Effects of bilateral kindling or bilateral sub-threshold stimulation of the amygdala or septum on muricide, ranacide, intraspecific aggression and passive avoidance in the rat

Bawden, Harry N.; Racine, R.

doi:10.1016/0031-9384(79)90412-8

Cited by 22 publications

(6 citation statements)

References 47 publications

(56 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Seizures induced by pilocarpine or lithium–pilocarpine were staged by the methods developed by Racine and modified by Gilbert (Bawden and Racine, 1979; McIntyre and Racine, 1986; Gilbert, 1995). For the experiments described herein, staging of limbic seizures was performed by video EEG monitoring.…”

Section: Resultsmentioning

confidence: 99%

Antagonism of peripheral inflammation reduces the severity of status epilepticus

Marchi

Fan

Ghosh

et al. 2009

Neurobiology of Disease

253

230

View full text Add to dashboard Cite

Status epilepticus (SE) is one of the most serious manifestations of epilepsy. Systemic inflammation and damage of blood-brain barrier (BBB) are etiologic cofactors in the pathogenesis of pilocarpine SE while acute osmotic disruption of the BBB is sufficient to elicit seizures. Whether an inflammatory-vascular-BBB mechanism could apply to the lithium–pilocarpine model is unknown. LiCl facilitated seizures induced by low-dose pilocarpine by activation of circulating T-lymphocytes and mononuclear cells. Serum IL-1β levels increased and BBB damage occurred concurrently to increased theta EEG activity. These events occurred prior to SE induced by cholinergic exposure. SE was elicited by lithium and pilocarpine irrespective of their sequence of administration supporting a common pathogenetic mechanism. Since IL-1β is an etiologic trigger for BBB breakdown and its serum elevation occurs before onset of SE early after LiCl and pilocarpine injections, we tested the hypothesis that intravenous administration of IL-1 receptor antagonists (IL-1ra) may prevent pilocarpine-induced seizures. Animals pre-treated with IL-1ra exhibited significant reduction of SE onset and of BBB damage. Our data support the concept of targeting systemic inflammation and BBB for the prevention of status epilepticus.

show abstract

Section: Resultsmentioning

confidence: 99%

Antagonism of peripheral inflammation reduces the severity of status epilepticus

Marchi

Fan

Ghosh

et al. 2009

Neurobiology of Disease

253

230

View full text Add to dashboard Cite

show abstract

“…Seizures induced by pilocarpine are staged by the methods developed by Racine and modified by Gilbert (Bawden and Racine, 1979; McIntyre and Racine 1986; Gilbert, 1995). For the experiments described herein, staging of limbic seizures was performed by video EEG monitoring.…”

Section: Resultsmentioning

confidence: 99%

In Vivo and In Vitro Effects of Pilocarpine: Relevance to Ictogenesis

Marchi¹,

Oby²,

Batra³

et al. 2007

Epilepsia

135

144

View full text Add to dashboard Cite

Summary:Objectives: A common experimental model of status epilepticus (SE) utilizes intraperitoneal administration of the cholinergic agonist pilocarpine preceded by methylscopolamine treatment. Currently, activation of cholinergic neurons is recognized as the only factor triggering pilocarpine SE. However, cholinergic receptors are also widely distributed systemically and pretreatment with methyl-scopolamine may not be sufficient to counteract the effects of systemically injected pilocarpine. The extent of such peripheral events and the contribution to SE are unknown and the possibility that pilocarpine also induces SE by peripheral actions is yet untested.Methods: We measured in vivo at onset of SE: brain and blood pilocarpine levels, blood-brain barrier (BBB) permeability, Tlymphocyte activation and serum levels of IL-1β and TNF-α. The effects of pilocarpine on neuronal excitability was assessed in vitro on hippocampal slices or whole guinea pig brain preparations in presence of physiologic or elevated [K + ] out .Results: Pilocarpine blood and brain levels at SE were 1400 ± 200 µM and 200 ± 80 µM, respectively. In vivo, after pilocarpine injection, increased serum IL-1β, decreased CD4:CD8 T-lymphocyte ratios and focal BBB leakage were observed. In vitro, pilocarpine failed to exert significant synchronized epileptiform activity when applied at concentrations identical or higher to levels measured in vivo. Intense electrographic seizure-like events occurred only in the copresence of levels of K + (6 mM) mimicking BBB leakage.Conclusions: Early systemic events increasing BBB permeability may promote entry of cofactors (e. g. K + ) into the brain leading to pilocarpine-induced SE. Disturbance of brain homeostasis represents an etiological factor contributing to pilocarpine seizures.

show abstract

“…Long-lasting increases in irritable behavior and resistance to capture have been found with pharmacologic kindling with lidocaine (Post et al, 1984). In addition, some (Pinel et al, 1977; Adamec and Stark-Adamec, 1983) but not all researchers (Bawden and Racine, 1979) have reported changes in behavior following electrical kindling of the amygdala and hippocampus. The persisting interictal emotional lability observed in our animals and those of other investigators is qualitatively different from the transient postictal irritability and increased defensive state observed after seizures.…”

Section: Discussionmentioning

confidence: 99%

Behavioral Effects of Kainic Acid Administration on the Immature Brain

et al. 1988

View full text Add to dashboard Cite

Prepubescent male rats with an amygdaloid electrode in place were administered kainic acid (KA) intraperitoneally (i.p.) while controls received phosphate-buffered saline (PBS). All KA-treated animals developed status epilepticus with bilateral forelimb clonus and ictal discharges on the EEG. The rats were then tested as adults for learning, memory, emotionality, social interaction, and activity level using the T maze, water maze, handling test, home cage intruder test, and open field test. KA-treated rats learned at a slower rate in the water maze and T maze than the controls. In addition, KA-treated rats had evidence of impaired memory during spatial bias testing in the water maze. In the home cage intruder test, KA-treated animals were more submissive and less aggressive than control animals. Finally, KA-treated animals were significantly more active than control animals in the open field test. This study demonstrates that KA administration to the immature brain, in a convulsant dose, results in permanent changes in behavior, learning, and memory.

show abstract

Effects of bilateral kindling or bilateral sub-threshold stimulation of the amygdala or septum on muricide, ranacide, intraspecific aggression and passive avoidance in the rat

Cited by 22 publications

References 47 publications

Antagonism of peripheral inflammation reduces the severity of status epilepticus

Antagonism of peripheral inflammation reduces the severity of status epilepticus

In Vivo and In Vitro Effects of Pilocarpine: Relevance to Ictogenesis

Behavioral Effects of Kainic Acid Administration on the Immature Brain

Contact Info

Product

Resources

About