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EnglishNitric 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.
Carletti, F., Ferraro, G., Rizzo, V., Friscia, S., & Sardo, P. (2012). Modulation of in vivo GABA-evoked responses by nitric oxide-active compounds in the globus pallidus of rat. JOURNAL OF NEURAL TRANSMISSION, 119(8), 911-921.
| Data di pubblicazione: | 2012 |
| Titolo: | Modulation of in vivo GABA-evoked responses by nitric oxide-active compounds in the globus pallidus of rat |
| Autori: | |
| Citazione: | Carletti, F., Ferraro, G., Rizzo, V., Friscia, S., & Sardo, P. (2012). Modulation of in vivo GABA-evoked responses by nitric oxide-active compounds in the globus pallidus of rat. JOURNAL OF NEURAL TRANSMISSION, 119(8), 911-921. |
| Rivista: | |
| Digital Object Identifier (DOI): | http://dx.doi.org/10.1007/s00702-011-0760-0 |
| 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. |
| Settore Scientifico Disciplinare: | Settore BIO/09 - Fisiologia |
| Appare nelle tipologie: | 1.01 Articolo in rivista |
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http://hdl.handle.net/10447/63345
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