The infusion of an NMDA antagonist into perirhinal cortex suppresses amygdala-kindled seizures

Holmes, Keith H.; Bilkey, David K.; Laverty, R.

doi:10.1016/0006-8993(92)91009-4

Cited by 41 publications

(18 citation statements)

References 21 publications

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“…This propensity of the PC to develop and sustain epileptiform activity is further corroborated by studies demonstrating that PC kindling occurs faster and results in an earlier generalization of seizures than kindling in the amygdala, hippocampus, and piriform cortex Plant, 1989, 1993;. In addition, a pivotal role for the PC in the generalization of seizures has also been presented by studies demonstrating that local application of an NMDA receptor antagonist to the PC/insular cortex can block amygdala-kindled seizures in rats (Holmes et al, 1992). Lesional studies have also indicated that the PC is required for the generation of hippocampal motor seizures (Kelly and McIntyre, 1996;McIntyre and Kelly, 2000).…”

Section: Discussionmentioning

confidence: 76%

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Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

et al. 2011

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The perirhinal cortex (PC), which is heavily connected with several epileptogenic regions of the limbic system such as the entorhinal cortex and amygdala, is involved in the generation and spread of seizures. However, the functional alterations occurring within an epileptic PC network are unknown. Here, we analyzed this issue by using in vitro electrophysiology and immunohistochemistry in brain tissue obtained from pilocarpine-treated epileptic rats and agematched, nonepileptic controls (NECs). Neurons recorded intracellularly from the PC deep layers in the two experimental groups had similar intrinsic and firing properties and generated spontaneous depolarizing and hyperpolarizing postsynaptic potentials with comparable duration and amplitude. However, spontaneous and stimulus-induced epileptiform discharges were seen with field potential recordings in over one-fifth of pilocarpine-treated slices but never in NEC tissue. These network events were reduced in duration by antagonizing NMDA receptors and abolished by NMDA + non-NMDA glutamatergic receptor antagonists. Pharmacologically isolated isolated inhibitory postsynaptic potentials had reversal potentials for the early GABA A receptor-mediated component that were significantly more depolarized in pilocarpine-treated cells. Experiments with a potassium-chloride cotransporter 2 antibody identified, in pilocarpine-treated PC, a significant immunostaining decrease that could not be explained by neuronal loss. However, interneurons expressing parvalbumin and neuropeptide Y were found to be decreased throughout the PC, whereas cholecystokinin-positive cells were diminished in superficial layers. These findings demonstrate synaptic hyper-excitability that is contributed by attenuated inhibition in the PC of pilocarpine-treated epileptic rats and underscore the role of PC networks in temporal lobe epilepsy.

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Section: Discussionmentioning

confidence: 76%

“…In addition, the PC is also more likely to generate electrographic seizures in vitro than adjacent limbic structures (Klueva et al, 2003;de Guzman et al, 2004). A primary role for PC in seizure generalization has also been reported (Holmes et al, 1992;Kelly and McIntyre, 1996;McIntyre and Kelly, 2000).…”

Section: Introductionmentioning

confidence: 90%

Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

et al. 2011

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“…Excessive NMDA receptor activation is associated with seizure activity and neuronal death in TLE (for reviews, see Chapman, 2000;Fujikawa, 2005). Previous studies in TLE animal models have shown that injection of NMDA antagonists into the PC or the IC of rats is able to protect against the development of kindled seizures (Holmes et al, 1992;Kodama et aL, 2001;Raisinghani and Faingold, 2005), and that NMDA receptors are important in mediating network hyperexcitability within the non-epileptic IC (Inaba et aL, 2006). AMPA receptors also appear to be important in the propagation of kindled and convulsant-induced seizure activity in these structures in rats in vivo (Tortorella et aL, 1997;Kodama et aL, 2001).…”

