Characteristics of limbic seizures evoked by peripheral injections of lithium and pilocarpine

Persinger, Michael A.; Makarec, Katherine; Bradley, Jean‐Claude

doi:10.1016/0031-9384(88)90342-3

Cited by 100 publications

(37 citation statements)

References 11 publications

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“…Thus, increased EAAC1 levels observed during the acute and latent period in the lithium-pilocarpine model might be an important compensatory change that both enhances clearance of glutamate from the synaptic cleft and may serve to enhance inhibitory synaptic transmission by increasing GABA production. This upregulation of EAAC1 could be sufficient to prevent neuronal death in the Tu, and granular and molecular layers of the DG, where no degenerating cells or axon terminals were detected 24 h after the injection of lithium-pilocarpine, in accordance with previous studies (Turski et al, 1989;Persinger et al, 1988;Motte et al, 1998;André et al, 2001;Roch et al, 2002). In all these structures, the upregulation of EAAC1 persisting up to 144 h after the onset of SE could be a protective mechanism against the potentially deleterious consequences of seizureenhanced glutamatergic neurotransmission.…”

Section: Eaac1 Glutamate Transporters In Epilepsy B Voutsinos-porche supporting

confidence: 90%

“…Recurrent seizures started around 20 to 25 mins after pilocarpine administration. These seizures which associated episodes of head and bilateral forelimb myoclonus with rearing and falling progressed to SE at approximately 35 to 40 mins after pilocarpine injection, as described previously (Persinger et al, 1988;Dubé et al, 2001;Roch et al, 2002). For the study of the acute phase, rats (n = 3) were killed at 24 h after the onset of SE.…”

Section: Lithium-pilocarpine-induced Status Epilepticusmentioning

confidence: 99%

“…Likewise, in surgical resections from human epileptic structures (Mathern et al, 1999;Meldrum et al, 1999;Tessler et al, 1999;Proper et al, 2002) and in animal models of epilepsy (Miller et al, 1997;Akbar et al, 1998;Ghijsen et al, 1999;Simantov et al, 1999; Doi et al 2000; Ueda and Willmore, 2000;Ueda et al, 2001;Crino et al, 2002), an increase or a decrease of EAAC1 transporter expression has been reported. Systemic injection of pilocarpine, a non-subtypespecific partial muscarinic agonist, alone or combined with lithium in the rat, is frequently used to produce an animal model of temporal lobe epilepsy (Persinger et al, 1988;Turski et al, 1989;Dubé et al, 2001). After status epilepticus (SE), extended neuronal loss and reactive gliosis occur mainly in forebrain limbic structures, including the hippocampus, amygdala, septum, thalamus, piriform and entorhinal cortex (Ent) (Turski et al, 1989;Motte et al, 1998;Fujikawa et al, 1999;Dubé et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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EAAC1 Glutamate Transporter Expression in the Rat Lithium-Pilocarpine Model of Temporal Lobe Epilepsy

Voutsinos-Porche

Koning

Clément

et al. 2006

J Cereb Blood Flow Metab

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Glutamate excitotoxicity has been involved in the pathophysiology of epilepsy. Normal functioning of glutamate transporters clears the synaptically released glutamate to prevent excitotoxic neuronal death. Using densitometric immunohistochemical analysis, we examined the temporal expression of the neuronal glutamate transporter (EAAC1) in the lithium-pilocarpine rat model of temporal lobe epilepsy. During the acute period of lithium-pilocarpine-induced status epilepticus, EAAC1 transporter expression increased in the pyramidal neurons of cornus ammonis (CA)1, CA2 and CA3 (fields of the hippocampus), in dentate gyrus (DG) granule cells and in olfactory tubercle (Tu). During the latent period, EAAC1 expression was strongly expressed in the DG granular and molecular layers, Tu, cerebral cortex and septum, and went back to control levels in CA1, CA2 and CA3 layers. The overexpression of EAAC1 occurred mainly in structures prone to develop FluoroJade-B-positive degenerating neurons. It is, however, not clear to what extent the overexpression of EAAC1 contributes to epileptogenesis and in which area it may represent a preventive or compensatory or response to injury.

