Impaired learning in rats in a 14-unit T-maze by 7-nitroindazole, a neuronal nitric oxide synthase inhibitor, is attenuated by the nitric oxide donor, molsidomine

Meyer, Rainer-Peter; Spangler, Edward L.; Patel, Namisha; London, Edythe D.; Ingram, Donald K.

doi:10.1016/s0014-2999(97)01428-3

Cited by 72 publications

(47 citation statements)

References 32 publications

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“…These antagonists have also been found to protect against NMDAinduced neurotoxicity (Haberny et al, 1992;Dawson et al, 1993;Ayata et al, 1997). They also block NMDA-mediated convulsions (Nakamura et al, 1995), and impair learning and memory in several animal models (Ward et al, 1990;Chapman et al, 1992;BoÈ hme et al, 1993;HoÈ lscher & Rose, 1993;HoÈ lscher et al, 1995;Yamada et al, 1995;Harder et al, 1998;Ingram et al, 1998a,b;Meyer et al, 1998;Zou et al, 1998). However, there is also evidence that inhibition of NOS does not impair learning or prevent the induction of long-term potentiation and NMDA-induced convulsions in animals (Buisson et al, 1993;Bannerman et al, 1994a,b).…”

Section: Discussionmentioning

confidence: 99%

Blockade of phencyclidine‐induced effects by a nitric oxide donor

Bujas‐Bobanovic

Bird

Robertson

et al. 2000

British J Pharmacology

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1 Phencyclidine (PCP) is widely used as an animal model of schizophrenia. The aim of this study was to better understand the role of nitric oxide (NO) in the mechanism of action of PCP and to determine whether positive NO modulators may provide a new approach to the treatment of schizophrenia. 2 The eects of the NO donor, sodium nitroprusside (SNP), were studied in PCP-treated rats. Following drug administration, behavioural changes and the expression of c-fos, a metabolic marker of functional pathways in the brain, were simultaneously monitored. 3 Acute PCP (5 mg kg 71 , i.p.) treatment induced a complex behavioural syndrome, consisting of hyperlocomotion, stereotyped behaviours and ataxia. Treatment with SNP (2 ± 6 mg kg 71 , i.p.) by itself produced no eect on any behaviour studied but completely abolished PCP-induced behaviour in a dose-and time-dependent manner. 4 PCP had dierential regional eects on c-fos expression in rat brain, suggesting regionally dierent patterns of neuronal activity. The most prominent immunostaining was observed in the cortical regions. Pre-treatment with SNP blocked PCP-induced c-fos expression at doses similar to those that suppress PCP-induced behavioural eects. 5 These results implicate the NO system in the mechanism of action of PCP. The fact that SNP abolished eects of PCP suggests that drugs targeting the glutamate-NO system may represent a novel approach to the treatment of PCP-induced psychosis and schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Blockade of phencyclidine‐induced effects by a nitric oxide donor

Bujas‐Bobanovic

Bird

Robertson

et al. 2000

British J Pharmacology

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“…Systemic administration of 7-NI at doses within this range have been found to inhibit spatial learning. Meyer et al (1998) found that spatial learning was significantly impaired in 3-4-mo-old male rats by administration of 65 mg/kg 7-NI 30 min prior to training. Administration of 10 or 30 mg/kg 7-NI immediately after object discrimination training impaired recall in 3-mo-old male Tryon-Maze-Bright rats 1 h after training (Prickaerts et al 1997).…”

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confidence: 89%

“…Nonetheless, studies with rats have shown an effect of 7-NI when administered 30 min before (Hölscher et al 1995;Meyer et al 1998) or 'after' training (Prickaerts et al 1997). The aim in Experiment 2 was to systematically explore the effects of posttraining administration for a wider range of doses of a specific nNOS inhibitor.…”

Section: Experiments 2: Dose Response Study Of Nnos Inhibitor Nplamentioning

confidence: 99%

Hemispheric Dissociation of the Involvement of NOS Isoforms in Memory for Discriminated Avoidance in the Chick

Rickard¹,

Gibbs²

2003

Learn. Mem.

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Previous research has indicated a role for both the neuronal (nNOS) and endothelial (eNOS) nitric oxide isoforms in memory formation. In addition, two distinct periods of activity of nitric oxide activity, dissociated by hemispheric localization, are implicated following passive avoidance training in the chick. In the present study, we trained black Australorp-white Leghorn chicks on a color discrimination avoidance task. Diphenyleneiodonium chloride (1 μM) or N-propyl-l-arginine (50 μM) was administered into either the left or right hemisphere of the chick brain in an attempt to differentiate the effects of inhibiting eNOS or nNOS, respectively. The memory loss previously observed following administration of diphenyleneiodonium chloride between 10 and 20 min posttraining was found to be lateralized to the right hemisphere, although administration of this agent into the left hemisphere around the time of training was also amnestic. In contrast, N-propyl-l-arginine caused memory loss only when administered to the left hemisphere around the time of training. These findings suggest that activation of both eNOS and nNOS isoforms may be essential for long-term memory consolidation of this task. Further, these two periods of activity are defined temporally and by hemisphere localization, although confirmation with more selective inhibitors when they become available is advised

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“…7-NI is a common pharmacological tool used to study NO effect in the central nervous system (CNS) since it preferentially inhibits nNOS in vivo [54] and above all it does not have any appreciable confounding pressor effects as does L-NAME [55]. However, 7-NI shows a strong monoamine oxidase (MAO) type B inhibitory activity [56][57][58][59].…”

Section: No Modulation Of the Activity Of Daergic Nigrostriatal Systemmentioning

confidence: 99%

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

Pierucci

Galati

Valentino

et al. 2011

CNSNDDT

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Several recent studies have emphasized a crucial role for the nitrergic system in movement control and the pathophysiology of the basal ganglia (BG). These observations are supported by anatomical evidence demonstrating the presence of nitric oxide synthase (NOS) in all the basal ganglia nuclei. In fact, nitrergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high expression of nitric oxide (NO)-producing neurons, with the striatum having the greatest number, together with important NO afferent input. In this paper, the distribution of NO in the BG nuclei will be described. Furthermore, evidence demonstrating the nitrergic control of BG activity will be reviewed. The new avenues that the increasing knowledge of NO in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. For example, inhibition of striatal NO/guanosine monophosphate signal pathway by phosphodiesterases seems to be effective in levodopa-induced dyskinesia. However, the results of experimental studies have to be interpreted with caution given the complexities of nitrergic signalling and the limitations of animal models. Nevertheless, the NO system represents a promising pharmacological intervention for treating Parkinson's disease and related disorders.

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Impaired learning in rats in a 14-unit T-maze by 7-nitroindazole, a neuronal nitric oxide synthase inhibitor, is attenuated by the nitric oxide donor, molsidomine

Cited by 72 publications

References 32 publications

Blockade of phencyclidine‐induced effects by a nitric oxide donor

Blockade of phencyclidine‐induced effects by a nitric oxide donor

Hemispheric Dissociation of the Involvement of NOS Isoforms in Memory for Discriminated Avoidance in the Chick

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

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