repeated cerebral ischemia and kainate-induced seizures in rat",

abstract = "Global cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression (T(ES)) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate-induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a 'four-vessel occlusion' model. We devised an automatic method of T(ES) estimation based on the decay of the root mean square of two-channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared T(ES) with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, T(ES) was approximately 15 s and remained unchanged when five ischemic episodes were separated by 10-min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion T(ES) progressively increased, reaching a plateau value of approximately 24 s. A similar plateau was reached during kainate-induced seizures. The T(ES) plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro.",

author = "Andrei Ilie and Stefan Spulber and Sinziana Avramescu and Nita, {Dragos Alexandru} and Ana-Maria Zagrean and Leon Zagrean and Mihai Moldovan",

note = "Keywords: Animals; Brain Ischemia; Cerebral Cortex; Electrodes; Electroencephalography; Evoked Potentials, Visual; Kainic Acid; Male; Rats; Rats, Wistar; Reperfusion; Seizures; Time Factors",

year = "2006",

doi = "10.1111/j.1460-9568.2006.04747.x",

language = "English",

volume = "23",

pages = "2135--2144",

journal = "European Journal of Neuroscience",

issn = "0953-816X",

publisher = "Wiley-Blackwell",

number = "8",

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TY - JOUR

T1 - Delayed ischemic electrocortical suppression during rapid repeated cerebral ischemia and kainate-induced seizures in rat

AU - Ilie, Andrei

AU - Spulber, Stefan

AU - Avramescu, Sinziana

AU - Nita, Dragos Alexandru

AU - Zagrean, Ana-Maria

AU - Zagrean, Leon

AU - Moldovan, Mihai

N1 - Keywords: Animals; Brain Ischemia; Cerebral Cortex; Electrodes; Electroencephalography; Evoked Potentials, Visual; Kainic Acid; Male; Rats; Rats, Wistar; Reperfusion; Seizures; Time Factors

PY - 2006

Y1 - 2006

N2 - Global cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression (T(ES)) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate-induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a 'four-vessel occlusion' model. We devised an automatic method of T(ES) estimation based on the decay of the root mean square of two-channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared T(ES) with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, T(ES) was approximately 15 s and remained unchanged when five ischemic episodes were separated by 10-min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion T(ES) progressively increased, reaching a plateau value of approximately 24 s. A similar plateau was reached during kainate-induced seizures. The T(ES) plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro.

AB - Global cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression (T(ES)) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate-induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a 'four-vessel occlusion' model. We devised an automatic method of T(ES) estimation based on the decay of the root mean square of two-channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared T(ES) with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, T(ES) was approximately 15 s and remained unchanged when five ischemic episodes were separated by 10-min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion T(ES) progressively increased, reaching a plateau value of approximately 24 s. A similar plateau was reached during kainate-induced seizures. The T(ES) plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro.

U2 - 10.1111/j.1460-9568.2006.04747.x

DO - 10.1111/j.1460-9568.2006.04747.x

M3 - Journal article

C2 - 16630060

SN - 0953-816X

VL - 23

SP - 2135

EP - 2144

JO - European Journal of Neuroscience

JF - European Journal of Neuroscience

IS - 8

ER -

Delayed ischemic electrocortical suppression during rapid repeated cerebral ischemia and kainate-induced seizures in rat

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