Section: Methodsmentioning

confidence: 99%

“…indicators of neuronal excitation (Ferland et aL, 1998;Sato et aL, 1998). Further, infusion of NMDA receptor antagonists into the IC of rats in vivo can protect against the development of kindled seizures (Holmes et aL, 1992;Kodama et aL, 2001). Finally, a recent study reported substantial neuronal loss in the IC in pilocarpine-treated rats (Chen et aL, 2006), while a clinical case study reported volumetrie reduction in the IC (Bauer et al, 2006).…”

Section: Extrahippocampal Involvement In Tle: the Insular Cortexmentioning

confidence: 99%

Epileptiform synchronization in the rat insular and perirhinal cortices in vitro

Sudbury

Avoli

2007

Eur J of Neuroscience

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The hippocampus plays a primary role in temporal lobe epilepsy, a common form of partial epilepsy in adults. Recent studies, however, indicate that extrahippocampal areas such as the perirhinal and insular cortices represent important participants in this epileptic disorder. By employing field potential recordings in the in vitro 4‐aminopyridine model of temporal lobe epilepsy, we have investigated here the contribution of glutamatergic and GABAergic signaling to epileptiform activity in these structures. First, we provide evidence of epileptiform synchronicity between the perirhinal and insular cortices, and resolve some pharmacological and network mechanisms involved in sustaining the interictal‐ and ictal‐like discharges recorded there. Second, we report that in the absence of ionotropic glutamatergic transmission, GABAergic networks produce synchronous potentials that spread between the perirhinal and insular cortices. Finally, we have established that such activity is modulated by activating µ‐opioid receptors. Our findings support clinical and experimental evidence concerning the involvement of the perirhinal and insular cortex networks in temporal lobe epilepsy, and provide observations that may impact research focussing on the role of the insular cortex in nociception.

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“…For example, the lateral orbital and agranular insular cortices as well as the claustrum projected strongly to the frontal Fr2i 1 cortex. Importantly, interference with any one of these three areas has been shown to interfere with the generalization of amygdala kindled seizures (Corcoran et al, 1976;Kudo and Wada, 1990;Holmes et al, 1992). In addition, the parietal cortex also sent numerous projections to the frontal F r 2 i l area, although its role in convulsive seizure expression has not been defined.…”

Section: Cortical Projectionsmentioning

confidence: 97%

Efferent projections of the anterior perirhinal cortex in the rat

1996

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Because convulsive seizures develop very rapidly from kindling sites in the anterior perirhinal cortex, we studied perirhinal efferents by using the anterograde tracer Phaseolus vulgaris leucoagglutinin (PhAL). PhAL injections into the anterior perirhinal cortex labelled a prominent network of fibers within the frontal cortex that was most dense within layers I and II and layer VI. As individual PhAL injection sites within the perirhinal cortex were restricted to one or two adjacent laminae, we were able to determine that layer V was the main source of the perirhinofrontal projection. This was confirmed by frontal cortex injections of the retrograde tracer Fluorogold (FG). Other cortical areas with densely labelled fibers following perirhinal PhAL injections included the agranular insular, infralimbic, orbital, parietal, and entorhinal cortices. Moderate to mild fiber labelling was also noted in the posterior piriform, temporal and occipital cortices, and the claustrum. Subcortical labelling was seen in the nucleus accumbens; fundus striati; basal and lateral amygdala nuclei; the "acoustic thalamus"; and the central grey. Several of these cortical and subcortical projections were bilateral. The different laminar origin of these perirhinal efferents is discussed. These results confirmed our prediction of extensive direct projections from the anterior perirhinal cortex to the frontal cortex in the rat. The significance of this projection is discussed with special reference to the anatomical basis of convulsive limbic seizures.

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The infusion of an NMDA antagonist into perirhinal cortex suppresses amygdala-kindled seizures

Cited by 41 publications

References 21 publications

Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

Epileptiform synchronization in the rat insular and perirhinal cortices in vitro

Efferent projections of the anterior perirhinal cortex in the rat

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