Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Posttraining administration of the L-enantiomer of the competitive inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl ester (L-NAME, 3-100 mg/kg, ip), impaired 48-h retention of a one-trial step-through inhibitory shock-avoidance task in male Swiss mice. The effects were dose-dependent and were not observed when the D-enantiomer (D-NAME, 3-100 mg/kg, ip) was injected instead of L-NAME. Retention latencies of mice that had not received a footshock during training were not affected by L-NAME. The memory impairment produced by L-NAME was time-dependent, suggesting an action on memory storage. The effects of L-NAME on memory were overcome by the injection of L-(but not D-)arginine (300 mg/kg, ip) along with the inhibitor. Considered together, these findings suggest that the L-arginine/nitric oxide pathway may be involved in memory storage of an inhibitory avoidance response in mice.
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PMID:A nitric oxide synthase inhibitor impairs memory storage in mice. 861 82

The present experiments examined the role of the central cholinergic system in the memory impairment induced by post-training administration of a nitric oxide synthase (NOS) inhibitor in mice. Male Swiss mice received a one-trial inhibitory avoidance training (0.8 mA, 50 Hz, 1-s footshock) followed immediately by an ip injection of the NOS inhibitor L-NG-nitroarginine methyl ester (L-NAME; 100 mg/kg). Retention (cut-off time, 300 s) was tested 48 h after training. The administration of L-NAME results in memory impairment for the inhibitory avoidance task. The effects of L-NAME (100 mg/kg, ip) on retention were reversed in a dose-related manner by the centrally acting anticholinesterase physostigmine (35, 70, or 150 microg/kg, sc) administered 30 min after the NOS inhibitor. Further, L-NAME (100 mg/kg, ip)-induced memory impairment was completely antagonized by the centrally acting muscarinic cholinergic agonist oxotremorine (OTM; 25, 50, or 100 microg/kg, sc) when given 30 min after L-NAME. The peripherally acting anticholinesterase neostigmine (150 microg/kg, sc) did not modify the memory-impairing effects of L-NAME. These findings suggest that the memory impairment following post-training administration of a NOS inhibitor is mediated, at least in part, by a reduction of the activity of central muscarinic cholinergic mechanisms and are consistent with our previous view that nitric oxide may be involved in post-training neural processes underlying the storage of newly acquired information.
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PMID:Enhancement of the post-training cholinergic tone antagonizes the impairment of retention induced by a nitric oxide synthase inhibitor in mice. 861 84

Inhibition of nitric oxide (NO) synthesis has been found to produce learning deficits in spatial tasks. Recent studies also suggest a regulatory effect of endogenous NO on hippocampal serotonin (5-HT) release and have shown that NO-synthase (NOS) inhibitors increased extracellular levels of serotonin (5-HT) in the rat hippocampus. To clarify possible interactions between NO and 5-HT in the hippocampus on learning processes, the effect of selective hippocampal 5-HT depletion on NOS inhibition-induced spatial learning deficits was investigated. Rats received bilateral injections of 5,7-dihydroxytryptamine (5,7-DHT), a 5-HT neurotoxin, or its vehicle in the CA1 region of hippocampus following pretreatment with desipramine. Rats were subjected to 5 days of training in the Morris water maze (MWM); 4 days with the invisible platform to test spatial learning and the 5th day with the visible platform to test motivation and sensorimotor coordination. Nomega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, was administered to either sham-operated or 5,7-DHT-lesioned groups 30 min before training each day. Results showed that L-NAME significantly impaired the ability of rats to locate the hidden platform. This impairment was reversed by co-administration of mole equivalent dose of L-arginine, the NO precursor. Although the 5,7-DHT-induced lesion had no effect by itself on rat performance in the MWM, it attenuated the memory impairment caused by L-NAME. The observed effect suggests an interaction between NO and 5-HT in the hippocampus on spatial memory formation; however, the mechanism of interaction is still unclear and requires further investigation.
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PMID:Serotonin depletion in rat hippocampus attenuates L-NAME-induced spatial learning deficits. 1256 Jan 30

