Brainstem Experimental Seizures Produced by Microinjections of Carbachol

Elazar, Zeev; Feldman, Zeev

doi:10.1111/j.1528-1157.1987.tb03674.x

Cited by 53 publications

(8 citation statements)

References 28 publications

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“…In several animals, the induction of high muscle tone by infusion of carbachol into the DLPT was followed within 2–4 min by pronounced convulsions of the limbs, head and tail, as well as foaming at the mouth. These observations are consistent with previous studies reporting that microinjections of carbachol into the pontine and mesencephalic reticular formation of adult rats produces electroencephalographic seizures, including convulsions (Elazar & Feldman, 1987; Elazar & Berchanski, 2000).…”

Section: Resultssupporting

confidence: 93%

Brainstem cholinergic modulation of muscle tone in infant rats

Gall

Poremba

Blumberg

2007

Eur J of Neuroscience

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In week-old rats, lesions of the dorsolateral pontine tegmentum (DLPT) and nucleus pontis oralis (PnO) have opposing effects on nuchal muscle tone. Specifically, pups with DLPT lesions exhibit prolonged bouts of nuchal muscle atonia (indicative of sleep) and pups with PnO lesions exhibit prolonged bouts of high nuchal muscle tone (indicative of wakefulness). Here we test the hypothesis that nuchal muscle tone is modulated, at least in part, by cholinergically mediated interactions between these two regions. First, in unanesthetized pups, we found that chemical infusion of the cholinergic agonist carbachol (22 mm, 0.1 microL) within the DLPT produced high muscle tone. Next, chemical lesions of the PnO were used to produce a chronic state of high nuchal muscle tone, at which time the cholinergic antagonist scopolamine (10 mm, 0.1 microL) was infused into the DLPT. Scopolamine effectively decreased nuchal muscle tone, thus suggesting that lesions of the PnO increase muscle tone via cholinergic activation of the DLPT. Using 2-deoxyglucose autoradiography, metabolic activation throughout the DLPT was observed after PnO lesions. Finally, consistent with the hypothesis that PnO inactivation produces high muscle tone, infusion of the sodium channel blocker lidocaine (2%) into the PnO of unanesthetized pups produced rapid increases in muscle tone. We conclude that, even early in infancy, the DLPT is critically involved in the regulation of muscle tone and behavioral state, and that its activity is modulated by a cholinergic mechanism that is directly or indirectly controlled by the PnO.

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Section: Resultssupporting

confidence: 93%

Brainstem cholinergic modulation of muscle tone in infant rats

Gall

Poremba

Blumberg

2007

Eur J of Neuroscience

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“…The involvement of brainstem sites in seizure development and generalization has been investigated through a variety of interventions. For example, administration of convulsive drugs to thalamic and brainstem sites produces AD and convulsions (Elazar & Feldman, 1987; Peterson, 1995; Ishimoto et al, 2000; Raisinghani & Faingold, 2003; Ishimoto et al, 2004). Furthermore, lesions of brainstem nuclei can disrupt development of audiogenic seizures (Browning, 1986).…”

mentioning

confidence: 99%

Susceptibility of brainstem to kindling and transfer to the forebrain

Lam

Whelan²,

Corcoran

2010

Epilepsia

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SUMMARYPurpose: The kindling of seizures with stimulation of brainstem sites has been reported inconsistently in the literature. The characteristics of the kindling observed, involving high intensities of stimulation and immediate onset of generalized tonic-clonic convulsions, raise questions regarding the nature of kindling from these sites. Methods: We implanted chronic electrodes in either the nucleus reticularis pontis oralis (RPO), mesencephalic reticular formation (MRF), dorsal periaqueductal gray (dPAG), or ventrolateral periaqueductal gray (vlPAG) in male Long-Evans rats, with a recording electrode in the amygdala. Rats received conventional high-frequency kindling stimulation once daily for 30 days. To test for transfer, we kindled the amygdala beginning 7 weeks after the last brainstem kindling trial. Results: Tonic-clonic seizures were evoked by stimulation from all brainstem sites. Seizures were brief and were associated with characteristic low-amplitude highfrequency afterdischarge (AD). Kindling of the dPAG resulted in the development of classic AD and increased AD duration. Prior kindling of the dPAG facilitated subsequent kindling of the amygdala; however, no transfer was observed with prekindling of other brainstem sites. Discussion: The variability in the response to kindling stimulation suggests that certain brainstem sites are resistant to kindling, whereas other sites are more susceptible to kindling but are still relatively resistant in comparison to sites in the forebrain. The development of classic AD in later trials of dPAG stimulation suggests that epileptogenesis can occur even in the initial absence of classic AD when low-amplitude high-frequency AD is present.

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“…Similarly one might consider cataleptic responses as an additional type of generalization of AGS. In this regard, carbachol injected into the midbrain reticular formation or into nuclei of the pontine reticular formation was shown to cause not only behavioral wild running seizures and EEG seizures, but also in some instances an apparently identical catalepsy (Elazar and Feldman, 1987). Unfortunately, little is understood about the relationship between catalepsy and AGSs or the dir ct evocation of catatonia by auditory stimulation as escribed in this study.…”

Section: Influence Of Exposure Durationmentioning

confidence: 70%

Ontogenetic Features of Audiogenic Seizure Susceptibility Induced in Immature Rats by Noise

Pierson

Swann

1991

Epilepsia

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Although numerous models are currently used for systematic study of the mechanisms of epileptogenesis in mature brain, few animal models have been developed that allow similar explorations in the developing nervous system. One experimental model of epilepsy supports a premise that perinatal experience can lead to eventual seizure susceptibility, however. Audiogenic seizure (AGS) susceptibility can be induced during a critical developmental period in normal mice by auditory deprivation and therefore by cochlear trauma. We studied the developmental parameters that affect success of both induction and testing of AGS-susceptibility in the rat. Intense high-frequency noise exposure was used as the traumatizing agent. The Wistar rat strain used is inherently seizure-resistant because in greater than 400 trials, untreated rats have never exhibited susceptibility at any age. Although single prolonged exposures to high-intensity noise were administered to groups of rats at ages between postnatal days (PNDs) 12 and 36, PND 14 was the age when exposure was most likely to result in eventual seizure susceptibility. Furthermore, duration of initial exposure on PND 14 determined the rate of susceptibility when measured 2 weeks later. Accordingly, we noted that single noise exposures at an intensity of 125 dB and ranging between 6 and 10 min in duration induced susceptibility in 100% of rats tested on PND 28; nonetheless, seizures among the rats exposed for 8 min were the most severe. Typically, these seizures began as wild running attacks and were followed by tonic/clonic convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)

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Brainstem Experimental Seizures Produced by Microinjections of Carbachol

Cited by 53 publications

References 28 publications

Brainstem cholinergic modulation of muscle tone in infant rats

Brainstem cholinergic modulation of muscle tone in infant rats

Susceptibility of brainstem to kindling and transfer to the forebrain

Ontogenetic Features of Audiogenic Seizure Susceptibility Induced in Immature Rats by Noise

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