Role of excitatory amino acid transmission in the genesis of seizures elicited from the deep prepiriform cortex

Piredda, S.; Gale, Karen

doi:10.1016/0006-8993(86)90859-0

Cited by 101 publications

(20 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Widespread increases in NGF mRNA (but not in trkA mRNA (Bengzon et al, 1993)) and protein were found following kindling-induced seizures (Bengzon et al, 1992; Morimoto et al, 1998; Sato et al, 1996). Moreover, an increase in mRNA for NGF has been demonstrated following brief, noninjurious, recurrent limbic seizures evoked by focal administration of the GABA receptor antagonist bicuculline into the area tempestas , an epileptogenic site within the anterior piriform cortex (Piredda and Gale 1985; Piredda and Gale 1986) as well as after ECS exposure (Follesa et al, 1994; Kondratyev et al, 2002). The latter NGF increase is independent of injury since ECS treatment (either minimal or maximal), even when given repeatedly over several days, has not been found to induce neuronal injury (Devanand et al, 1994; Kondratyev et al, 2001; Masco et al, 1999; Orzi et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical evaluation of the protein expression of nerve growth factor and its TrkA receptor in rat limbic regions following electroshock seizures

Conti

Gale

Kondratyev

2009

Neuroscience Research

Self Cite

View full text Add to dashboard Cite

Repeated (but not acute) exposure to brief, noninjurious seizures evoked by minimal electroconvulsive shock (ECS) decreases neuronal death in limbic system and increases mRNA levels for nerve growth factor (NGF). Thus, the induction of NGF is a potential mechanism for the neuroprotection evoked by repeated ECS. The neuroprotective action of NGF is mediated by the TrkA receptor. This study determined whether repeated ECS exposure increased TrkA and NGF protein levels. To determine the functional significance of changes in these proteins, we compared the effects of ECS given daily either for 7 days (chronic ECS) or for 1 day (acute ECS). After chronic ECS, upregulation of both NGF and TrkA was found in perirhinal cortex, thalamus, and amygdala. In hippocampus, TrkA was upregulated in CA2, CA3 and CA4. NGF increase in hippocampus was found in CA1 and dentate gyrus. In frontal cortex and substantia innominata, an increase in NGF (but not in TrkA) was found. In most brain regions, TrkA and NGF remained unchanged after acute ECS. Our results demonstrate that repeated exposure to ECS causes an upregulation of TrkA and NGF proteins in several limbic areas in which neuroprotective effects are observed suggesting that NGF contributes to ECS-evoked neuroprotection.

show abstract

Section: Introductionmentioning

confidence: 99%

Immunohistochemical evaluation of the protein expression of nerve growth factor and its TrkA receptor in rat limbic regions following electroshock seizures

Conti

Gale

Kondratyev

2009

Neuroscience Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…A tonic balance between excitatory glutamatergic input and inhibitory GABAergic input exists within AT, and the unilateral disruption of this balance in favor of excitation triggers seizures. Accordingly, focal injection of bicuculline, a GABA A receptor antagonist, removes the endogenous inhibitory control in AT and allows the endogenous excitatory drive to evoke limbic motor seizures (Piredda and Gale, 1986a). In the rat, the local blockade of either NMDA or AMPA receptors protects against seizure activity elicited by focal bicuculline, indicating that both subtypes of Glu receptor are necessary for seizure initiation from AT (Piredda and Gale, 1986a;Tortorella et al, 1997).…”

Section: Abstract: Area Tempestas; Piriform Cortex; Bicuculline; Gabmentioning

confidence: 99%

Mediodorsal Thalamus Plays a Critical Role in the Development of Limbic Motor Seizures

