Inhibition of nitric oxide synthesis impairs two different forms of learning

Chapman, Paul F.; Atkins, Coleen M.; Allen, Michelle; Haley, Jane E.; Steinmetz, Joseph E.

doi:10.1097/00001756-199207000-00005

Cited by 226 publications

(100 citation statements)

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“…impairment (Chapman et al, 1992;Bannerman et al, 1994a,b,c;Fin et al, 1995;Good, 1996). We have demonstrated previously that neonatal nonhandling can lead to an attenuation of latent inhibition (Weiner et al, 1985(Weiner et al, , 1987Weiner, 1988, 1992;Feldon et al, 1990).…”

Section: Discussionmentioning

confidence: 94%

Neonatal Nonhandling andIn UteroPrenatal Stress Reduce the Density of NADPH-Diaphorase-Reactive Neurons in the Fascia Dentata and Ammon’s Horn of Rats

et al. 1997

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The density of nitric oxide (NO)-producing neurons in the fascia dentata and Ammon's horn was assessed in 6-month-old male rats using NADPH-diaphorase (NADPH-d) histochemistry. Two separate experiments investigated whether (1) the complete absence of neonatal handling or (2) the administration of periodic prenatal stress could affect the expression and distribution of NADPH-d reactivity in the hippocampus, when compared with rats raised in normal standard laboratory conditions. Experiment 1 demonstrated that adult rats that received no handling during neonatal development (from birth to postnatal day 22) showed a very substantial reduction in NADPH-d-positive neurons per unit area throughout the entire hippocampus when compared with rats that received regular daily handling in this period. Quantitative analysis further revealed that this effect was significantly more pronounced in Ammon's horn than in the fascia dentata, and within Ammon's horn the dorsal region was selectively more affected. Experiment 2 showed that prenatal stress, which involved the administration of daily restraint stress to pregnant dams throughout the gestation period, also led to a reduction in NADPH-d reactivity in the hippocampus of the offspring of these dam when they reached adulthood.The present results suggest that behavioral manipulations in the early neonatal or prenatal period can significantly alter the neurodevelopment of the hippocampal NO system and these changes might be related to some of the behavioral abnormalities that emerge later in adulthood.

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Section: Discussionmentioning

confidence: 94%

Neonatal Nonhandling andIn UteroPrenatal Stress Reduce the Density of NADPH-Diaphorase-Reactive Neurons in the Fascia Dentata and Ammon’s Horn of Rats

et al. 1997

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“…Regarding the CNS, research on different neurobiological models from vertebrates and invertebrates has produced fundamental findings on the role of NO in the normal physiology of several areas. It is known that NO is involved in the behavior of animals, i.e., feeding processes, visual functionality, memory, and learning (Chapman et al, 1992;Moroz et al, 1993;Elphick et al, 1995Elphick et al, , 1996Mü ller, 1996Mü ller, , 1997Seidel and Bicker, 1997;Conforti et al, 1999;Pisu et al, 1999).…”

Section: What Is the Role Of No After Axotomy?mentioning

confidence: 99%

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

et al. 2002

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When vestibular damage occurs, nitric oxide synthase (NOS) expression in rat cerebellar flocculus is affected. Since compensation for postural symptoms occurs and Purkinje cells play an important role in movement coordination and motor learning, we analyzed in situ the induction of NOS in the Purkinje cell population of the cerebellum (corpus cerebelli) of frog after unilateral transection of the eighth statoacoustic nerve to gain insight into the role of NO in neural plasticity after injury. Three days after neurectomy, the early effects induced NADPH diaphorase reactivity in most of the Purkinje cells on the ipsilateral side, while on the contralateral side the highest labeling was observed at 15 days. This finding can give information on the dynamics of vestibular compensation, in which NOS involvement was investigated. At 30 days, NADPH diaphorase reactivity was present in a large number of Purkinje cells of the whole cerebellum, while at 60 days a down-regulation for NADPH diaphorase reactivity was evident. A similar trend was observed for NOS-immunoreactivity, which was still present at 60 days in a high percentage of Purkinje cells, mainly on the ipsilateral side. On the basis of cell density evaluations, it was proposed that the early induction of NOS after neurectomy was linked to the degeneration of a part of the Purkinje neurons, while the permanence of NOS labeling might be due to a neuroprotective role of NO in the restoration phase of the vestibular compensation process. Anat Rec 268: 73-83, 2002.

