Vagus Nerve Prolonged Stimulation in Cats: Effects on Epileptogenesis (Amygdala Electrical Kindling): Behavioral and Electrographic Changes

Fernández-Guardiola, Augusto; Martínez, Adrián; Valdés-Cruz, Alejandro; Magdaleno-Madrigal, Víctor Manuel; Martinez, Daniel Godoy; Fernández-Mas, Rodrigo

doi:10.1111/j.1528-1157.1999.tb00787.x

Cited by 85 publications

(38 citation statements)

References 33 publications

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“…Important evidence for the role of the peripheral nervous system in seizure activity is the use of vagus nerve stimulation as a mode of treatment in human epilepsy (reviewed in Ref. 4), as well as to dramatically reduce seizure activity in dogs, cats, and rodents models of epilepsy (22,58,63,67). However, other experiments have suggested that the peripheral nAChR subunits do not play a key role in nicotine-induced seizures.…”

Section: Discussionmentioning

confidence: 99%

Mice lacking neuronal nicotinic acetylcholine receptor β4-subunit and mice lacking both α5- and β4-subunits are highly resistant to nicotine-induced seizures

Kedmi

Beaudet

Orr-Urtreger

2004

Physiological Genomics

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Kedmi, Merav, Arthur L. Beaudet, and Avi Orr-Urtreger. Mice lacking neuronal nicotinic acetylcholine receptor ␤4-subunit and mice lacking both ␣5-and ␤4-subunits are highly resistant to nicotineinduced seizures. Physiol Genomics 17: 221-229, 2004. First published March 2, 2004 10.1152/physiolgenomics.00202.2003.-Nicotine, the main addictive component of tobacco, evokes a wide range of dose-dependent behaviors in rodents, and when administrated in high doses, it can induce clonic-tonic seizures. Nicotine acts through the nicotinic acetylcholine receptors (nAChRs). Mutations in the human ␣4-and the ␤2-nAChR subunit genes cause autosomal dominant nocturnal frontal lobe epilepsy. Using transgenic mice with mutations in nAChR subunits, it was demonstrated previously that the ␣4-, ␣5-, and ␣7-subunits are involved in nicotine-induced seizures. To examine the possibility that the ␤4-subunit is also involved in this phenotype, we tested mice with homozygous ␤4-subunit deficiency. The ␤4 null mice were remarkably resistant to nicotine-induced seizures compared with wild-type and ␣5 null mice. We also generated mice with double deficiency of both ␣5-and ␤4-nAChR subunits and demonstrated that they were more resistant to nicotine's convulsant effect than either the ␣5 or the ␤4 single mutant mice. In addition, the single ␣5 mutants and the double ␣5␤4-deficient mice exhibited a significantly shorter latency time to seizure than that of the wild-type mice. Our results thus show that ␤4-containing nAChRs have a crucial role in the pathogenesis of nicotine-induced seizures. Furthermore, by comparing multiple mutant mice with single and double subunit deficiency, we suggest that nicotinic receptors containing either ␣5-or ␤4-subunits are involved in nicotine-induced seizures and that receptors containing both subunits are likely to contribute to this phenomena as well. However, the ␣5-subunit, but not the ␤4-subunit, regulates the rate of response to high doses of nicotine.neuronal nicotinic acetylcholine receptor ␣5-and ␤4-subunits; knockout mice NICOTINE ACTS THROUGH THE nicotinic acetylcholine receptors (nAChRs) and can be toxic in high doses in mice, inducing tremors, seizures, and even death (41). The nAChRs are allosteric membrane proteins that belong to a large family of ligand-gated ion channels. Each receptor is composed of a combination of five subunits. To date, 12 neuronal subunits (␣2-␣10 and ␤2-␤4) have been identified (reviewed in Ref. 29). They are widely distributed in the central and peripheral nervous systems and are also expressed in nonneuronal cells (11,14,23,30,37).In humans, nAChRs are associated with a number of pathological conditions, including epilepsy (reviewed in Ref. 35). Mutations in the ␣4-and ␤2-subunit genes were associated with familial cases of autosomal dominant nocturnal frontal lobe epilepsy (15, 45, 52-54). In addition, genetic linkage was found between juvenile myoclonic epilepsy and the chromosomal region encompassing the ␣7-subunit gene (18).In mice, a genetic linkage was shown betw...

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Section: Discussionmentioning

confidence: 99%

Mice lacking neuronal nicotinic acetylcholine receptor β4-subunit and mice lacking both α5- and β4-subunits are highly resistant to nicotine-induced seizures

Kedmi

Beaudet

Orr-Urtreger

2004

Physiological Genomics

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“…Since that time numerous clinical trials have confirmed the effectiveness of VNS in controlling seizures (Ben-Menachem 1996;Handforth et al, 1998;Morris and Mueller, 1999;Boon, et al, 2002;Wheless and Baumgartner, 2004). Moreover, VNS exerts anticonvulsant effects in a variety of experimental animal models of epilepsy including rat (Takaya et al, 1996), dog (Zabara, 1992), and cat models (Fernandez-Guardiola et al, 1999). In addition, VNS suppresses seizures in a variety of populations including children (Crumrine, 2000;Amar et al, 2001;Wakai and Kotagal, 2001;Nagarajan et al, 2002;Kossoff and Pyzik, 2004), adolescents (Crumrine, 2000;Wakai and Kotagal, 2001;Nagarajan et al, 2002), adults (Tanganelli et al, 2002;Chavel et al, 2003;Koszewski et al, 2003;Holmes et al, 2004;Hui et al, 2004), the aged (Sirven et al, 2000) and, recently, in low IQ residents of long-term care facilities (Huf et al, 2005).…”

