1984
DOI: 10.1016/0165-3806(84)90085-3
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Kainic-acid-induced seizures: A developmental study

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Cited by 359 publications
(208 citation statements)
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“…The substantia nigra pars reticulata (SNr), a main basal ganglia output structure, is thought to be crucially involved in the propagation and modulation of different types of experimental seizures including complex-partial seizures as observed in TLE (Iadarola and Gale, 1982;Garcia-Cairasco and Sabbatini, 1983;Le Gal La Salle et al, 1983;Albala et al, 1984;De Sarro et al, 1984McNamara et al, 1984;Moshé and Albala, 1984;Sperber et al, 1987;Moshé et al, 1992;Gale et al, 2008). Using in vivo recordings, numerous plastic network changes were shown for basal ganglia structures including the SNr in amygdalakindled rats as a model for TLE (Gernert et al, 2004;Nolte et al, 2006;Kücker et al, 2010).…”
Section: Introductionmentioning
confidence: 99%
“…The substantia nigra pars reticulata (SNr), a main basal ganglia output structure, is thought to be crucially involved in the propagation and modulation of different types of experimental seizures including complex-partial seizures as observed in TLE (Iadarola and Gale, 1982;Garcia-Cairasco and Sabbatini, 1983;Le Gal La Salle et al, 1983;Albala et al, 1984;De Sarro et al, 1984McNamara et al, 1984;Moshé and Albala, 1984;Sperber et al, 1987;Moshé et al, 1992;Gale et al, 2008). Using in vivo recordings, numerous plastic network changes were shown for basal ganglia structures including the SNr in amygdalakindled rats as a model for TLE (Gernert et al, 2004;Nolte et al, 2006;Kücker et al, 2010).…”
Section: Introductionmentioning
confidence: 99%
“…On the othe~. hand, both published and unpublished experimental studies in immature animals of most, although not all, species have failed to demonstrate that even prolonged seizures (status epilepticus) lead to overt brain injury (1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14] (see "Discussion").…”
mentioning
confidence: 99%
“…The observation that changes in the hippocampus tend to be region specific may explain the many conflicting reports on hippocampal alterations following excitatory intervention, particularly in the neonate. Some authors report longterm hippocampal changes following neonatal excitotoxicity [44][45][46][47][48][49], while others report that the hippocampus is relatively resistant to these changes [28,[50][51][52][53][54]. It is possible that some of these discrepancies result from methodological differences whereby only select regions of the hippocampus were examined.…”
Section: Discussionmentioning
confidence: 99%
“…Administration of low doses of DOM in neonatal rats does not produce overt toxicity or status epilepticus but results in permanent alterations in adult rat behavior that manifest as changes in cognition [17][18][19], attentional processing [20][21][22], anxiety [18,23], seizure threshold [24], and sleep patterns [25] that are consistent with the development of temporal lobe epilepsy (TLE). Moreover, these changes in behavior have been shown to correlate with neuropathological changes in the hippocampal formation such as mossy fiber sprouting (MFS) [17,26] and selective loss of parvalbumin-positive GABAergic interneurons [27] that are also present in both animal models of TLE produced by kainic acid [13,28] as well as human TLE patients [29]. Collectively, these multiple reports have led us to propose that low dose neonatal DOM initiates a slowly developing epileptogenic process that creates an animal model for studying the development of epilepsy and the identification of presymptomatic biomarkers of epileptogenesis (for review, see [30][31][32]).…”
Section: Introductionmentioning
confidence: 99%