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Kindling antagonism: an arrest of epileptogenesis?Kirkby, Robert Duncan 09 July 2018 (has links)
Concurrent alternating stimulation of two limbic sites culminates in
typical kindling of generalized seizures from one site (dominant), whereas the
other site (suppressed) supports only nongeneralized seizures for as long as
stimulation of the dominant site continues (kindling antagonism). Burchfiel
and Applegate (1989; 1990) claimed that antagonism reflects a frank arrest
of kindling from the suppressed site at an intermediate stage. They argued,
moreover, that the eventual generalization of seizures provoked from the
suppressed site after the termination of stimulation of the dominant site
reflects a resumption of kindling from its previous state of arrest.
Burchfiel and Applegate also claimed that the behaviorally stereotyped
arrest of kindling from the suppressed site reveals critical transitions
between sequentially expressed mechanisms that govern both antagonism
and kindling. They therefore viewed kindling as a stepwise process that is
mediated by qualitatively and temporally distinct mechanisms. This position
hinges on the assumption that antagonism reflects a true arrest of kindling
from the suppressed site rather than a transient inhibition of seizures. I
conducted the following experiments to determine whether the assumption
is justified,
In Experiment 1, I replicated and extended the observations of
Burchfiel and Applegate concerning the expression of antagonism during
alternating stimulation of limbic as well as nonlimbic sites. The results of
Experiment 1 thus indicate that antagonism is indeed a robust phenomenon
and therefore worthy of further study.
In Experiment 2, the imposition of a prolonged stimulation-free period
(30 d) after the termination of stimulation of the dominant site (amygdala)
did not significantly reduce the number of stimulations of the suppressed
site (septal area) required to elicit a generalized seizure. Also, epileptiform
after discharge provoked from the septal area increased during alternating
stimulation, and the septal area supported generalized seizures after fewer
stimulations in rats previously expressing antagonism as compared to control
rats previously kindled from the amygdala. Collectively, these data are
consistent with the view of Burchfiel and Applegate that kindling from the
suppressed site progresses to an intermediate stage during alternating
stimulation and resumes after the termination of stimulation of the dominant
site.
The results of Experiment 2 also suggest the possibility that the
development of seizures from the suppressed site after the termination of
stimulation of the dominant site is dictated by the additive expression of:
first, the well-documented facilitation of kindling from one site that reliably
follows kindling from another (i.e., transfer between the amygdala, which
supported generalized seizures, and the septal area); second, (partial)
kindling from the septal area, which previously supported nonconvulsive or
partial seizures, during the Initial Phase. The results of Experiment 3
revealed that the facilitation of seizure development from the septal area
observed in rats previously exposed to alternating stimulation, which
perhaps is attributable to partial kindling from the suppressed site, was site specific.
Rats subjected to alternating stimulation of the left amygdala and
right septal area and control rats previously stimulated only in the left
amygdala subsequently demonstrated generalized seizures following similar
numbers of stimulations of the previously unstimulated right amygdala.
Another plausible view is that antagonism reflects a long-lasting (>
30 d) form of inhibition that is perhaps uniquely invoked by alternating
stimulation, While the results of Experiments 1 - 3 do not rule out this
possibility, the results of Experiment 4 clearly indicate that the persistence
of any such effects of alternating stimulation is not mediated by continuing
influences of the dominant site: After the establishment of antagonism,
radio-frequency lesions of the dominant site (amygdala) failed to alter the
development of seizures provoked by stimulation of the suppressed site
(septal area). / Graduate
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Mechanisms of hyperexcitability in the kindling model of epilepsyElmér, Eskil. January 1997 (has links)
Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.
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Mechanisms of hyperexcitability in the kindling model of epilepsyElmér, Eskil. January 1997 (has links)
Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.
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An Investigation into temporal lobe seizure networks : role of the piriform and perirhinal cortices in hippocampal kindled motor seizures.Kelly, Mary Ellen, January 1900 (has links)
Thesis (Ph. D.)--Carleton University, 1995. / Also available in electronic format on the Internet.
