In limbic seizures, neuronal excitation is conveyed from the entorhinal cortex directly to CA1 and subicular regions. This phenomenon is associated with a reduced ability of CA3 to respond to entorhinal cortex inputs. Here, we describe a lesion that destroys the perforant path in CA3 after status epilepticus (SE) induced by pilocarpine injection in 8-week-old rats. Using magnetic resonance imaging, immunohistochemical, and ultrastructural analyses, we determined that this lesion develops after 30 minutes of SE and is characterized by microhemorrhages and ischemia. After a longer period of SE, the lesion invariably involves the upper blade of the dentate gyrus. Adult rats treated with subcutaneous diazepam (20 mg kg-1 for 3 days) did not develop the dentate gyrus lesion and had less frequent spontaneous recurrent seizures (p < 0.01). Young (3-week-old) rats rarely (20%) developed the CA3 lesion, and their spontaneous seizures were delayed (p < 0.01). To investigate the role of the damaged CA3 in seizure activity, we reinduced SE in adult and young epileptic rats. Using FosB/[DELTA]FosB markers, we found induction of FosB/[DELTA]FosB immunopositivity in CA3 neurons of young but not in adult rats. These experiments indicate that SE can produce a focal lesion in the perforant path that may affect the roles of the hippocampus in epileptic rats

Proepileptic influence of a focal vascular lesion affecting entorhinal cortex-CA3 connections after status epilepticus / G. Biagini, E. Baldelli, D. Longo, M. Baccarani Contri, U. Guerrini, L. Sironi, P. Gelosa, I. Zini, D.S. Ragsdale, M. Avoli. - In: JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY. - ISSN 0022-3069. - 67:7(2008), pp. 687-701.

Proepileptic influence of a focal vascular lesion affecting entorhinal cortex-CA3 connections after status epilepticus

U. Guerrini;L. Sironi;P. Gelosa;
2008

Abstract

In limbic seizures, neuronal excitation is conveyed from the entorhinal cortex directly to CA1 and subicular regions. This phenomenon is associated with a reduced ability of CA3 to respond to entorhinal cortex inputs. Here, we describe a lesion that destroys the perforant path in CA3 after status epilepticus (SE) induced by pilocarpine injection in 8-week-old rats. Using magnetic resonance imaging, immunohistochemical, and ultrastructural analyses, we determined that this lesion develops after 30 minutes of SE and is characterized by microhemorrhages and ischemia. After a longer period of SE, the lesion invariably involves the upper blade of the dentate gyrus. Adult rats treated with subcutaneous diazepam (20 mg kg-1 for 3 days) did not develop the dentate gyrus lesion and had less frequent spontaneous recurrent seizures (p < 0.01). Young (3-week-old) rats rarely (20%) developed the CA3 lesion, and their spontaneous seizures were delayed (p < 0.01). To investigate the role of the damaged CA3 in seizure activity, we reinduced SE in adult and young epileptic rats. Using FosB/[DELTA]FosB markers, we found induction of FosB/[DELTA]FosB immunopositivity in CA3 neurons of young but not in adult rats. These experiments indicate that SE can produce a focal lesion in the perforant path that may affect the roles of the hippocampus in epileptic rats
English
Hemorrhage ; Hippocampus ; Immediate early genes ; Ischemia ; Magnetic resonance imaging ; Pilocarpine ; Temporal lobe epilepsy
Settore BIO/14 - Farmacologia
Articolo
Sì, ma tipo non specificato
2008
Lippincott Williams & Wilkins
67
7
687
701
Periodico con rilevanza internazionale
info:eu-repo/semantics/article
Proepileptic influence of a focal vascular lesion affecting entorhinal cortex-CA3 connections after status epilepticus / G. Biagini, E. Baldelli, D. Longo, M. Baccarani Contri, U. Guerrini, L. Sironi, P. Gelosa, I. Zini, D.S. Ragsdale, M. Avoli. - In: JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY. - ISSN 0022-3069. - 67:7(2008), pp. 687-701.
none
Prodotti della ricerca::01 - Articolo su periodico
10
262
Article (author)
si
G. Biagini, E. Baldelli, D. Longo, M. Baccarani Contri, U. Guerrini, L. Sironi, P. Gelosa, I. Zini, D.S. Ragsdale, M. Avoli
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/53581
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