Literature DB >> 23505998

Seizure-like discharges induced by 4-aminopyridine in the olfactory system of the in vitro isolated guinea pig brain.

Laura Uva1, Federica Trombin, Giovanni Carriero, Massimo Avoli, Marco de Curtis.   

Abstract

PURPOSE: The study of the interactions leading to network- or region-specific propagation of seizures is crucial to understand ictogenesis. We have recently found that systemic (arterial) application of the potassium channel blocker, 4-aminopyridine (4AP), induces different and independent seizure activities in olfactory and in limbic structures. Here, we have characterized the network and cellular features that support 4AP-induced seizure-like events in the olfactory cortex.
METHODS: Simultaneous extracellular recordings were performed from the piriform cortex, the entorhinal cortex, the olfactory tubercle, and the amygdala of the in vitro isolated guinea pig brain preparation. Intracellular, sharp electrode recordings were obtained from neurons of different layers of the region of ictal onset, the piriform cortex. Seizure-like discharges were induced by both arterial perfusion and local intracortical injections of 4AP. KEY
FINDINGS: Arterial application of 4AP induces independent seizure activities in limbic and olfactory cortices. Both local applications of 4AP and cortico-cortical disconnections demonstrated that region-specific seizure-like events initiated in the primary olfactory cortex and propagate to anatomically related areas. Seizures induced by arterial administration of 4-AP are preceded by runs of fast activity at circa 30-40 Hz and are independently generated in the hemispheres. Simultaneous extracellular and intracellular recordings in the piriform cortex revealed that the onset of seizure correlates with (1) a gradual amplitude increase of fast activity runs, (2) a large intracellular depolarization with action potential firing of superficial layer neurons, and (3) no firing in a subpopulation of deep layers neurons. During the ictal event, neuronal firing was abolished for 10-30 s in all neurons and gradually restored and synchronized before seizure termination. SIGNIFICANCE: Our data show that olfactory neuronal networks sustain the generation of seizure-like activities that are independent from those observed in adjacent and connected limbic cortex regions. The data support the concept that functionally and anatomically hard-wired networks generate region-specific seizure patterns that could be substrates for system epilepsy. Wiley Periodicals, Inc.
© 2013 International League Against Epilepsy.

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Year:  2013        PMID: 23505998      PMCID: PMC4891192          DOI: 10.1111/epi.12133

Source DB:  PubMed          Journal:  Epilepsia        ISSN: 0013-9580            Impact factor:   5.864


  63 in total

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Authors:  Gilles van Luijtelaar; Evgenia Sitnikova
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2.  Distribution of the olfactory fiber input into the olfactory tubercle of the in vitro isolated guinea pig brain.

Authors:  Giovanni Carriero; Laura Uva; Vadym Gnatkovsky; Marco de Curtis
Journal:  J Neurophysiol       Date:  2008-10-15       Impact factor: 2.714

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Journal:  J Comp Neurol       Date:  1990-02-08       Impact factor: 3.215

Review 5.  Pathophysiological mechanisms of genetic absence epilepsy in the rat.

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6.  Single-neuron dynamics in human focal epilepsy.

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Authors:  P Perreault; M Avoli
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8.  A GABAergic depolarizing potential in the hippocampus disclosed by the convulsant 4-aminopyridine.

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Journal:  Brain Res       Date:  1987-01-01       Impact factor: 3.252

9.  Convulsant actions of 4-aminopyridine on the guinea-pig olfactory cortex slice.

Authors:  M Galvan; P Grafe; G ten Bruggencate
Journal:  Brain Res       Date:  1982-06-03       Impact factor: 3.252

10.  Inputs from the olfactory bulb and olfactory cortex to the entorhinal cortex in the cat. I. Anatomical observations.

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Journal:  Exp Brain Res       Date:  1984       Impact factor: 1.972

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  11 in total

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Review 4.  Complex metabolically demanding sensory processing in the olfactory system: implications for epilepsy.

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6.  Role of inhibitory control in modulating focal seizure spread.

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8.  α-Amino-3-Hydroxy-5-Methyl-4-Isoxazolepropionic Acid Receptor Plasticity Sustains Severe, Fatal Status Epilepticus.

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9.  How do we use in vitro models to understand epileptiform and ictal activity? A report of the TASK1-WG4 group of the ILAE/AES Joint Translational Task Force.

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10.  Suppression of cortical seizures by optic stimulation of the reticular thalamus in PV-mhChR2-YFP BAC transgenic mice.

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