Mossy fiber sprouting is dissociated from kindling of generalized seizures in the guinea-pig

Mohapel, Paul; Armitage, Lisa L.; Gilbert, Trevor H.; Hannesson, Darren K.; Teskey, G. Campbell; Corcoran, Michael E.

doi:10.1097/00001756-200009110-00014

Cited by 17 publications

(8 citation statements)

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“…In experiments 4 and 5 we also examined mossy fiber sprouting using the Timm stain (Sloviter, 1991;Buckmaster and Dudek, 1997) and immunohistochemical staining for Met-enkephalin, neuropeptide Y, and synaptophysin (Table 2). Timm stain was performed with our routine protocol (Mohapel et al, 1997(Mohapel et al, , 2000Armitage et al, 1998). Immunohistochemical staining was performed using a conventional avidin -biotin -immunoperoxidase technique as described previously (Z hang et al, 1997, 2001).…”

Section: Methodsmentioning

confidence: 99%

“…In addition, some kainic acid (KA)-treated rats showing frequent SRS exhibit no detectable neuronal loss in the hippocampus (Sloviter, 1992;Buckmaster and Dudek, 1997). Numerous dissociations between epileptogenesis and mossy fiber sprouting have been described in the rat kindling and KA preparations of TLE (Elmer et al, 1997;Mohapel et al, 1997Mohapel et al, , 2000Armitage et al, 1998;Mello, 1998, 1999). In the present study we sought to test this hypothesis further, using both the traditional KA preparation of TLE in rats (Ben-Ari, 1985;Fisher, 1989;Sperk, 1994;Hellier et al, 1998) and a novel version of the preparation.…”

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confidence: 99%

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Relations between Brain Pathology and Temporal Lobe Epilepsy

et al. 2002

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Temporal lobe epilepsy, the most common type of epilepsy in adult humans, is characterized clinically by the progressive development of spontaneous recurrent seizures of temporal lobe origin and pathologically by hippocampal neuronal loss and mossy fiber sprouting. In this study, we sought to test the prominent hypothesis that neuronal loss and mossy fiber sprouting play a critical role in the genesis and progression of temporal lobe epilepsy. Rats receiving a single kainic acid injection experienced a single sustained episode of epileptic status with massive neuronal loss and mossy fiber sprouting, whereas rats receiving triple kainic acid injections experienced two priming episodes and one sustained episode of epileptic status with no detectable neuronal loss and mossy fiber sprouting. Early in the process of chronic seizure development, primed rats that failed to show detectable neuronal loss and mossy fiber sprouting exhibited a starting date and a frequency of spontaneous recurrent seizures similar to those of nonprimed rats that showed massive neuronal loss and mossy fiber sprouting. However, nonprimed rats displayed significantly prolonged episodes of spontaneous recurrent seizures over the whole process of chronic seizure development and more frequent severe seizures later in the process. Similar results were observed in both Fischer-344 and Wistar rats as well as in the rat pilocarpine preparation of temporal lobe epilepsy. These results fail to reveal a relation between neuronal loss-mossy fiber sprouting and the genesis of temporal lobe epilepsy but suggest that neuronal loss, mossy fiber sprouting, or both contribute to the intensification of chronic seizures.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Relations between Brain Pathology and Temporal Lobe Epilepsy

et al. 2002

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“…Whether such severe, widely damaging, and often lethal seizures are at all comparable in severity to the antecedent insults experienced by most patients with temporal lobe epilepsy has not, to our knowledge, been addressed. Regardless, spontaneous seizures develop in severely brain-damaged animals whether or not hippocampal damage and synaptic reorganization occur (Sloviter, 1992;Elmer et al, 1997;Longo and Mello, 1998;Mohapel et al, 2000;Nissinen et al, 2001;Longo et al, 2002;Zhang et al, 2002). Because the development of spontaneous behavioral seizures does not necessarily indicate a damaged or hyperexcitable hippocampus (Sloviter, 1992) or any hippocampal involvement in the spontaneous seizures (Michalakis et al, 1998), electrophysiological studies in slices from hippocampi of epileptic animals in which the hippocampus has not been analyzed in vivo to verify principal cell hyperexcitability, nor anatomically to verify the presence of hippocampal sclerosis, seem of dubious value.…”

Section: Hippocampal Neuron Loss and Survival In Human Epilepsymentioning

confidence: 99%

“Dormant basket cell” hypothesis revisited: Relative vulnerabilities of dentate gyrus mossy cells and inhibitory interneurons after hippocampal status epilepticus in the rat