In the present study, we investigated the effects of N(G)-nitro-L-arginine (L-NAME), an inhibitor of nitric oxide synthase, on repeated cerebral ischemia-induced impairment of spatial memory of the 8-arm radial maze in rats. Repeated ischemia (10 min ischemia x 2 times with 1 h interval) impaired the spatial memory in the 8-arm radial maze test and produced apoptosis in the hippocampus 7 days after final occlusion, and gradually increased the NO(x)(-) levels approximately 30-180 min after the second reperfusion. Post-ischemic administration of L-NAME at a dose of 50 mg/kg, i.p. 30 min following the second occlusion, significantly attenuated the repeated ischemia-induced impairment of spatial memory in the 8-arm radial maze test and suppressed apoptosis in the hippocampus, and also significantly suppressed a delayed increase in the NO(x)(-) levels induced by repeated ischemia. However, pre-ischemic administration of L-NAME at a dose of 50 mg/kg, i.p. 30 min before the first occlusion, caused about 90% mortality (the mortality rate of vehicle-treated group was 10%). These results suggest that the delayed generation of NO(x)(-) may cause spatial memory impairment and induction of apoptosis in the hippocampus in rats subjected to repeated ischemia.
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PMID:Post-ischemic administration [correction of administeration] but not pre-ischemic administration [correction of administeration] of NG-nitro-L-arginine prevents spatial memory impairments and apoptosis by an inhibition of a delayed increase in NOx- in the hippocampus following repeated cerebral ischemia. 1264 90

Learning and memory processes were tested in adult male rats using a traditional pole-climbing apparatus 30 min after the administration of L-arginine (500 and 1000 mg/kg), the precursor of nitric oxide (NO), and N-nitro-L-arginine methyl ester (L-NAME) (50 and 100 mg/kg), the inhibitor of NO synthesis. The effects of the convulsant (5.0 mg/kg) and a smaller nonconvulsant (2.5 mg/kg) dose of picrotoxin were tested on learning and memory 120 min and 24 h after their administration. The tests were carried out 30 min after L-arginine in animals treated 120 min previously with the convulsant dose of picrotoxin. A dose-dependent enhancement and an inhibition of learning and memory were observed in animals treated with L-arginine and L-NAME, respectively. The convulsant dose of picrotoxin impaired both learning and memory processes. The effect of picrotoxin was reverted following the administration of L-arginine (1000 mg/kg). An interpretation of these results indicates that convulsions induced by picrotoxin produces learning and memory impairment, and that this defect is reversible if NO synthesis is increased in the brain by the systemic administration of L-arginine.
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PMID:Prevention of picrotoxin convulsions-induced learning and memory impairment by nitric oxide increasing dose of L-arginine in rats. 1287 23

An aging rat model of chronic brain hypoperfusion (CBH) that mimics human mild cognitive impairment (MCI) was used to examine the role of nitric oxide synthase (NOS) isoforms on spatial memory function. Rats with CBH underwent bilateral common carotid artery occlusion (2-vessel occlusion (2-VO)) for either 26 or 8 weeks and were compared with nonoccluded sham controls (S-VO). The neuronal and endothelial (nNOS/eNOS) constitutive inhibitor nitro-L-arginine methyl ester (L-NAME) 20 mg/kg was administered after 26 weeks for 3 days to 2-VO and S-VO groups and spatial memory was assessed with a modified Morris watermaze test. Only 2-VO rats worsened their spatial memory ability after L-NAME. Electron microscopic immunocytochemical examination using an antibody against eNOS showed 2-VO rats had significant loss or absence of eNOS-containing positive gold particles in hippocampal endothelium and these changes were associated with endothelial cell compression, mitochondrial damage and heavy amyloid deposition in hippocampal capillaries and perivascular region. In the 8-week study, three groups of 2-VO rats were administered an acute dose of 7-NI, aminoguanidine or L-NIO, the relatively selective inhibitors of nNOS, inducible NOS and eNOS. Only rats administered the eNOS inhibitor L-NIO worsened markedly their watermaze performance (P = 0.009) when compared with S-VO nonoccluded controls. We conclude from these findings that vascular nitric oxide derived from eNOS may play a critical role in spatial memory function during CBH possibly by keeping cerebral perfusion optimal through its regulation of microvessel tone and cerebral blood flow and that disruption of this mechanism can result in spatial memory impairment. These findings may identify therapeutic targets for preventing MCI and treating Alzheimer's disease.
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PMID:Inhibition of vascular nitric oxide after rat chronic brain hypoperfusion: spatial memory and immunocytochemical changes. 1570

