Alteration in dentate neuronal activities associated with perforant path kindling

Maru, Eiichi; Goddard, Graham V.

doi:10.1016/0014-4886(87)90165-8

Cited by 103 publications

(43 citation statements)

References 24 publications

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“…Although others have described an increase in paired-pulse inhibition after seizures (Tuff et al, 1983;King et al, 1985;Oliver and Miller, 1985;de Jonge and Racine, 1987;Maru and Goddard, 1987;Milgram et al, 1991;Sperber et al, 1991), the locus for this change has not been determined. Up to now, it has not been clear whether enhanced granule cell inhibition is produced by a heightened postsynaptic response to GABA or an increase in inhibitory synaptic transmission impinging on granule cells.…”

Section: Discussionmentioning

confidence: 95%

“…The blockade of early inhibition unmasked equal paired-pulse facilitation in both groups, but late, GABA B receptor-mediated inhibition in slices from K A-treated rats still was enhanced significantly compared with controls (asterisks, p Ͻ 0.05, one-way ANOVA; points with no error bars had SEMs smaller than symbols). Goddard, 1987;Gilbert, 1991;Milgram et al, 1991;Spiller and Racine, 1994). In contrast, aberrant supragranular Timm staining requires at least 4 d to develop, increases in intensity over several weeks, and appears to be permanent (Cavazos et al, 1991;Mello et al, 1993;Okazaki et al, 1995).…”

Section: Discussionmentioning

confidence: 96%

“…In contrast to these persistent changes that promote hyperexcitability, inhibition of dentate gyrus granule cells is lost only transiently during and immediately after seizures (Maru and Goddard, 1987;Milgram et al, 1991;Spiller and Racine, 1994). Within 24 hr, PP-evoked inhibition of granule neurons recovers to levels higher than those preceding K A administration (Milgram et al, 1991) or kindled stimulation (Tuff et al, 1983;King et al, 1985;Oliver and Miller, 1985;de Jonge and Racine, 1987;Maru and Goddard, 1987;Gilbert, 1991;Milgram et al, 1995), although this inhibition may be subject to more rapid fatigue (Sloviter, 1992;Buhl et al, 1996).…”

mentioning

confidence: 99%

“…Within 24 hr, PP-evoked inhibition of granule neurons recovers to levels higher than those preceding K A administration (Milgram et al, 1991) or kindled stimulation (Tuff et al, 1983;King et al, 1985;Oliver and Miller, 1985;de Jonge and Racine, 1987;Maru and Goddard, 1987;Gilbert, 1991;Milgram et al, 1995), although this inhibition may be subject to more rapid fatigue (Sloviter, 1992;Buhl et al, 1996). Little is known about the underlying mechanisms or the functional role of this enhanced inhibition.…”

mentioning

confidence: 99%

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Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABA_BReceptors

Haas¹,

Sperber

Moshé

et al. 1996

J. Neurosci.

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Seizures cause a persistent enhancement in dentate synaptic inhibition concurrent with, and possibly compensatory for, seizure-induced hippocampal hyperexcitability. To study this phenomenon, we evoked status epilepticus in rats with systemic kainic acid (K A), and 2 weeks later assessed granule cell inhibition with paired-pulse stimulation of the perforant path (PP) in vitro. Controls demonstrated three components of paired-pulse inhibition: early inhibition (10 -30 msec), intermediate facilitation (30 -120 msec), and late inhibition (120 msec to 120 sec). After seizures, inhibition in all components was enhanced significantly. The GABA A antagonist bicuculline blocked only early enhanced inhibition, demonstrating that both GABA A and GABA B postsynaptic receptors contribute to seizure-induced enhanced inhibition. In controls, the GABA B antagonist CGP 35348 increased both GABA A and GABA B responses in granule cells, suggesting that CGP 35348 acts presynaptically, blocking receptors that suppress GABA release. In contrast, slices from K A-treated rats were markedly less sensitive to CGP 35348. To test the hypothesis that GABA B receptors regulating GABA release are downregulated after seizures, we measured paired-pulse suppression of recurrent IPSPs, or disinhibition, using mossy fiber stimuli. Early disinhibition (Ͻ 200 msec) was reduced after seizures, whereas late disinhibition remained intact. CGP 35348 blocked the early component of disinhibition in controls and, to a lesser extent, reduced disinhibition in K A slices. However, paired monosynaptic IPSPs recorded intracellularly showed no difference in disinhibition between groups. Our findings indicate that seizure-induced enhancement in dentate inhibition is caused, at least in part, by reduced GABA B function in the polysynaptic recurrent inhibitory circuit, resulting in reduced disinhibition and heightened GABA release.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABA_BReceptors

