A nitric oxide (NO) synthase inhibitor accelerates amygdala kindling

Neuroreport ◽  
1992 ◽  
Vol 3 (9) ◽  
pp. 805-808 ◽  
Author(s):  
Gérard Rondouin ◽  
Mireille Lerner-Natoli ◽  
Olivier Manzoni ◽  
Mireille Lafon-Cazal ◽  
Joel Bockaert
Keyword(s):  
Nitric Oxide ◽  
No Synthase ◽  
No Synthase Inhibitor ◽  
Amygdala Kindling ◽  
Synthase Inhibitor

Peculiarities of influence of NO-synthase inhibitors on behavioral parameters of rats

2020 ◽  
Vol 28 (3) ◽  
pp. 275-282
Author(s):  
Valentina G. Bashkatova ◽  
Natalia G. Bogdanova ◽  
Elena V. Alexeeva ◽  
Galina A. Nazarova ◽  
Sergey K. Sudakov
Keyword(s):  
Nitric Oxide ◽  
Locomotor Activity ◽  
Motor Activity ◽  
Pain Sensitivity ◽  
Selective Inhibitor ◽  
No Synthase ◽  
Anxiety Level ◽  
Male Rats ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

Aim. A comparative study of the influence of nitric oxide synthase (NO-synthase) inhibitors on the parameters of anxiety, motor activity and pain sensitivity of rats. Materials and Methods. The work was conducted on male rats of Wistar line. The anxiety level and locomotor activity of rats were studied in the elevated plus maze (EPM) test. Pain sensitivity of the animals was tested on the hotplate apparatus. In the work, selective inhibitor of inducible isoform of NO-synthase aminoguanidine at a dose of 50 mg/kg, and non-selective inhibitor of this enzyme N-nitro-L-arginine at a dose of 50 mg/kg, were used. Rats of the control group were introduced the equivalent quantity of normal saline. NO-synthase inducible inhibitor aminoguadinine did not produce any influence on the anxiety level, but led to reduction of the horizontal motor activity of rats. Introduction of non-selective NO-synthase inhibitor N-nitro-L-arginine was accompanied by reduction of the anxiety and of the locomotor activity of animals in the EPM test. Both investigated NO-synthase inhibitors induced alteration of pain sensitivity of rats in the form of hypoalgesia. Here, the most pronounced nociceptive effect was observed with introduction of non-selective NO-synthase inhibitor. Conclusion. In the work the evidence of participation of inducible isoform of NO-synthase in realization of the motor activity and pain sensitivity processes in rats is shown. In result of the conducted experiments it was found that introduction of non-selective NO-synthase inhibitor N-nitro-L-arginine was accompanied by evident alterations of anxious behavior, locomotor activity and nociceptive sensitivity of rats. The results obtained confirm the important role of the system of regulation of nitric oxide synthesis in neurochemical mechanisms of behavioral reactions in rats.

scholarly journals Role of Nitric Oxide in Regulating Cerebrocortical Oxygen Consumption and Blood Flow during Hypercapnia

1994 ◽  
Vol 14 (3) ◽  
pp. 503-509 ◽  
Author(s):  
Ildiko Horvath ◽  
Norbert T. Sandor ◽  
Zoltan Ruttner ◽  
Alan C. McLaughlin
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Methyl Ester ◽  
Superior Sagittal Sinus ◽  
No Synthase ◽  
Sagittal Sinus ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

The effect of the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (Paco2 ∼ 60 mm Hg and Paco2 ∼ 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety–Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. l-NAME treatment did not have a significant effect on either CMRO2 or CBE under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.

Donor of nitric oxide improves, while NO-synthase inhibitor impairs resistance and adaptation to strenous physical exercise

1998 ◽  
Vol 125 (4) ◽  
pp. 336-339
Author(s):  
N. P. Aimasheva ◽  
E. B. Manukhina ◽  
M. G. Pshennikova ◽  
A. F. Vanin ◽  
I. Yu. Malyshev
Keyword(s):  
Nitric Oxide ◽  
Physical Exercise ◽  
No Synthase ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

Systemic injection of a nitric oxide synthase inhibitor suppresses sleep responses to sleep deprivation in rats

2000 ◽  
Vol 278 (4) ◽  
pp. R1048-R1056 ◽  
Author(s):  
Ana Cristina Ribeiro ◽  
John G. Gilligan ◽  
Levente Kapás
Keyword(s):  
Nitric Oxide ◽  
Sleep Deprivation ◽  
Dark Period ◽  
Intraperitoneal Administration ◽  
No Synthase ◽  
Sleep Regulation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Systemic Injection ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

We hypothesized that nitric oxide (NO) may play a role in homeostatic sleep regulation. To test this hypothesis, we studied the sleep deprivation (SD)-induced homeostatic sleep responses after intraperitoneal administration of an NO synthase inhibitor, Nω-nitro-l-arginine methyl ester (l-NAME, a cumulative dose of 100 mg/kg). Amounts and intensity of sleep were increased in response to 8 h of SD in control rats ( n = 8). Sleep amounts remained above baseline for 16 h after SD followed by a negative rebound. Rapid eye movement sleep (REMS) and non-REMS (NREMS) intensities were elevated for 16 and 4 h, respectively. l-NAME treatment ( n = 8) suppressed the rebound increases in NREMS amount and intensity. REMS rebound was attenuated by l-NAME in the first dark period after SD; however, a second rebound appeared in the subsequent dark period. REMS intensity did not increase after SD in l-NAME-injected rats. The finding that the NO synthase inhibitor suppressed rebound increases in NREMS suggests that NO may play a role as a signaling molecule in homeostatic regulation of NREMS.

Electrophysiological effects of nitric oxide in mouse superior mesenteric ganglion

1996 ◽  
Vol 270 (2) ◽  
pp. G324-G331 ◽  
Author(s):  
B. Mazet ◽  
S. M. Miller ◽  
J. H. Szurszewski
Keyword(s):  
Nitric Oxide ◽  
Direct Action ◽  
No Synthase ◽  
Excitatory Postsynaptic Potential ◽  
Repetitive Nerve Stimulation ◽  
Membrane Hyperpolarization ◽  
No Synthase Inhibitor ◽  
Mesenteric Ganglion ◽  
Synthase Inhibitor

Effects of nitric oxide (NO) generated from sodium nitroprusside (SNP) on neurons of mouse superior mesenteric ganglion (SMG) were studied in vitro using intracellular recording techniques. SNP solutions caused a membrane hyperpolarization in the majority (64%) of the neurons tested or a hyperpolarization followed by a depolarization in 8% of the neurons tested. The SNP-induced hyperpolarization persisted in a low-Ca2+ high-Mg2+ solution, indicating a direct effect of NO on the postsynaptic membrane. The hyperpolarizing effect of SNP was reduced or abolished by oxyhemoglobin. Electrical stimulation of the colonic nerves evoked a late slow excitatory postsynaptic potential (late sEPSP) in a population of neurons in normal Krebs solution. The amplitude of the late sEPSP was significantly enhanced in the presence of NG-nitroL-arginine, a NO synthase inhibitor. The results, particularly those observed with the NO synthase inhibitor, suggest that endogenous NO was released in the mouse SMG by repetitive nerve stimulation and that it modulated slow synaptic transmission, presumably by a direct action on ganglionic neurons.

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