Huntington's disease is a neurodegenerative disorder characterized by symptoms like chorea and dementia. There is no exact therapeutic agent available to manage and cure this disease. 3-Nitropropionic acid, a neurotoxin causes gait and memory impairment which leads to oxidative damage and upsets glutathione defense in animals. 3-NP model is a useful tool to develop suitable therapeutic agent in the treatment of Huntington's disease. Present study compares the effects of lycopene and epigallocatechin-3-gallate (EGCG) on memory impairment and disturbs glutathione system against 3-NP treatment. 3-NP treatment significantly impaired memory as assessed in Morris water maze and elevated plus maze tasks. On the 15 day, the levels of reduced glutathione, total glutathione and glutathione-S-transferase were also significantly decreased in the striatum, hippocampus and cortex areas of the brain. The treatment with lycopene (2.5, 5 and 10mg/kg) and EGCG (10, 20 and 40 mg/kg) significantly improved memory and restored glutathione system functioning. Further, L-arginine and L-NAME pretreatment with the sub effective dose of lycopene (5mg/kg) and EGCG (20mg/kg) reversed and potentiate their protective effects respectively. In conclusion, lycopene and EGCG could be used to mange 3-NP induced behavioral and biochemical alterations by involving nitric oxide pathways.
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PMID:Effect of lycopene and epigallocatechin-3-gallate against 3-nitropropionic acid induced cognitive dysfunction and glutathione depletion in rat: a novel nitric oxide mechanism. 1961 97

Chronic infusion of human amyloid-beta 1-40 (Abeta) in the lateral ventricle (LV) of rats is associated with memory impairment and increase of kinin receptors in cortical and hippocampal areas. Deletion of kinin B1 or B2 receptors abolished memory impairment caused by an acute single injection of Abeta in the LV. As brain tissue and kinin receptors could unlikely react to acute or chronic administration of a similar quantity of Abeta, we evaluated the participation of B1 or B2 receptors in memory impairment after chronic infusion of Abeta. Male C57Bl/6J (wt), knock-out B1 (koB1) or B2 (koB2) mice (12weeks of age) previously trained in a two-way shuttle-box and achieving conditioned avoidance responses (CAR, % of 50 trials) were infused with AB (550pmol, 0.12microL/h, 28days) or vehicle in the LV using a mini-osmotic pump. They were tested before the surgery (T0), 7 and 35days after the infusion started (T7; T35). In T0, no difference was observed between CAR of the control (Cwt=59.7+/-6.7%; CkoB1=46.7+/-4.0%; CkoB2=64.4+/-5.8%) and Abeta (Abetawt=66.0+/-3.0%; AbetakoB1=66.8+/-8.2%; AbetakoB2=58.7+/-5.9%) groups. In T7, AbetakoB2 showed a significant decrease in CAR (41.0+/-8.6%) compared to the control-koB2 (72.8+/-2.2%, P<0.05). In T35, a significant decrease (P<0.05) was observed in Abetawt (40.7+/-3.3%) and AbetakoB2 (41.2+/-10.7%) but not in the AbetakoB1 (64.0+/-14.0%) compared to their control groups. No changes were observed in the controls at T35. We suggest that in chronic infusion of BA, B1 receptors could play an important role in the neurodegenerative process. Conversely, the premature memory impairment of koB2 suggests that it may be a protective factor.
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PMID:Participation of kinin receptors on memory impairment after chronic infusion of human amyloid-beta 1-40 peptide in mice. 1992 31

