A crucial epileptogenic site in the deep prepiriform cortex

Piredda, S.; Gale, Karen

doi:10.1038/318586d0

Cited by 59 publications

(98 citation statements)

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“…The excitability and level of synchronization of pyramidal neuron discharge control the degree of involvement of the associative fibres and regulate the distributed positive synaptic feedback generated by the associative output. The functional aspect of this pattern of connectivity could account for the operational process of olfactory encoding and for an associative form of synaptic plasticity (Gustafsson and Wigstrom, 1986), as suggested by Haberly and Bower (l989), as well as for the mechanisms of generation and propagation of epileptiform activity (Piredda and Gale, 1985; de Curtis ef a/., 1994b).…”

Section: Discussionmentioning

confidence: 92%

Associative Synaptic Potentials in the Piriform Cortex of the Isolated Guinea‐pig Brain In Vitro

Biella

Curtis

1995

Eur J of Neuroscience

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The involvement of local and remote associative fibres in the generation of piriform cortex synaptic potentials was investigated in the isolated guinea-pig brain maintained in vitro by arterial perfusion by implementing current source density analysis (CSD) on cortical field potential profiles. Previous hypotheses were verified using acute surgical isolation of piriform cortical areas to study different synaptic events separately. Stimulation of the lateral olfactory tract activated associative potentials throughout the piriform cortex. In the anterior piriform cortex, the current sinks responsible for the generation of associative potentials were located in the superficial portion of layer Ib and in layer III. In the posterior piriform cortex, two associative events were observed: an early sink located in the superficial part of layer Ib, followed by a sink in the deep part of the same layer. In the anterior piriform cortex, local associative synaptic potentials were separated from the component carried by long projective fibres by surgically isolating a small area of cortex monosynaptically activated by lateral olfactory tract stimulation. In this patch of lateral olfactory tract-connected anterior piriform cortex, local associative sinks were observed in the superficial Ib layer and in layer III. Monosynaptic activation of the isolated patch of anterior piriform cortex induced purely associative potentials throughout the piriform cortex. These potentials were mediated by the synaptic activation of apical dendrites in the superficial Ib layer and selectively abolished by severing the long associative fibres. The anterior piriform cortex layer III sink and the posterior piriform cortex deep Ib associative component were evoked by the activation of large population spikes in the monosynaptic anterior piriform cortex and the disynaptic posterior piriform cortex response respectively. These two sinks are presumably generated locally through a polysynaptic circuit, whose activation depends on the degree of cortical excitation. Olfactory signal processing in the guinea-pig piriform cortex during states of normal excitability is supported by the interactions between associative inputs impinging on the synapses located separately on the dendrites of pyramidal neurons. An increase in the synchronization of piriform cortex neuron discharge activates usually silent local circuit synapses.

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Section: Discussionmentioning

confidence: 92%

Associative Synaptic Potentials in the Piriform Cortex of the Isolated Guinea‐pig Brain In Vitro

Biella

Curtis

1995

Eur J of Neuroscience

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“…Our data from experiments with lidocaine, a nonspecific blocker of neural transmission, indicate that the suppression of the activity of mNTS efferents is anticonvulsant. Because vagal afferents to the mNTS are thought to be predominantly excitatory ( I [9][10][11][12][13][14][15][16][17][18][19][20][21], the question arises as to how the anticonvulsant effects of high-frequency vagal nerve stimulation (2-10) can be reconciled with the anticonvulsant effects of mNTS inhibition. Evidence that high-frequency afferent vagal stimulation may in fact suppress activity in the mNTS derives from metabolic mapping studies with 2-deoxyglucose, which demonstrated that vagal nerve stimulation induced reductions of glucose metabolism in the NTS (46).…”

Section: Relation To Vagal Nerve Stimulationmentioning

confidence: 99%

Regulation of Limbic Motor Seizures by GABA and Glutamate Transmission in Nucleus Tractus Solitarius