Sloviter

Zappone

Harvey

et al. 2003

J of Comparative Neurology

225

175

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The "dormant basket cell" hypothesis suggests that postinjury hippocampal network hyperexcitability results from the loss of vulnerable neurons that normally excite insult-resistant inhibitory basket cells. We have reexamined the experimental basis of this hypothesis in light of reports that excitatory hilar mossy cells are not consistently vulnerable and inhibitory basket cells are not consistently seizure resistant. Prolonged afferent stimulation that reliably evoked granule cell discharges always produced extensive hilar neuron degeneration and immediate granule cell disinhibition. Conversely, kainic acid-induced status epilepticus in chronically implanted animals produced similarly extensive hilar cell loss and immediate granule cell disinhibition, but only when granule cells discharged continuously during status epilepticus. In both preparations, electron microscopy revealed degeneration of presynaptic terminals forming asymmetrical synapses in the mossy cell target zone, including some terminating on gamma-aminobutyric acid-immunoreactive elements, but no evidence of axosomatic or axoaxonic degeneration in the adjacent granule cell layer. Although parvalbumin immunocytochemistry and in situ hybridization revealed decreased staining, this apparently was due to altered parvalbumin expression rather than basket cell death, because substance P receptor-positive interneurons, some of which contained residual parvalbumin immunoreactivity, survived. These results confirm the inherent vulnerability of dendritically projecting hilar mossy cells and interneurons and the relative resistance of dentate inhibitory basket and chandelier cells that target granule cell somata. The variability of hippocampal cell loss after status epilepticus suggests that altered hippocampal structure and function cannot be assumed to cause the spontaneous seizures that develop in these animals and highlights the importance of confirming hippocampal pathology and pathophysiology in vivo in each case.

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“…Several previous studies have demonstrated kindling-induced morphological alterations at the cellular, dendritic, and synaptic level in the hippocampus (Armitage et al, 1998;Binder et al, 1999;Cavazos et al, 1994;Cavazos and Sutula, 1990;Geinisman et al, 1988Geinisman et al, , 1990Geinisman et al, , 1992Hawrylak et al, 1993;Hovorka et al, 1997;Jiang et al, 1998;Mohapel et al, 2000;Spiller and Racine, 1994;Sutula, 1990), amygdala (Nishizuka et al, 1991;Okada et al, 1993), and neocortex (Teskey et al, 1999(Teskey et al, , 2001. The two later studies that examined dendritic alterations in the neocortex following kindling focused on layer III pyramidal cells because earlier work had shown a sexual dimorphism at the structural level (Kolb and Stewart, 1991) and a differential plastic response to midline frontal lesions (Kolb and Whishaw, 1991) and gonadal hormones (Kolb and Stewart, 1995) in that layer.…”

Section: Introductionmentioning

confidence: 99%

Neocortical kindling is associated with opposing alterations in dendritic morphology in neocortical layer V and striatum from neocortical layer III

Teskey

Monfils

Silasi

et al. 2005

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Previous research has shown that seizures kindled in the corpus callosum result in a persistent enhancement of the callosal-neocortical evoked response but only a transient reduction in layer III pyramidal cell morphology. To date, there are no reports on the direct effects of repeated seizures on dendritic morphology in layer V, the pyramidal layer thought to mediate the kindling-induced enhanced evoked response. This experiment examined the effect of repeated seizures elicited from the corpus callosum, at the level of the frontal neocortex, on the morphology of sensorimotor frontal (Fr1) and occipital (OC1) neocortical layer V, as well as striatal and neuronal dendrites, in male rats. After 25 days of electrically elicited seizures or handling control, rats were sacrificed either 2 days or 3 weeks following the last seizure and processed for Golgi-Cox staining. Analysis of the impregnated pyramidal cell dendrites indicated a significant increase in the amount of dendritic length and branching in rats 2 days, but a decrease 3 weeks, following the last seizure. There was no effect at the distant occipital site. The differential effect between layer V pyramidal neurons and layer III pyramidal neurons suggests that these areas play different roles in the expression of seizures and the adaptation of the brain to the persistent effect of kindling.

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Mossy fiber sprouting is dissociated from kindling of generalized seizures in the guinea-pig

Cited by 17 publications

References 10 publications

Relations between Brain Pathology and Temporal Lobe Epilepsy

Relations between Brain Pathology and Temporal Lobe Epilepsy

“Dormant basket cell” hypothesis revisited: Relative vulnerabilities of dentate gyrus mossy cells and inhibitory interneurons after hippocampal status epilepticus in the rat

Neocortical kindling is associated with opposing alterations in dendritic morphology in neocortical layer V and striatum from neocortical layer III

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