Endogenous activation of adenosine A(1) receptors accelerates ischemic suppression of spontaneous electrocortical activity
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Endogenous activation of adenosine A(1) receptors accelerates ischemic suppression of spontaneous electrocortical activity. / Ilie, Andrei; Ciocan, Dragos; Zagrean, Ana-Maria; Nita, Dragos Alexandru; Zagrean, Leon; Moldovan, Mihai.
In: Journal of Neurophysiology, Vol. 96, No. 5, 2006, p. 2809-14.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Endogenous activation of adenosine A(1) receptors accelerates ischemic suppression of spontaneous electrocortical activity
AU - Ilie, Andrei
AU - Ciocan, Dragos
AU - Zagrean, Ana-Maria
AU - Nita, Dragos Alexandru
AU - Zagrean, Leon
AU - Moldovan, Mihai
N1 - Keywords: Animals; Brain Ischemia; Cerebral Cortex; Electrocardiography; Electroencephalography; Electrophysiology; Male; Rats; Rats, Wistar; Receptor, Adenosine A1; Reperfusion; Synaptic Transmission; Xanthines
PY - 2006
Y1 - 2006
N2 - Cerebral ischemia induces a rapid suppression of spontaneous brain rhythms prior to major alterations in ionic homeostasis. It was found in vitro during ischemia that the rapidly formed adenosine, resulting from the intracellular breakdown of ATP, may inhibit synaptic transmission via the A(1) receptor subtype. The link between endogenous A(1) receptor activation during ischemia and the suppression of spontaneous electrocortical activity has not yet been established in the intact brain. The aim of this study was to investigate in vivo the effects of A(1) receptor antagonism by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) on the time to electrocortical suppression during global cerebral ischemia. Adult male Wistar rats under chloral hydrate anesthesia were subjected to 1-min transient "four-vessel occlusion" ischemic episodes, separated by 20-min reperfusion. The rats were injected intraperitoneally with either 1.25 mg/kg DPCPX dissolved in 2 ml/kg dimethyl sulfoxide (DMSO) or the same volume of DMSO alone, 15 min before the third ischemic episode. Time to electrocortical suppression was estimated based on the decay of the root mean square of two-channel electrocorticographic recordings. During the first two ischemic episodes, electrocortical suppression appeared after approximately 12 s in both groups. After DMSO administration, ischemic suppression remained unchanged. After DPCPX administration, the time to electrocortical suppression was increased by approximately 10 s, and bursts of activity were recorded during the entire ischemia. These effects disappeared within 15 h after DPCPX administration. Our data provide evidence that during cerebral ischemia endogenous activation of A(1) receptors accelerates the electrical "shut-down" of the whole brain.
AB - Cerebral ischemia induces a rapid suppression of spontaneous brain rhythms prior to major alterations in ionic homeostasis. It was found in vitro during ischemia that the rapidly formed adenosine, resulting from the intracellular breakdown of ATP, may inhibit synaptic transmission via the A(1) receptor subtype. The link between endogenous A(1) receptor activation during ischemia and the suppression of spontaneous electrocortical activity has not yet been established in the intact brain. The aim of this study was to investigate in vivo the effects of A(1) receptor antagonism by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) on the time to electrocortical suppression during global cerebral ischemia. Adult male Wistar rats under chloral hydrate anesthesia were subjected to 1-min transient "four-vessel occlusion" ischemic episodes, separated by 20-min reperfusion. The rats were injected intraperitoneally with either 1.25 mg/kg DPCPX dissolved in 2 ml/kg dimethyl sulfoxide (DMSO) or the same volume of DMSO alone, 15 min before the third ischemic episode. Time to electrocortical suppression was estimated based on the decay of the root mean square of two-channel electrocorticographic recordings. During the first two ischemic episodes, electrocortical suppression appeared after approximately 12 s in both groups. After DMSO administration, ischemic suppression remained unchanged. After DPCPX administration, the time to electrocortical suppression was increased by approximately 10 s, and bursts of activity were recorded during the entire ischemia. These effects disappeared within 15 h after DPCPX administration. Our data provide evidence that during cerebral ischemia endogenous activation of A(1) receptors accelerates the electrical "shut-down" of the whole brain.
U2 - 10.1152/jn.00466.2006
DO - 10.1152/jn.00466.2006
M3 - Journal article
C2 - 16885523
VL - 96
SP - 2809
EP - 2814
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 5
ER -
ID: 21662282