Modulation of in vivo GABA-evoked responses by nitric oxide-active compounds in the globus pallidus of rat

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Abstract

Nitric oxide (NO) is a gaseous molecule acting as a messenger in both the peripheral and the central nervous systems. NO affects synaptic activity by modulating neurotransmitter release and/or receptor function. We previously observed that NO-active compounds modify the bioelectric activity of basal ganglia (BG) units. In this study, we applied microiontophoresis to extracellular in vivo recordings to investigate the effect of NO-active compounds on GABA-evoked responses in the globus pallidus (GP) of anesthetized rats. The changes induced by NO-active drugs on the GABA-induced inhibition were used as indicators of NO modulation. The response to GABA release was tested on recorded GP neurons before and during the administration of S-nitroso-glutathione (SNOG, a NO donor) and/or Nω-nitro-L: -arginine methyl ester (L: -NAME), an inhibitor of nitric oxide synthase (NOS); furthermore, SNOG and L: -NAME were tested at different ejection currents in order to highlight the possibility of a current-dependent effect in the nitrergic modulation of GABA transmission. In general, during SNOG ejection the magnitude of GABA-evoked responses was reduced, whereas the administration of L: -NAME produced the opposite effect. The results suggest that NO-active drugs modulate the response of GP neurons to GABA transmission; the effects induced by SNOG and L: -NAME were strictly related to the ejection currents. Then, the modulation of GABAergic transmission by NO could represent a mechanism to finely regulate the GP neurons activity with important consequences on the overall BG function.
Lingua originaleEnglish
pagine (da-a)911-921
Numero di pagine11
RivistaJournal of Neural Transmission
Volume119
Stato di pubblicazionePublished - 2012

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Globus Pallidus
gamma-Aminobutyric Acid
Nitric Oxide
NG-Nitroarginine Methyl Ester
Basal Ganglia
Neurons
GABAergic Neurons
Nitric Oxide Donors
Peripheral Nervous System
Nitric Oxide Synthase
Pharmaceutical Preparations
Glutathione
Neurotransmitter Agents
Central Nervous System

All Science Journal Classification (ASJC) codes

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

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title = "Modulation of in vivo GABA-evoked responses by nitric oxide-active compounds in the globus pallidus of rat",
abstract = "Nitric oxide (NO) is a gaseous molecule acting as a messenger in both the peripheral and the central nervous systems. NO affects synaptic activity by modulating neurotransmitter release and/or receptor function. We previously observed that NO-active compounds modify the bioelectric activity of basal ganglia (BG) units. In this study, we applied microiontophoresis to extracellular in vivo recordings to investigate the effect of NO-active compounds on GABA-evoked responses in the globus pallidus (GP) of anesthetized rats. The changes induced by NO-active drugs on the GABA-induced inhibition were used as indicators of NO modulation. The response to GABA release was tested on recorded GP neurons before and during the administration of S-nitroso-glutathione (SNOG, a NO donor) and/or Nω-nitro-L: -arginine methyl ester (L: -NAME), an inhibitor of nitric oxide synthase (NOS); furthermore, SNOG and L: -NAME were tested at different ejection currents in order to highlight the possibility of a current-dependent effect in the nitrergic modulation of GABA transmission. In general, during SNOG ejection the magnitude of GABA-evoked responses was reduced, whereas the administration of L: -NAME produced the opposite effect. The results suggest that NO-active drugs modulate the response of GP neurons to GABA transmission; the effects induced by SNOG and L: -NAME were strictly related to the ejection currents. Then, the modulation of GABAergic transmission by NO could represent a mechanism to finely regulate the GP neurons activity with important consequences on the overall BG function.",
author = "Pierangelo Sardo and Giuseppe Ferraro and Fabio Carletti and Valerio Rizzo and Simonetta Friscia",
year = "2012",
language = "English",
volume = "119",
pages = "911--921",
journal = "Journal of Neural Transmission",
issn = "0300-9564",
publisher = "Springer Verlag",

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TY - JOUR

T1 - Modulation of in vivo GABA-evoked responses by nitric oxide-active compounds in the globus pallidus of rat

AU - Sardo, Pierangelo

AU - Ferraro, Giuseppe

AU - Carletti, Fabio

AU - Rizzo, Valerio

AU - Friscia, Simonetta

PY - 2012

Y1 - 2012

N2 - Nitric oxide (NO) is a gaseous molecule acting as a messenger in both the peripheral and the central nervous systems. NO affects synaptic activity by modulating neurotransmitter release and/or receptor function. We previously observed that NO-active compounds modify the bioelectric activity of basal ganglia (BG) units. In this study, we applied microiontophoresis to extracellular in vivo recordings to investigate the effect of NO-active compounds on GABA-evoked responses in the globus pallidus (GP) of anesthetized rats. The changes induced by NO-active drugs on the GABA-induced inhibition were used as indicators of NO modulation. The response to GABA release was tested on recorded GP neurons before and during the administration of S-nitroso-glutathione (SNOG, a NO donor) and/or Nω-nitro-L: -arginine methyl ester (L: -NAME), an inhibitor of nitric oxide synthase (NOS); furthermore, SNOG and L: -NAME were tested at different ejection currents in order to highlight the possibility of a current-dependent effect in the nitrergic modulation of GABA transmission. In general, during SNOG ejection the magnitude of GABA-evoked responses was reduced, whereas the administration of L: -NAME produced the opposite effect. The results suggest that NO-active drugs modulate the response of GP neurons to GABA transmission; the effects induced by SNOG and L: -NAME were strictly related to the ejection currents. Then, the modulation of GABAergic transmission by NO could represent a mechanism to finely regulate the GP neurons activity with important consequences on the overall BG function.

AB - Nitric oxide (NO) is a gaseous molecule acting as a messenger in both the peripheral and the central nervous systems. NO affects synaptic activity by modulating neurotransmitter release and/or receptor function. We previously observed that NO-active compounds modify the bioelectric activity of basal ganglia (BG) units. In this study, we applied microiontophoresis to extracellular in vivo recordings to investigate the effect of NO-active compounds on GABA-evoked responses in the globus pallidus (GP) of anesthetized rats. The changes induced by NO-active drugs on the GABA-induced inhibition were used as indicators of NO modulation. The response to GABA release was tested on recorded GP neurons before and during the administration of S-nitroso-glutathione (SNOG, a NO donor) and/or Nω-nitro-L: -arginine methyl ester (L: -NAME), an inhibitor of nitric oxide synthase (NOS); furthermore, SNOG and L: -NAME were tested at different ejection currents in order to highlight the possibility of a current-dependent effect in the nitrergic modulation of GABA transmission. In general, during SNOG ejection the magnitude of GABA-evoked responses was reduced, whereas the administration of L: -NAME produced the opposite effect. The results suggest that NO-active drugs modulate the response of GP neurons to GABA transmission; the effects induced by SNOG and L: -NAME were strictly related to the ejection currents. Then, the modulation of GABAergic transmission by NO could represent a mechanism to finely regulate the GP neurons activity with important consequences on the overall BG function.

UR - http://hdl.handle.net/10447/63345

M3 - Article

VL - 119

SP - 911

EP - 921

JO - Journal of Neural Transmission

JF - Journal of Neural Transmission

SN - 0300-9564

ER -