The nitric oxide synthesis inhibitor L-name facilitates associative learning

Du, Wei; Harvey, J.

doi:10.1016/s0278-5846(96)00105-4

Cited by 18 publications

(10 citation statements)

References 26 publications

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“…The fact that the activation of ionotropic glutamate receptors generates NO production by a calcium-dependent process led to the hypothesis that NO could be involved in excitotoxicity (Kiedrowski et al, 1992). Also, a role for NO in certain neurodegenerative processes (Southam and Garthwaite, 1993) and memory disorders (Du and Harvey, 1996;Du et al, 2000) has been proposed. NO production is increased in kainic acid (KA)-induced seizures (Mulsch et al, 1994) and inhibition of NOS activity with 7-nitroindazole, a selective nNOS inhibitor, and N-nitro-L-arginine (L-NAME), a NOS inhibitor, decreases NO production and hippocampal damage, and attenuates seizure activity (Takei et al, 1999;Takei et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus

Byun

Lee

Jeon

et al. 2009

Korean J Physiol Pharmacol

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Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. W e tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS − /− ) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.

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Section: Introductionmentioning

confidence: 99%

Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus

Byun

Lee

Jeon

et al. 2009

Korean J Physiol Pharmacol

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“…The role of NO in learning and memory is unclear. NOS inhibition was reported to slow down (Chapman et al, 1992), as well as to accelerate (Du and Harvey, 1996), classical conditioning. Application of an NO donator improved or impaired avoidance learning, depending on dose (Huang and Lee, 1995).…”

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confidence: 99%

Superior Water Maze Performance and Increase in Fear-Related Behavior in the Endothelial Nitric Oxide Synthase-Deficient Mouse Together with Monoamine Changes in Cerebellum and Ventral Striatum

Frisch¹,

Dere²,

Silva³

et al. 2000

J. Neurosci.

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Nitric oxide (NO) has been implicated in the control of emotion, learning, and memory. We have examined endothelial NO synthase-deficient mice (eNOSϪ/Ϫ) in terms of habituation to an open field, elevated plus-maze behavior, Morris water maze performance, and changes in cerebral monoamines. In the open field, eNOSϪ/Ϫ animals were less active than wild-type controls but showed unimpaired habituation. In the plus-maze, an anxiogenic effect was observed. Proceeding from previous findings of deficits in hippocampal and neocortical long-term potentiation (LTP) in our eNOSϪ/Ϫ mice, we investigated whether these animals also express deficits in learning tasks that have been linked to hippocampal function and LTP. Unexpectedly, eNOS gene disruption led to accelerated place learning in the water maze. Furthermore, during long-term retention and reversal learning, eNOSϪ/Ϫ mice showed improved performance. In a cued version of the water maze task, eNOSϪ/Ϫ and control mice did not differ, implying that the superior performance of eNOSϪ/Ϫ animals on the former tasks cannot be attributed solely to differences in sensorimotor capacities. The neurochemical evaluation of the eNOSϪ/Ϫ mice revealed increases in the concentrations of the serotonin metabolite 5-HIAA in the cerebellum, together with an accelerated serotonin turnover in the frontal cortex. Furthermore, eNOSϪ/Ϫ mice had a higher dopamine turnover in the ventral striatum. These findings are discussed in terms of possible concomitant effects on physiological parameters, such as a decreased reactivity of GABAergic neurotransmission or changes in vascular functions, and effects on behavioral processes related to reinforcement, learning, and emotion.

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“…Acquisition of the conditioned NM response has been demonstrated to provide an excellent model for separating learning from performance variables (Harvey and Welsh 1996) and is acknowledged to provide an unambiguous measure of associative learning (Harvey 1987). We found that systemic (IV) administration of the NO donor SNP retarded (Du et al 1995) and IP injection of the NOS inhibitor L-NAME enhanced (Du and Harvey 1996) the acquisition of CRs. These alterations in learning occurred in the absence of any effects on performance variables or non-associative processes (Du et al 1995;Du and Harvey 1996).…”

Section: Introductionmentioning

confidence: 94%

“…We found that systemic (IV) administration of the NO donor SNP retarded (Du et al 1995) and IP injection of the NOS inhibitor L-NAME enhanced (Du and Harvey 1996) the acquisition of CRs. These alterations in learning occurred in the absence of any effects on performance variables or non-associative processes (Du et al 1995;Du and Harvey 1996). The purpose of the present study was to determine whether the effects of L-NAME and SNP were due to their direct central effects on brain NO.…”

Section: Introductionmentioning

confidence: 94%

“…Knepper and Kurylo (1998) G. Classical conditioning -increased amplitude of response -whisker pairing -one CS Rat L-NAME, microiontophoresis in barrel cortex Enhanced Maalouf et al (1998) H. Classical conditioning -percent CRs -eye blink EMG -one CS Rabbit L-NAME, 10, 25, 75 mg/kg, IP?, 120 trials Impaired at all three doses* Chapman et al (1992) I. Classical conditioning -percent CRs -nictitating membrane response -one CS Rabbit L-NAME, 25 mg/kg, IP, 60 trials Enhanced at 25 mg/kg Du and Harvey (1996) Rabbit 7-NI, 10, 25, 50 mg/kg, SC, 60 trials Enhanced at 50 mg/kg Present study Rabbit AR-R 17477, 0.1, 1.0, 10 mg/kg, SC, 60 trials Enhanced at 10 mg/kg Present study *The effect was not dose-dependent L-NA Nω-nitro-L-arginine, L-NAME Nω-nitro-L-arginine methyl ester Cannulae and surgery Rabbits were anesthetized with sodium pentobarbital and a guide cannula/obturator assembly (Welsh and Harvey 1991) was implanted into the left lateral ventricle as previously described (Aloyo et al 1993). Rabbits were allowed 5 days of post-surgical recovery before beginning behavioral training.…”

Section: Subjectsmentioning

confidence: 99%

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Associative learning is enhanced by selective neuronal nitric oxide synthase inhibitors and retarded by a nitric oxide donor in the rabbit

Weiss

Harvey

2000

Psychopharmacology

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The nitric oxide synthesis inhibitor L-name facilitates associative learning

Cited by 18 publications

References 26 publications

Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus

Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus

Superior Water Maze Performance and Increase in Fear-Related Behavior in the Endothelial Nitric Oxide Synthase-Deficient Mouse Together with Monoamine Changes in Cerebellum and Ventral Striatum

Associative learning is enhanced by selective neuronal nitric oxide synthase inhibitors and retarded by a nitric oxide donor in the rabbit

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