Section: Vns In Epilepsymentioning

confidence: 99%

Increased extracellular concentrations of norepinephrine in cortex and hippocampus following vagus nerve stimulation in the rat

Roosevelt¹,

et al. 2006

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The vagus nerve is an important source of afferent information about visceral states and it provides input to the locus coeruleus (LC), the major source of norepinephrine (NE) in the brain. It has been suggested that the effects of electrical stimulation of the vagus nerve on learning and memory, mood, seizure suppression, and recovery of function following brain damage are mediated, in part, by the release of brain NE. The hypothesis that left vagus nerve stimulation (VNS) at the cervical level results in increased extracellular NE concentrations in the cortex and hippocampus was tested at four stimulus intensities 0.0, 0.25, 0.5, and 1.0 mA. Stimulation at 0.0 and 0.25 mA had no effect on NE concentrations, while the 0.5 mA stimulation increased NE concentrations significantly in the hippocampus (23%), but not the cortex. However, 1.0 mA stimulation significantly increased NE concentrations in both the cortex (39%) and hippocampus (28%) bilaterally. The increases in NE were transient and confined to the stimulation periods. VNS did not alter NE concentrations in either structure during the inter-stimulation baseline periods. No differences were observed between NE levels in the initial baseline and the post-stimulation baselines. These findings support the hypothesis that VNS increases extracellular NE concentrations in both the hippocampus and cortex.

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“…At the same time, it has been observed that vagal afferents robustly promote REM intrusion. Even the electrical stimulation of the vagus nerve enhances REM (Puizillout & Foutz, 1976;Valdes-Cruz et al, 2002;Fernandez-Guardiola et al, 1999), elicits parieto-occipital geniculate (PGO) waves (Valdes-Cruz et al, 2002;Fernandez-Guardiola et al, 1999) and causes atonia in various animal preparations (Valdes-Cruz et al, 2002;Puizillout Foutz et al, 1977). This phenomena of transition from wakefulness to REM sleep has been termed variously as "reflex REM narcolepsy" and "narcoleptic reflex" (Valdes-Cruz et al, 2002).…”

Section: There Are Also Distinct Lines Of Evidences Showing That Rem mentioning

confidence: 99%

“…Activation of these vagal afferents robustly promotes REM intrusion. Even the electrical stimulation of the vagus nerve enhances REM (Puizillout & Foutz, 1976;Valdes-Cruz et al, 2002;Fernandez-Guardiola et al, 1999) and elicits PGO waves which are most prominent in REM sleep (Valdes-Cruz et al, 2002;Fernandez-Guardiola et al, 1999).…”

Section: The Neurobiological Perspectivementioning

confidence: 99%

A REM Intrusion Model for Death Bed Visions: A Palliative Nursing Perspective

Zhang¹,

Zhao²,

Xu³

et al. 2014

Neuroquantology

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Nurses often face the end of life conditions in resulting from several etiologies. It may be the end of life situations in chronic debilitating conditions like renal failures, oncological conditions and even progressive old age as such. Often around the clock nursing remains the primary mode of care for such patients. End of life care is complicated by several psychological and physical conditions. One of these psychological conditions which remain poorly understood is the presence of unusual end of life experiences where the exact role of nurses becomes controversial. In this article, we present a review of present literature on the end of life experiences. We will introduce by highlighting the importance of nursing position in observing these experiences. Subsequently, we will touch the neurobiological and psychological theories of near death experiences. We will then move towards the similarities between near death experiences and end of life dreams and visions. We will then elaborate on the REM intrusion model for near death experiences (NDEs). Finally, we will propound a REM intrusion model for end of life dreams and visions (ELDVs) and will see that the conditions of End of life predispose the patients for developing REM intrusions. Additionally, this model explains many of the features of ELDVs in both the phenomenological and neurological contexts.Key Words: death bed visions, end of life dreams, end of life visions, near death experiences, REM intrusion, neurobiology

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Vagus Nerve Prolonged Stimulation in Cats: Effects on Epileptogenesis (Amygdala Electrical Kindling): Behavioral and Electrographic Changes

Cited by 85 publications

References 33 publications

Mice lacking neuronal nicotinic acetylcholine receptor β4-subunit and mice lacking both α5- and β4-subunits are highly resistant to nicotine-induced seizures

Mice lacking neuronal nicotinic acetylcholine receptor β4-subunit and mice lacking both α5- and β4-subunits are highly resistant to nicotine-induced seizures

Increased extracellular concentrations of norepinephrine in cortex and hippocampus following vagus nerve stimulation in the rat

A REM Intrusion Model for Death Bed Visions: A Palliative Nursing Perspective

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