Walker¹,

Easton²,

Gale³

1999

Epilepsia

139

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Summary:Purpose: The nucleus of the solitary tract (NTS) is a primary site at which vagal afferents terminate. Because afferent vagal nerve stimulation has been demonstrated to have anticonvulsant effects, it is likely that changes in synaptic transmission in the NTS can regulate seizure susceptibility. We tested this hypothesis by examining the influence of y-aminobutyric acid (GABA) ergic and glutamatergic transmission in the NTS on seizures evoked by systemic and focal bicuculline and systemic pentylenetetrazol (PTZ) in rats.Methods: Muscimol (256 pmol), a GABA,-receptor agonist, bicuculline methiodide ( 1 77 pmol), a GABA,-receptor antagonist, kynurenate (634 pmol), a glutamate-receptor antagonist, or lidocaine (100 nl; 5%), a local anesthetic, was microinjected into the mediocaudal (m)NTS. Ten minutes later, seizure activity was induced by either a focal microinfusion of bicuculline methiodide ( I77 pmol) into the rostral piriform cortex, systemic PTZ (50 mg/kg, i.p.), or systemic bicuculline (0.35 mg/kg, i.v.).Results: Muscimol in mNTS (but not in adjacent regions of NTS) attenuated seizures in all seizure models tested, whereas bicuculline methiodide into mNTS did not alter seizure responses. Kynurenate infusions into mNTS significantly reduced the severity of seizures evoked both systemically and focally. Anticonvulsant effects also were obtained with lidocaine application into the same region of mNTS. Unilateral injections were sufficient to afford seizure protection.Conclusions: Our results demonstrate that an increase in GABA transmission or a decrease in glutamate transmission in the rat mNTS reduces susceptibility to limbic motor seizures. This suggests that inhibition of mNTS outputs enhances seizure resistance in the forebrain and provides a potential mechanism for the seizure protection obtained with vagal stimulation.

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“…These data suggest that, in the relative absence of GABAergic inhibition, either muscarinic receptor activation or nondesensitizing AMPA receptor activation triggers a state of severe, continuous and long-lasting seizure activity. It is well established that glutamate activity in AT plays a major role in eliciting seizures (Piredda & Gale, 1985). Nonetheless, the synergism between bicuculline and carbachol was not reproduced by combining bicuculline with either AMPA or NMDA glutamate receptor agonists.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, an EEG recording was performed in selected rats from each experimental group. EEG recordings started before the microinfusions and were continued during and for 1 h after each treatment according to the methods previously described (Piredda & Gale, 1985;Maggio et al, 1990;Browning et al, 1993).…”

Section: Convulsions Elicited By Microinjection Into Atmentioning

confidence: 99%

“…Within 'area tempestas' (AT), an epileptogenic site in the anterior extent of the piriform cortex, muscarinic acetylcholine and glutamate receptors provide excitatory drive for triggering seizures (Piredda & Gale, 1985). This excitatory drive is counteracted by GABAergic inhibitory inputs, so that seizures can be initiated from AT either by focal application of a GABA receptor antagonist (bicuculline) or by agonists for muscarinic or ionotropic glutamate receptors (Piredda & Gale, 1985). Previous studies have suggested that the AMPA subtype of glutamate receptor is essential for seizures evoked by removal of GABAergic inhibition (Tortorella et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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

Fornai

Busceti

Kondratyev

et al. 2005

Eur J of Neuroscience

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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.

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A crucial epileptogenic site in the deep prepiriform cortex

Cited by 59 publications

References 0 publications

Associative Synaptic Potentials in the Piriform Cortex of the Isolated Guinea‐pig Brain In Vitro

Associative Synaptic Potentials in the Piriform Cortex of the Isolated Guinea‐pig Brain In Vitro

Regulation of Limbic Motor Seizures by GABA and Glutamate Transmission in Nucleus Tractus Solitarius

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

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