Facilitation of focal cobalt-induced epilepsy after lesions of the noradrenergic locus coeruleus system

Trottier, Suzanne; Lindvall, Olle; Chauvel, Patrick; ̈rklund, Anders Bjo

doi:10.1016/0006-8993(88)90831-1

Cited by 34 publications

(14 citation statements)

References 19 publications

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“…Similarly, Mason and Corcoran [78] showed a greater susceptibility to seizures induced by the chemoconvulsant metrazol and electroconvulsive shock in NE-lesioned rats. A facilitation of focal cobalt-induced seizures was observed in rats after removal of their forebrain NE projection from the LC [79]. Similarly, pre-treatment with DSP-4 reduced the threshold for facial and forelimb clonus obtained by corneal electroshock stimulation in rats, while maximal electroshock performed in NE-depleted rats confirmed increased susceptibility to brainstem seizures [9].…”

Section: The Antiepileptic Role Of Ne In Classic Seizure Modelsmentioning

confidence: 65%

The role of norepinephrine in epilepsy: from the bench to the bedside

Giorgi

Pizzanelli

Biagioni

et al. 2004

Neuroscience & Biobehavioral Reviews

161

113

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Section: The Antiepileptic Role Of Ne In Classic Seizure Modelsmentioning

confidence: 65%

The role of norepinephrine in epilepsy: from the bench to the bedside

Giorgi

Pizzanelli

Biagioni

et al. 2004

Neuroscience & Biobehavioral Reviews

161

113

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“…Although many studies have implicated NE as an endogenous neuromodulator of seizure activity (Chen et al, 1954;Arnold et al, 1973;Libet et al, 1977;Jerlicz et al, 1978;Mason and Corcoran, 1979;Snead, 1987;Trottier et al, 1988;Turski et al, 1989;Sullivan and Osorio, 1991;Mishra et al, 1994), the evidence has not always been consistent. The data presented here demonstrate that a selective loss of NE from noradrenergic terminals is proconvulsant.…”

Section: Without Dopsmentioning

confidence: 91%

“…(1) selective lesioning of noradrenergic neurons (with 6-hydroxydopamine or DSP-4) increases seizure susceptibility to a variety of convulsant stimuli (Arnold et al, 1973;Jerlicz et al, 1978;Mason and Corcoran, 1979;Snead, 1987;Trottier et al, 1988;Sullivan and Osorio, 1991;Mishra et al, 1994); (2) direct stimulation of the locus coeruleus (LC, the major concentration of noradrenergic cell bodies in the C NS) and the subsequent release of N E reduce C NS sensitivity to convulsant stimuli (Libet et al, 1977;T urski et al, 1989); (3) genetically epilepsy-prone rats (GEPRs), a widely used animal model of epilepsy, have deficient presynaptic N E content, N E turnover, tyrosine hydroxylase levels, dopamine ␤-hydroxylase (DBH) levels, and N E uptake (Jobe et al, 1984;Dailey and Jobe, 1986;Browning et al, 1989;Lauterborn and Ribak, 1989;Dailey et al, 1991); and (4) adrenergic agonists acting at the ␣-2 adrenoreceptor (␣2-AR) have anticonvulsant action (Papanicolaou et al, 1982;Baran et al, 1985;Loscher and C zuczwar, 1987;Fletcher and Forster, 1988;Jackson et al, 1991).…”

mentioning

confidence: 99%

Norepinephrine-Deficient Mice Have Increased Susceptibility to Seizure-Inducing Stimuli

Szot

Weinshenker

White³

et al. 1999

J. Neurosci.

127

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Several lines of evidence suggest that norepinephrine (NE) can modulate seizure activity. However, the experimental methods used in the past cannot exclude the possible role of other neurotransmitters coreleased with NE from noradrenergic terminals. We have assessed the seizure susceptibility of genetically engineered mice that lack NE. Seizure susceptibility was determined in the dopamine ␤-hydroxylase null mutant (Dbh Ϫ/Ϫ) mouse using four different convulsant stimuli: 2,2,2-trifluroethyl ether (flurothyl), pentylenetetrazol (PTZ), kainic acid, and high-decibel sound. Dbh Ϫ/Ϫ mice demonstrated enhanced susceptibility (i.e., lower threshold) compared with littermate heterozygous (Dbh ϩ/Ϫ) controls to flurothyl, PTZ, kainic acid, and audiogenic seizures and enhanced sensitivity (i.e., seizure severity and mortality) to flurothyl, PTZ, and kainic acid. c-Fos mRNA expression in the cortex, hippocampus (CA1 and CA3), and amygdala was increased in Dbh Ϫ/Ϫ mice in association with flurothyl-induced seizures. Enhanced seizure susceptibility to flurothyl and increased seizure-induced c-fos mRNA expression were reversed by pretreatment with L-threo-3,4-dihydroxyphenylserine, which partially restores the NE content in Dbh Ϫ/Ϫ mice. These genetically engineered mice confirm unambiguously the potent effects of the noradrenergic system in modulating epileptogenicity and illustrate the unique opportunity offered by Dbh Ϫ/Ϫ mice for elucidating the pathways through which NE can regulate seizure activity.

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“…Because the locus coeruleus projects widely throughout the neocortex, [40] and because norepinephrine has been shown to have anticonvulsant effects, [31457479] it is plausible that the locus coeruleus plays a role in the mechanism(s) of TNS and VNS. One key piece of evidence for such a mechanism comes from Krahl and colleagues, [42] who demonstrated that lesions of the locus coeruleus in rats prevented the anticonvulsant effects of VNS.…”

Section: Introductionmentioning

confidence: 99%

Central mechanisms of cranial nerve stimulation for epilepsy

Fanselow¹

2012

Surg Neurol Int

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Stimulation of peripheral cranial nerves has been shown to exert anticonvulsant effects in animal models as well as in human patients. Specifically, stimulation of both the trigeminal and vagus nerves has been shown in multiple clinical trials to be anticonvulsant, and stimulation of these nerves at therapeutic levels does not cause pain or negatively affect brain function. However, the neuronal mechanisms by which such stimulation exerts therapeutic effects are not well understood. In this review, the possible locations of action for trigeminal nerve stimulation (TNS) and vagus nerve stimulation (VNS) are explored. Additionally, the multiple time scales on which TNS and VNS function are discussed.

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Facilitation of focal cobalt-induced epilepsy after lesions of the noradrenergic locus coeruleus system

Cited by 34 publications

References 19 publications

The role of norepinephrine in epilepsy: from the bench to the bedside

The role of norepinephrine in epilepsy: from the bench to the bedside

Norepinephrine-Deficient Mice Have Increased Susceptibility to Seizure-Inducing Stimuli

Central mechanisms of cranial nerve stimulation for epilepsy

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