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Section: Eaac1 Glutamate Transporters In Epilepsy B Voutsinos-porche supporting

confidence: 90%

Section: Lithium-pilocarpine-induced Status Epilepticusmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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EAAC1 Glutamate Transporter Expression in the Rat Lithium-Pilocarpine Model of Temporal Lobe Epilepsy

Voutsinos-Porche

Koning

Clément

et al. 2006

J Cereb Blood Flow Metab

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“…Numerous studies over the last few decades have identified sex and cycle-dependent differences in seizure susceptibility in rodents. These studies have used various methods to induce seizures, including kindling, electroshock, and chemoconvulsant administration Buterbaugh, 1989;Edwards et al, 1999;Finn and Gee, 1994;Hoffman et al, 2003;Hom and Buterbaugh, 1986;Hudson and Buterbaugh, 1991;Kalkbrenner and Standley, 2003;Matejovska et al, 1998;Nicoletti et al, 1985;Pericic and Bujas, 1997;Persinger et al, 1988;Pesce et al, 2000;Schwartz-Giblin et al, 1989;Slamberova and Vathy, 2000;Tan and Tan, 2001;Tominaga et al, 2001;Valente et al, 2002;Velisek et al, 1999;Wahnschaffe and Loscher, 1992;Woolley, 2000). However, these studies have failed to provide a clear picture of the relationship between ovarian hormone levels and seizure susceptibility.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, mid-morning comparisons of cycling rats allowed optimal comparisons of physiological changes of reproductive steroids (e.g., estradiol is elevated during the morning on proestrus but progesterone is not, allowing specific insight into the influence of physiological levels of estradiol). Since age and body weight may also influence the response to convulsants Darbin et al, 2004;Hunter et al, 1989;Pericic and Bujas, 1997;Persinger et al, 1988;Turski et al, 1989), we included animals from a range of ages and body weights in each reproductive condition, to determine whether age and/or body weight might affect the outcome.…”

Section: Introductionmentioning

confidence: 99%

Seizure susceptibility in intact and ovariectomized female rats treated with the convulsant pilocarpine

Scharfman

Goodman

Rigoulot

et al. 2005

Experimental Neurology

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Despite numerous neuroendocrinological studies of seizures, the influence of estrogen and progesterone on seizures and epilepsy remains unclear. This may be due to the fact that previous studies have not systematically compared distinct endocrine conditions and included all relevant controls. The goal of the present study was to conduct such a study using pilocarpine as chemoconvulsant. Thus, age and weight-matched, intact or ovariectomized rats were tested to determine incidence of status epilepticus and to study events leading to status. Intact female rats were sampled at each cycle stage (proestrus, estrus, metestrus, or diestrus 2). Convulsant was administered at the same time of day, 10:00-10:30 a.m. Statistical analysis showed that there was a significantly lower incidence of status on the morning of estrus, but differences were attenuated in older animals. Ovariectomized rats were distinct in their rapid progression to status. These results show that the incidence of status in female rats following pilocarpine injection, and the progression to pilocarpineinduced status, are influenced by reproductive state as well as age. The hormonal milieu present specifically on the morning of estrus appears to decrease susceptibility to pilocarpine-induced status, particularly at young ages. In contrast, the chronic absence of reproductive steroids that characterizes the ovariectomized rat leads to a more rapid progression to status. This dissociation between incidence vs. progression provides new insight into the influence of estrogen and progesterone on seizures.

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Expression of c‐fos protein in the experimental epilepsy induced by pilocarpine

Barone

Morelli

Cicarelli

et al. 1993

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The expression of the c-fos proto-oncogene, as estimated by immunohistochemistry of the FOS nuclear protein, was studied in both focal and generalized seizures induced in rats by systemic administration of pilocarpine. Focal seizures, as indicated by the occurrence of stereotyped oral movements, chewing and sniffing, were evoked by either a subconvulsant dose of pilocarpine (200 mg/kg) or the association of a convulsant dose of pilocarpine (400 mg/kg) with SCH 23390, a selective D-1 dopamine receptor antagonist. This seizure pattern resulted in FOS accumulation in certain limbic areas, namely, the piriform cortex, amygdala, and olfactory tubercle. On the other hand, in rats developing generalized seizures, accumulation of FOS was also found in hippocampus, cingulate cortex, frontal cortex, striatum, accumbens, as well as in certain thalamic nuclei. Generalized seizures, including motor limbic seizures and status epilepticus, were induced by either a convulsant dose of pilocarpine (400 mg/kg) or a low dose of pilocarpine (15-200 mg/kg) combined with either lithium or the D-1 selective agonist SKF 38393. These findings indicate a close correlation between the sequence of behavioural alterations induced by pilocarpine and the proto-oncogene activation. The results provide the basis for mapping the areas of origin and the pathways of generalization of seizure activity. As shown by the effects of dopamine receptor agonists and antagonists, the process of generalization appears to be controlled by the dopamine system.

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Characteristics of limbic seizures evoked by peripheral injections of lithium and pilocarpine

Cited by 100 publications

References 11 publications

EAAC1 Glutamate Transporter Expression in the Rat Lithium-Pilocarpine Model of Temporal Lobe Epilepsy

EAAC1 Glutamate Transporter Expression in the Rat Lithium-Pilocarpine Model of Temporal Lobe Epilepsy

Seizure susceptibility in intact and ovariectomized female rats treated with the convulsant pilocarpine

Expression of c‐fos protein in the experimental epilepsy induced by pilocarpine

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