Inhibitory action of Nω-nitro-L-arginine methyl ester on in vivo long-term potentiation in the rat dentate gyrus

Iga, Yoshinori; Yoshioka, Mitsuhiro; Togashi, Hiroko; Saito, Hideya

doi:10.1016/0014-2999(93)90873-g

Cited by 33 publications

(18 citation statements)

References 14 publications

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“…S-Nitrosylation is thought to be a biological process involved in some physiologic and pathophysiologic states such as cerebral ischemia (5 -7). Translocating NO bioactivity from Hb can modulate these biological processes, where intracellular thiols might be a key element since the translocation is accelerated in the presence of low molecular weight thiols such as glutathione and a trace amount of copper ions (38,48). A nitrosylated molecule (S-nitrosothiol) such as S-nitrosoglutathione (GSNO) is known to be present in a micromolar concentration in the rat brain and might serve as signaling molecules between endothelial cells and neurons (48,49).…”

Section: Discussionmentioning

confidence: 99%

“…The rats were tracheotomized, and artificially respirated. Extracellular recordings of field EPSPs were made from the granule cell body layer of the dentate gyrus (DG) (coordinates: 3.5 mm posterior, 2.0 mm lateral to the bregma, 3.3 mm ventral from the cortical surface) after electrical stimulation of the perforant-path (coordinates: 8.1 mm posterior, 4.4 mm lateral to the bregma, 2.5 mm ventral from the cortical surface), according to the atlas of Paxinos and Watson (37), at a baseline frequency of 0.033 Hz and 250 m s in duration as described previously (38). The evoked responses were amplified and monitored with an oscilloscope (VC-10; Nihon Kohden, Tokyo) and were averaged with a data analysis system (MASSCOMP; Concurrent, Tokyo).…”

Section: Electrophysiological Recordingmentioning

confidence: 99%

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An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

et al. 2004

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Abstract. Evidence suggests that S-nitrosylation is a biological process involved in cerebral ischemia. The aim of the present study was to elucidate the effects of S-nitrosylated (SNO) polyethylene glycol-conjugated (PEG) hemoglobin (Hb) developed as an artificial oxygen carrier, which can absorb free NO and translocate NO to a sulfhydryl (SH) moiety, on ischemic cerebral dysfunction. Long-term potentiation (LTP) in the perforant path-dentate gyrus synapses of the rat hippocampus was evaluated as functional outcome 4 days after transient incomplete cerebral ischemia (2-vessel occlusion: 2VO, 10 min). SNO-PEG-Hb (250 mg / kg, i.v.) administered on Day 0, 1, 2, or 4 (immediately, 24 h, 48 h, or 96 h after reperfusion, respectively) alleviated 2VO-induced LTP impairment with a therapeutic time window. The effect was significant when SNO-PEG-Hb was administered on Day 1 or 2. SNO-PEG-Hb altered NOS features observed in the vehicle-treated 2VO rat, upregulation of eNOS, nNOS, and iNOS expressions at mRNA and protein levels; SNO-PEG-Hb further upregulated eNOS and nNOS and downregulated iNOS expressions. These findings suggest that SNO-PEG-Hb might have protective effects on the rat hippocampus from ischemia / reperfusion-induced functional damages, thereby increasing the therapeutic potential as an artificial oxygen carrier for use in the area of oxygen therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Electrophysiological Recordingmentioning

confidence: 99%

An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

et al. 2004

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“…For example, it may mediate the NMDA-induced increase in cGMP but simultaneously inhibit the NMDA-induced increase in intracellular Ca 2+ and NOS activity, and block NMDA receptors (20,23). The influence of NO on NMDA neurotransmission may vary widely according to drug concentration and site of injection, which might explain the range of conflicting results on the role of NO in NMDA-modulated events such as epilepsy, neurotoxicity, longterm potentiation and nociception (5,20,50,51). For instance, in a very recent study Proctor et al (52) demonstrated that exogenously applied NO or its precursors can This biphasic effect of NOS inhibitors is not unusual for drugs with anticonvulsant activity (53).…”

Section: L-noargmentioning

confidence: 99%

Anticonvulsant and proconvulsant roles of nitric oxide in experimental epilepsy models

Del‐Bel

Oliveira

et al. 1997

Braz J Med Biol Res

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The effect of acute (120 mg/kg) and chronic (25 mg/kg, twice a day, for 4 days) intraperitonial injection of the nitric oxide (NO) synthase (NOS) inhibitor N G -nitro-L-arginine (L-NOARG) was evaluated on seizure induction by drugs such as pilocarpine and pentylenetetrazole (PTZ) and by sound stimulation of audiogenic seizure-resistant (R) and audiogenic seizure-susceptible (S) rats. Seizures were elicited by a subconvulsant dose of pilocarpine (100 mg/kg) only after NOS inhibition. NOS inhibition also simultaneously potentiated the severity of PTZ-induced limbic seizures (60 mg/kg) and protected against PTZ-induced tonic seizures (80 mg/kg). The audiogenic seizure susceptibility of S or R rats did not change after similar treatments. In conclusion, proconvulsant effects of NOS inhibition are suggested to occur in the pilocarpine model and in the limbic components of PTZinduced seizures, while an anticonvulsant role is suggested for the tonic seizures induced by higher doses of PTZ, revealing inhibitorspecific interactions with convulsant dose and also confirming the hypothesis that the effects of NOS inhibitors vary with the model of seizure.

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“…Although some research groups found block or impairment of induction of LTP, others did not. In one study the NOS inhibitor N-nitro-L-arginine-methyl-ester (L-NAME) prevented LTP induction in vivo in the rat (Iga et al 1993;Mizutani et al 1993), whereas in another study, LTP induction was not affected (Bannerman et al 1994b) or only LTP of the population spike was inhibited (Bannerman et al 1994c). A third study found that L-NAME raised the threshold for the induction of LTP (P.F.…”

Section: Introductionmentioning

confidence: 99%

7-Nitro indazole, a selective neuronal nitric oxide synthase inhibitor in vivo, impairs spatial learning in the rat.

Hölscher

McGlinchey²,

Anwyl³

et al. 1996

Learn. Mem.

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Nitric oxide (NO) is an intercellular messenger that has been suggested to have a role in learning and memory formation. Previous studies with nonselective NO synthase inhibitors have produced contradictory results in learning experiments. However, these drugs also produced blood pressure changes, as NO is an endothelial-derived relaxing factor. A novel NO synthase inhibitor, 7-nitro indazole (7-NI), as a dose (30 mg/kg i.p.) shown previously to inhibit neuronal NO synthase by 85% without affecting blood pressure, produced amnesic effects both in a water maze and in an 8-arm radial maze. Latency as well as distance was greater in the 7-NI group in the water maze while swim speed was not affected. Latency, working memory (WM), and reference memory (RF) errors were also higher in the 7-NI group in the 8-arm maze. At the end of the second training day, these differences were no longer apparent. However, on the fourth training day, a transfer test in the water maze showed that 7-NI had produced a spatial memory deficit, reducing quadrant bias and the number of annulus crossings. Learning of a visual cue task was not affected. No difference between groups was visible in an open field test. We conclude that neuronal NO sythase activity plays a role in learning and memory formation in the rat. 3Corresponding author.

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Inhibitory action of Nω-nitro-L-arginine methyl ester on in vivo long-term potentiation in the rat dentate gyrus

Cited by 33 publications

References 14 publications

An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

Anticonvulsant and proconvulsant roles of nitric oxide in experimental epilepsy models

7-Nitro indazole, a selective neuronal nitric oxide synthase inhibitor in vivo, impairs spatial learning in the rat.

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