Haas¹,

Sperber

Moshé

et al. 1996

J. Neurosci.

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“…It has been suggested that LTP is involved in kindling epileptogenesis (37). In agreement, BDNF knock-out mice that exhibit kindling retardation (9) show deficits in LTP at Schaffer collateral-CA1 synapses (38).…”

Section: Discussionmentioning

confidence: 49%

Development and persistence of kindling epilepsy are impaired in mice lacking glial cell line-derived neurotrophic factor family receptor α2

Nanobashvili

Airaksinen

Kokaia

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Seizure activity regulates gene expression for glial cell linederived neurotrophic factor (GDNF) and neurturin (NRTN), and their receptor components, the transmembrane c-Ret tyrosine kinase and the glycosylphosphatidylinositol-anchored GDNF family receptor (GFR) ␣1 and ␣2 in limbic structures. We demonstrate here that epileptogenesis, as assessed in the hippocampal kindling model, is markedly suppressed in mice lacking GFR␣2. Moreover, at 6 to 8 wk after having reached the epileptic state, the hyperexcitability is lower in GFR␣2 knock-out mice as compared with wild-type mice. These results provide evidence that signaling through GFR␣2 is involved in mechanisms regulating the development and persistence of kindling epilepsy. Our data suggest that GDNF and NRTN may modulate seizure susceptibility by altering the function of hilar neuropeptide Y-containing interneurons and entorhinal cortical afferents at dentate granule cell synapses.

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Long‐lasting increased excitability differs in dentate gyrus vs. CA1 in freely moving chronic epileptic rats after electrically induced status epilepticus

et al. 2002

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A paired-pulse (PP) stimulation protocol was used to examine changes in field potentials (fEPSPs), locally evoked in CA1 via Schaffer/ commissural fiber stimulation and in the dentate gyrus (DG) through angular bundle stimulation, in freely moving epileptic rats. This epilepsy model is characterized by recurrent spontaneous seizures that occur after a latent period of 1-2 weeks following an electrically induced status epilepticus (SE). In the control period, i.e., before induction of SE, the PP stimulation protocol given at the appropriate intensity evoked fEPSPs with a pronounced paired-pulse depression (PPD). In the acute period, immediately after SE, the fEPSPs in the CA1 and DG areas were generally depressed. During the latent period in the CA1 stratum radiatum, the negative fEPSP was followed by a large positive potential that remained for the rest of the recording period. CA1 PPD, observed during the control period, was changed to paired-pulse facilitation (PPF) that remained for the rest of the recording period. Also during the latent period, a broad late component appeared in DG fEPSPs. The initial decrease in PPD was partly restored in the following weeks. Timm staining at different time points after SE showed an increase of mossy-fiber sprouting in the inner molecular layer within 6 days, which was robust within 6 weeks. We noted Timm granules positioned on parvalbumin immunoreactive neurons in the granule-cell layer of rats that had survived SE, suggesting that restoration of PPD could be partly due to reinnervation of a population of GABAergic neurons. The broad late component of DG fEPSPs, which was sensitive to the NMDA receptor antagonist ketamine, was still present for at least 6 weeks into the chronic epileptic phase, indicating lasting increased excitability. These observed changes indicate a lasting increased excitability in CA1 and DG networks that could play a role in the recurrence of spontaneous seizures.

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Alteration in dentate neuronal activities associated with perforant path kindling

Cited by 103 publications

References 24 publications

Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABA_BReceptors

Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABA_BReceptors

Development and persistence of kindling epilepsy are impaired in mice lacking glial cell line-derived neurotrophic factor family receptor α2

Long‐lasting increased excitability differs in dentate gyrus vs. CA1 in freely moving chronic epileptic rats after electrically induced status epilepticus

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Alteration in dentate neuronal activities associated with perforant path kindling

Cited by 103 publications

References 24 publications

Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABABReceptors

Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABABReceptors

Development and persistence of kindling epilepsy are impaired in mice lacking glial cell line-derived neurotrophic factor family receptor α2

Long‐lasting increased excitability differs in dentate gyrus vs. CA1 in freely moving chronic epileptic rats after electrically induced status epilepticus

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Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABA_BReceptors

Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABA_BReceptors