Sprouting of GABAergic and mossy fiber axons in dentate gyrus following intrahippocampal kainate in the rat

Davenport, Cynthia J.; Brown, W. J.; Babb, Thomas L.

doi:10.1016/0014-4886(90)90072-z

Cited by 237 publications

(93 citation statements)

References 22 publications

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“…Although mossy fibre sprouting is generally considered to be of excitatory nature, Davenport et al 7 found evidence of an increase of glutamate decarboxylase immunoreactivity in the dentate gyrus following intrahippocampal kainate. Therefore, it may be hypothesized that kindling-elicited sprouting in the dentate area may be accompanied by the formation of new GABAergic synapses, as revealed by the increased binding sites for [3H]muscimol41 and [3H]ftunitrazepam reported here.…”

Section: Resultsmentioning

confidence: 99%

Long-term and regional specific changes in [3H]flunitrazepam binding in kindled rat hippocampus

1995

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Section: Resultsmentioning

confidence: 99%

Long-term and regional specific changes in [3H]flunitrazepam binding in kindled rat hippocampus

1995

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“…For instance, robust periods of firing depression (presumably corresponding to IPSPs) have been recorded in electrophysiological studies performed presurgically with intracranial electrodes or extracellular unit recordings in TLE patients (Wilson and Engel, 1993;Isokawa-Akesson et al, 1989). Moreover, histochemical studies have demonstrated that some interneuron subtypes are preserved in both human and experimental animal epileptic tissue Davenport et al, 1990;Esclapez et al, 1997) even though some other subtypes are clearly decreased in number in specific limbic structures (de Guzman et al, 2006(de Guzman et al, , 2008.…”

Section: Gaba a Receptor-mediated Inhibition In Temporal Lobe Epilepsymentioning

confidence: 99%

“…Later studies, however, have challenged this assumption, by showing that inhibition per se or some types of inhibitory mechanisms are preserved in animal models of epilepsy (Davenport et al, 1990;Esclapez et al, 1997;Prince & Jacobs, 1998;Cossart et al, 2001Cossart et al, , 2005 and in post-surgical human temporal lobe tissue (Isokawa-Akesson et al, 1989;Babb et al, 1989;Avoli and Olivier, 1989;Avoli et al, 1995;Cohen et al, 2002). Moreover, more complex, at times ambiguous, roles for GABAergic signaling in epilepsy were identified.…”

Section: Introductionmentioning

confidence: 99%

GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity

Avoli¹,

Curtis²

2011

Progress in Neurobiology

222

253

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GABA is the main inhibitory neurotransmitter in the adult forebrain, where it activates ionotropic type A and metabotropic type B receptors. Early studies have shown that GABA A receptormediated inhibition controls neuronal excitability and thus the occurrence of seizures. However, more complex, and at times unexpected, mechanisms of GABAergic signaling have been identified during epileptiform discharges over the last few years. Here, we will review experimental data that point at the paradoxical role played by GABA A receptor-mediated mechanisms in synchronizing neuronal networks, and in particular those of limbic structures such as the hippocampus, the entorhinal and perirhinal cortices, or the amygdala. After having summarized the fundamental characteristics of GABA A receptor-mediated mechanisms, we will analyze their role in the generation of network oscillations and their contribution to epileptiform synchronization. Whether and how GABA A receptors influence the interaction between limbic networks leading to ictogenesis will be also reviewed. Finally, we will consider the role of altered inhibition in the human epileptic brain along with the ability of GABA A receptor-mediated conductances to generate synchronous depolarizing events that may lead to ictogenesis in human epileptic disorders as well.

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“…While the projection of GC axons (mossy fibers) to the ML is quite sparse in normal rodents (Claiborne et al, 1986;Ribak and Peterson, 1991;Sutula et al, 1998), it is remarkably augmented in animal models of TLE (reviewed in Houser, 1999), as well as in humans with this hippocampal epilepsy (deLanerolle et al, 1989;Sutula et al, 1989;Houser et al, 1990;Babb et al, 1991, Mikkonen et al, 1998. Because the majority of these "sprouted" supragranular mossy fibers terminate on GC dendrites (Okazaki et al, 1995;Wenzel et al, 2000;Buckmaster et al, 2002), they may increase the excitability of GCs and thus promote epileptogenesis (but see Longo and Mello, 1998;Nissinen et al, 2001).…”

Section: Mossy Fiber Collateral Density In Gc and Molecular Layers Ismentioning

confidence: 99%

Mossy fiber plasticity and enhanced hippocampal excitability, without hippocampal cell loss or altered neurogenesis, in an animal model of prolonged febrile seizures

et al. 2003

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Seizures induced by fever (febrile seizures) are the most frequent seizures affecting infants and children; however, their impact on the developing hippocampal formation is not completely understood. Such understanding is highly important because of the potential relationship of prolonged febrile seizures to temporal lobe epilepsy. Using an immature rat model, we have previously demonstrated that prolonged experimental febrile seizures render the hippocampus hyperexcitable throughout life. Here we examined whether (1) neuronal loss, (2) altered neurogenesis, or (3) mossy fiber sprouting, all implicated in epileptogenesis in both animal models and humans, were involved in the generation of a pro-epileptic, hyperexcitable hippocampus by these seizures. The results demonstrated that prolonged experimental febrile seizures did not result in appreciable loss of any vulnerable hippocampal cell population, though causing strikingly enhanced sensitivity to hippocampal excitants later in life. In addition, experimental febrile seizures on postnatal day 10 did not enhance proliferation of granule cells, whereas seizures generated by kainic acid during the same developmental age increased neurogenesis in the immature hippocampus. However, prolonged febrile seizures resulted in long-term axonal reorganization in the immature hippocampal formation: Mossy fiber densities in granule cell-and molecular layers were significantly increased by 3 months (but not 10 days) after the seizures. Thus, the data indicate that prolonged febrile seizures influence connectivity of the immature hippocampus long-term, and this process requires neither significant neuronal loss nor altered neurogenesis. In addition, the temporal course of the augmented mossy fiber invasion of the granule cell and molecular layers suggests that it is a consequence, rather than the cause, of the hyperexcitable hippocampal network resulting from these seizures.

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Sprouting of GABAergic and mossy fiber axons in dentate gyrus following intrahippocampal kainate in the rat

Cited by 237 publications

References 22 publications

Long-term and regional specific changes in [3H]flunitrazepam binding in kindled rat hippocampus

Long-term and regional specific changes in [3H]flunitrazepam binding in kindled rat hippocampus

GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity

Mossy fiber plasticity and enhanced hippocampal excitability, without hippocampal cell loss or altered neurogenesis, in an animal model of prolonged febrile seizures

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