In an effort to understand the involvement of dorsal hippocampal nitric oxide system in ethanol (ETOH)-induced state-dependent memory, the effects of microinjection of l-arginine (a precursor of nitric oxide) and/or l-NAME (a nitric oxide synthase inhibitor) into the CA1 regions of dorsal hippocampus on this kind of memory were examined. In order to assess memory retrieval, a single trial step-down inhibitory avoidance task was used in mice. Pre-training intraperitoneal administration of ETOH (0.5 and 1g/kg) dose dependently caused amnesia, while pre-test administration of the same doses of ETOH restored the retrieval and induced state-dependent memory. Pre-test microinjection of l-arginine (0.5, 0.75 and 1 microg/mouse), into the CA1 region of dorsal hippocampus (intra-CA1) had no effect on memory retrieval. However, pre-test intra-CA1 microinjection of the same doses of l-arginine interestingly inhibited ETOH-induced state-dependent memory. The maximum response was obtained with 1 microg/mouse of l-arginine. Furthermore, memory impairment was produced following pre-test intra-CA1 microinjection of l-NAME (0.5, 0.75 and 1 microg/mouse). Pre-test co-administration of a higher dose of l-NAME (1 microg/mouse, intra-CA1) with an ineffective dose of ETOH (0.25 g/kg), improved the memory retrieval. Pre-test intra-CA1 microinjection of l-arginine or l-NAME could not affect ETOH-induced amnesia. In addition, l-arginine-induced inhibition of the pre-test ETOH response was decreased by pre-test microinjection of l-NAME. The ensemble of these observations suggests that ETOH-induced state-dependent memory can be modulated through the dorsal hippocampal nitric oxide system.
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PMID:Inhibition of dorsal hippocampal nitric oxide synthesis potentiates ethanol-induced state-dependent memory in mice. 2010 98

In the present study, the effects of nitric oxide agents on WIN55, 212-2 induced state-dependent memory of passive avoidance task were examined in mice. One-trial step-down paradigm was used for the assessment of memory retention in adult male NMRI mice. Post-training intra-CA1 administration of CB1 and CB2 receptor agonists, WIN55, 212-2 (0.25, 0.5 and 1 microg/mouse), dose-dependently decreased memory retrieval. The memory impairment induced by post-training administration of WIN55, 212-2 (1 microg/mouse) was restored by pre-test administration of the same dose of the drug (1 microg/mouse, intra-CA1), showing the WIN55, 212-2 state-dependent memory. Single intra-CA1 administration of L-arginine (0.3, 1 and 3 microg/mouse) or L-NAME (0.3, 1 and 3 microg/mouse), 5 min pre-test could not alter memory retrieval. On the other hand, in the animals in which retrieval was impaired due to post-training administration of WIN55, 212-2 (1 microg/mouse), pre-test intra-CA1 administration of l-arginine (1 and 3 microg/mouse), but not L-NAME (0.3, 1 and 3 microg/mouse) 24h after training restored memory retrieval. Also, in the animals which received both post-training (1 microg/mouse) and pre-test injections of WIN55, 212-2 (1 microg/mouse), the injection of L-NAME (3 microg/mouse, intra-CA1), 2 min before pre-test administration decreased retrieval. Furthermore, in the animals under the influence of post-training administration of WIN55, 212-2 (1 microg/mouse), pre-test co-administration of non-effective doses of WIN55, 212-2 (0.25 microg/mouse) and L-arginine (0.3 and 1 microg/mouse), increased the restoration of memory by pre-test WIN55, 212-2. These findings may demonstrate the involvement of NO in state-dependent memory induced by intra-CA1 administration of WIN55, 212-2.
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PMID:Influence of intracerebral administration of NO agents in dorsal hippocampus (CA1) on cannabinoid state-dependent memory in the step-down passive avoidance test. 2022 32


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