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Kindling and activation induced hippocampal plasticity /Adams, Beth Chick. January 1998 (has links)
Thesis (Ph.D.) -- McMaster University, 1999. / Includes bibliographical references (leaves 130-151). Also available via World Wide Web.
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An investigation of the role of amygdaloid α-2 adrenoceptors in the kindling of seizuresPelletier, Marc Roger 06 July 2018 (has links)
It has been reported previously that systemic administration of clonidine, an
agonist of α-2 receptors for noradrenaline, significantly retards amygdaloid kindling,
by delaying the emergence from partial seizure, Conversely, systemic administration
of α-2 antagonists has been reported to facilitate amygdaloid kindling, The
experiments I conducted attempted to discover whether α-2 adrenoceptors in the
amygdala participated in these effects, I examined the effect of either systemic
administration (i,p.) or intraamygdaloid infusions of a variety of noradrenergic drugs
on the kindling of seizures with electrical stimulation of the amygdala, Rats received
either low-frequency stimulation of the amygdala, to induce rapid kindling, or
conventional high-frequency stimulation, Drugs and electrical stimulation were
administered once every 48 hrs, I observed a significant retardation of kindling in
rats receiving i,p. injections of clonidine (0.1 mg/kg) or unilateral infusions of
clonidine in concentrations of [special characters omitted] to [special characters omitted] M, regardless of the stimulation frequency.
The prophylactic effect was due to a delay in the progression out of partial seizure. I observed similar effects with infusions of xylazine, also an α-2 adrenoceptor agonist,
The effect was specific to the amygdala/pyriform region, because infusions of
clonidine dorsal lo the amygdala were without effect. Power spectral analysis of the
AD from the stimulated and the contralateral amygdala during the initial occurrence
of bilateral AD failed to reveal differences attributable to clonidine, Therefore,
clonidine might retard kindling by modifying the propagation of AD from the
stimulated amygdala to a midbrain or pontine brainstem area critical, for the
expression of generalized seizures. Clonidine had no effect on established generalized
seizures, suggesting that it was producing a genuine prophylactic effect against
kindling. Unexpectedly, intraamygdaloid infusions of either idazoxan, yohimbine, or
SK&F 104856, antagonists of α-2 receptors, failed to accelerate kindling.
Simultaneous infusion of idazoxan blocked clonidine’s prophylactic effect, which
suggests strongly that this effect was mediated at the α-2 adrenoceptor. Blockade of
amygdaloid α-1 adrenoceptors with corynanthine failed to affect kindling.
I conclude that the population of α-2 adrenoceptors in the amygdala/pyriform
region contributes to the antiepileptogenic effect observed after systemic
administration of clonidine and that the facilitation of kindling observed after systemic
administration of α-2 antagonists reported previously may have been mediated by the
blockade of a population of α -2 adrenoceptors in addition to, or outside of, the
amygdala/pyriform region. / Graduate
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Anxiogenic and anxiolytic effects in the elevated plus maze produced by kindling and low frequency stimulation of the basolateral amygdala /Young, Barbara Ann, January 2001 (has links)
Thesis (M.Sc.)--Memorial University of Newfoundland, 2001. / Bibliography: leaves 47-54.
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Perirhinal or postrhinal cortex lesions : effects on spatial versus fear learning, and on kindling /Bureau, Yves, January 1900 (has links)
Thesis (Ph. D.)--Carleton University, 2001. / Includes bibliographical references (p. 165-175). Also available in electronic format on the Internet.
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Influence of perinatal environment on impulsivity and seizure susceptibility differences in seizure-prone (fast) and seizure-resistant (slow) rodents /Patey, Andrea M. E. January 1900 (has links)
Thesis (M.Sc.) - Carleton University, 2005. / Includes bibliographical references (p. 86-97). Also available in electronic format on the Internet.
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A pharmacological examination of GABAb receptor-mediated inhibition in the amygdala of fast and slow kindling rat strains; in VIVO and in VITRO studies.Shin, Rick S. January 1900 (has links)
Thesis (Ph.D.) - Carleton University, 2005. / Includes bibliographical references (p. 175-191). Also available in electronic format on the Internet.
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