Involvement of nitric oxide-soluble guanylyl cyclase pathway in the control of maximal dentate gyrus activation in the rat.

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Abstract

Summary Nitric oxide=soluble Guanylyl cyclase (NO=sGC) pathway on the maximal dentate gyrus activation (MDA) was studied in rats. The cerebral NO levels were modified by administrating 7-Nitroindazole (7-NI), a selective inhibitor of neuronal NOS, and L-arginine, a precursor of the synthesis of NO. 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a specific inhibitor of the NO-sGC pathway, was administered to study the involvement of cGMP pathway. The epileptic activity of the dentate gyrus was obtained through the repetitive stimulation of the angular bundle; MDA parameters studied were: onset time, MDA duration and post-stimulus afterdischarge (AD) duration. 7-NI caused an increase of MDA onset time and a decrease of MDA and AD duration. L-arginine, induced an aggravation of the epileptiform phenomena. ODQ induced modifications of MDA parameters as those caused by 7-NI. Our results indicate that the nitrergic neurotransmission exerts a modulatory role in the proneness to the epileptogenic phenomena through the activation of sGC metabolic pathway.
Lingua originaleEnglish
pagine (da-a)1855-1861
Numero di pagine7
RivistaJournal of Neural Transmission
Volume113(12)
Stato di pubblicazionePublished - 2006

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Dentate Gyrus
Nitric Oxide
Arginine
Oxadiazoles
Quinoxalines
Metabolic Networks and Pathways
Soluble Guanylyl Cyclase
7-nitroindazole

All Science Journal Classification (ASJC) codes

  • Neurology
  • Biological Psychiatry
  • Psychiatry and Mental health
  • Clinical Neurology

Cita questo

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title = "Involvement of nitric oxide-soluble guanylyl cyclase pathway in the control of maximal dentate gyrus activation in the rat.",
abstract = "Summary Nitric oxide=soluble Guanylyl cyclase (NO=sGC) pathway on the maximal dentate gyrus activation (MDA) was studied in rats. The cerebral NO levels were modified by administrating 7-Nitroindazole (7-NI), a selective inhibitor of neuronal NOS, and L-arginine, a precursor of the synthesis of NO. 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a specific inhibitor of the NO-sGC pathway, was administered to study the involvement of cGMP pathway. The epileptic activity of the dentate gyrus was obtained through the repetitive stimulation of the angular bundle; MDA parameters studied were: onset time, MDA duration and post-stimulus afterdischarge (AD) duration. 7-NI caused an increase of MDA onset time and a decrease of MDA and AD duration. L-arginine, induced an aggravation of the epileptiform phenomena. ODQ induced modifications of MDA parameters as those caused by 7-NI. Our results indicate that the nitrergic neurotransmission exerts a modulatory role in the proneness to the epileptogenic phenomena through the activation of sGC metabolic pathway.",
author = "Pierangelo Sardo and Giuseppe Ferraro and Fabio Carletti and Valerio Rizzo and Stefania D'Agostino",
year = "2006",
language = "English",
volume = "113(12)",
pages = "1855--1861",
journal = "Journal of Neural Transmission",
issn = "0300-9564",
publisher = "Springer Verlag",

}

TY - JOUR

T1 - Involvement of nitric oxide-soluble guanylyl cyclase pathway in the control of maximal dentate gyrus activation in the rat.

AU - Sardo, Pierangelo

AU - Ferraro, Giuseppe

AU - Carletti, Fabio

AU - Rizzo, Valerio

AU - D'Agostino, Stefania

PY - 2006

Y1 - 2006

N2 - Summary Nitric oxide=soluble Guanylyl cyclase (NO=sGC) pathway on the maximal dentate gyrus activation (MDA) was studied in rats. The cerebral NO levels were modified by administrating 7-Nitroindazole (7-NI), a selective inhibitor of neuronal NOS, and L-arginine, a precursor of the synthesis of NO. 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a specific inhibitor of the NO-sGC pathway, was administered to study the involvement of cGMP pathway. The epileptic activity of the dentate gyrus was obtained through the repetitive stimulation of the angular bundle; MDA parameters studied were: onset time, MDA duration and post-stimulus afterdischarge (AD) duration. 7-NI caused an increase of MDA onset time and a decrease of MDA and AD duration. L-arginine, induced an aggravation of the epileptiform phenomena. ODQ induced modifications of MDA parameters as those caused by 7-NI. Our results indicate that the nitrergic neurotransmission exerts a modulatory role in the proneness to the epileptogenic phenomena through the activation of sGC metabolic pathway.

AB - Summary Nitric oxide=soluble Guanylyl cyclase (NO=sGC) pathway on the maximal dentate gyrus activation (MDA) was studied in rats. The cerebral NO levels were modified by administrating 7-Nitroindazole (7-NI), a selective inhibitor of neuronal NOS, and L-arginine, a precursor of the synthesis of NO. 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a specific inhibitor of the NO-sGC pathway, was administered to study the involvement of cGMP pathway. The epileptic activity of the dentate gyrus was obtained through the repetitive stimulation of the angular bundle; MDA parameters studied were: onset time, MDA duration and post-stimulus afterdischarge (AD) duration. 7-NI caused an increase of MDA onset time and a decrease of MDA and AD duration. L-arginine, induced an aggravation of the epileptiform phenomena. ODQ induced modifications of MDA parameters as those caused by 7-NI. Our results indicate that the nitrergic neurotransmission exerts a modulatory role in the proneness to the epileptogenic phenomena through the activation of sGC metabolic pathway.

UR - http://hdl.handle.net/10447/13008

M3 - Article

VL - 113(12)

SP - 1855

EP - 1861

JO - Journal of Neural Transmission

JF - Journal of Neural Transmission

SN - 0300-9564

ER -