1998

Self Cite

View full text Add to dashboard Cite

Limbic motor seizures in animals, analogous to complex partial seizures in humans, result in a consistent activation of the mediodorsal thalamus (MD) and, with prolonged seizures, damage to MD. This study examined the functional role of MD in focally evoked limbic motor seizures in the rat. GABA-and glutamate (Glu)-mediated synaptic transmissions in MD were evaluated for an influence on seizures evoked from area tempestas (AT), a discrete epileptogenic site in the rostral piriform cortex.A GABA A receptor agonist, Glu receptor antagonists, or a GABA-elevating agent were focally microinfused into MD before evoking seizures by focal application of bicuculline methiodide into the ipsilateral AT. Focal pretreatment of MD with the GABA A agonist muscimol (190 pmol) protected against seizures evoked from AT. Seizure protection was also obtained with the focal application of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)-quinoxaline (NBQX) (500 pmol), an antagonist of the AMPA subtype of Glu receptors, into MD. In contrast, focal pretreatment of MD with a competitive antagonist of the NMDA receptor 2-amino-7-phosphonoheptanoic acid (500 pmol) did not attenuate seizures. The anticonvulsant effects achieved with intra-MD injections of muscimol and NBQX were site-specific, because no seizure protection was obtained with injections placed 2 mm ventral or lateral to MD. Prolonged seizure protection was obtained following GABA elevation in MD after the application of the GABA transaminase inhibitor vigabatrin (194 nmol). These results suggest the following: (1) MD is a critical participant in the generation of seizures elicited focally from piriform cortex; (2) transmission via AMPA receptors, but not NMDA receptors, in MD regulates limbic seizure propagation; and (3) a GABA-mediated system exists within MD, the enhancement of which protects against focally evoked limbic motor seizures.

show abstract

“…Consistent with previous findings (Piredda & Gale, 1986), seizures induced by carbachol were prevented by pretreatment with 100 pmole of AP‐7 in AT. In six out of seven rats pretreated with AP‐7, carbachol induced only mild jaw clonus (score, 0.5) which appeared with a slow onset compared with animals treated with carbachol alone; the remaining rat showed no signs of seizure activity.…”

mentioning

confidence: 61%

AMPA receptor desensitization as a determinant of vulnerability to focally evoked status epilepticus

Fornai

Busceti

Kondratyev

et al. 2005

Eur J of Neuroscience

Self Cite

View full text Add to dashboard Cite

Within the area tempestas (AT) in the anterior piriform cortex, unilateral microinfusions of GABA receptor antagonists and glutamate receptor agonists trigger brief episodic limbic seizures. In the present study, we document a synergistic effect of coinfusing bicuculline (GABAA receptor antagonist) with either carbachol (muscarinic receptor agonist) or cyclothiazide (inhibitor of AMPA receptor desensitization) but not with glutamate receptor agonists (AMPA, NMDA or kainate) in the rat AT. In particular, coadministration of bicuculline (118 pmol) with either carbachol (328 pmol) or cyclothiazide (1.2 nmol) triggered continuous self-sustaining seizures (status epilepticus; SE). Cyclothiazide alone did not evoke seizures. Although blockade of NMDA receptors with AP-7 (100 or 500 pmol) prevented episodic seizures evoked by carbachol or bicuculline alone, it was without effect on the continuous seizures evoked by combined treatments. NMDA-insensitive self-sustaining seizures were also evoked by the combination of AMPA and cyclothiazide. Regardless of the mechanism by which SE was evoked, it was prevented only by an AMPA receptor antagonist, NBQX, thus reinforcing the crucial role of AMPA receptors in the transition to SE. Further evidence for AMPA receptor regulation of seizure severity came from the overexpression of the GluR1 AMPA receptor subunit in AT. This resulted in substantially increased severity of bicuculline-evoked seizures that was reversed by focal application of NBQX. Thus, desensitization of AMPA receptors appears to limit the duration and severity of seizure activity, and a failure of this mechanism, or an overabundance of slowly desensitizing AMPA receptors, predisposes to severe and prolonged seizures.

show abstract

Role of excitatory amino acid transmission in the genesis of seizures elicited from the deep prepiriform cortex

Cited by 101 publications

References 17 publications

Immunohistochemical evaluation of the protein expression of nerve growth factor and its TrkA receptor in rat limbic regions following electroshock seizures

Immunohistochemical evaluation of the protein expression of nerve growth factor and its TrkA receptor in rat limbic regions following electroshock seizures

Mediodorsal Thalamus Plays a Critical Role in the Development of Limbic Motor Seizures

AMPA receptor desensitization as a determinant of vulnerability to focally evoked status epilepticus

Contact Info

Product

Resources

About