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“…Consistent with the dual role of nitric oxide at NMDA receptors, previous research has shown that, although drugs that inhibit nitric oxide (NOS inhibitors) share some behavioral effects with NMDA antagonists, they also may attenuate other behaviors associated with NMDA antagonism. Shared properties include anxiolytic effects, memory impairment, and phencyclidine (PCP)-like discriminative stimulus effects (Chapman et al 1992;Jewett et al 1996;Volke et al 1997). In contrast, Deutsch et al (1996) found that NOS inhibitors blocked "popping" behavior in mice that was induced by the PCP-like noncompetitive NMDA antagonist, dizocilpine.…”

Section: Glutamate Stimulation Of N-methyl-d-aspartate (Nmda) Receptomentioning

confidence: 99%

“…Constitutive and inducible forms of NOS have been identified, but it is the constitutive, Ca 2 ϩ -calmodulin-dependent form that is found in the brain and is hypothesized to be involved in the centrally mediated properties of nitric oxide (Lambert et al 1991). These central effects may include roles in memory formation (Chapman et al 1992;Yamada et al 1995), development of tolerance or sensitization to drugs of abuse (Khanna et al 1993;Kolesnikov et al 1992;Majeed et al 1994;Pudiak and Bozarth 1993), and response to stroke or neurotrauma (Nagafusi et al 1995;Schulz et al 1995).…”

Section: Abstract : Antipsychotics; Nitric Oxide Synthase Inhibitorsmentioning

confidence: 99%

“…Shared properties include anxiolytic effects, memory impairment, and phencyclidine (PCP)-like discriminative stimulus effects (Chapman et al 1992;Jewett et al 1996;Volke et al 1997). In contrast, Deutsch et al (1996) found that NOS inhibitors blocked "popping" behavior in mice that was induced by the PCP-like noncompetitive NMDA antagonist, dizocilpine.…”

Section: Abstract : Antipsychotics; Nitric Oxide Synthase Inhibitorsmentioning

confidence: 99%

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Nitric Oxide Synthase Inhibitors Attenuate Phencyclidine-Induced Disruption of Prepulse Inhibition

Wiley

1998

Neuropsychopharmacology

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Glutamate stimulation of N-methyl-D-aspartate (NMDA) receptors results in release of nitric oxide which may mediate the effects of NMDA receptor stimulation and ր or may result in feedback inhibition of the presynaptic neuron. Results of a previous study showed that nitric oxide synthase (NOS) inhibitors blocked dizocilpine-induced behavior in mice. In the present study, NOS inhibitors were tested in combination with phencyclidine (PCP),Nitric oxide is a soluble gas that is synthesized from the amino acid L -arginine by nitric oxide synthase (NOS). Nicotinamide-adenine dinucleotide phosphate-diaphorase (NADPH) is a required co-factor and citrulline is a co-product of the reaction. Constitutive and inducible forms of NOS have been identified, but it is the constitutive, Ca 2 ϩ -calmodulin-dependent form that is found in the brain and is hypothesized to be involved in the centrally mediated properties of nitric oxide (Lambert et al. 1991). These central effects may include roles in memory formation (Chapman et al. 1992;Yamada et al. 1995), development of tolerance or sensitization to drugs of abuse (Khanna et al. 1993;Kolesnikov et al. 1992;Majeed et al. 1994;Pudiak and Bozarth 1993), and response to stroke or neurotrauma (Nagafusi et al. 1995;Schulz et al. 1995).Although NOS is not completely co-localized with any known neurotransmitter, a subset of N-methyl-Daspartate (NMDA) neurons is associated with NOS (Garthwaite 1991). In these neurons, depolarization of the NMDA receptor by the endogenous excitatory amino acid neurotransmitter glutamate produces an influx of Ca 2 ϩ which binds to calmodulin. This Ca 2 ϩ -calmodulin complex activates NOS directly, resulting in a brief "puff" of nitric oxide that diffuses out of the presynaptic terminal and into astrocytic processes to ac- (Manzoni et al. 1992). Consistent with the dual role of nitric oxide at NMDA receptors, previous research has shown that, although drugs that inhibit nitric oxide (NOS inhibitors) share some behavioral effects with NMDA antagonists, they also may attenuate other behaviors associated with NMDA antagonism. Shared properties include anxiolytic effects, memory impairment, and phencyclidine (PCP)-like discriminative stimulus effects (Chapman et al. 1992;Jewett et al. 1996;Volke et al. 1997). In contrast, Deutsch et al. (1996) found that NOS inhibitors blocked "popping" behavior in mice that was induced by the PCP-like noncompetitive NMDA antagonist, dizocilpine. Exploration of the effects of NOS inhibitors on other behavioral effects of NMDA antagonists, so far, has been minimal.Another procedure in which PCP-like NMDA antagonists produce characteristic effects is prepulse inhibition of acoustic startle. The acoustic startle response is a reflexive movement that occurs upon abrupt presentation of a loud acoustic stimulus. Prepulse inhibition refers to a decrease in the magnitude of this startle response that is observed when the loud noise is preceded by a weak acoustic stimulus (a "prepulse"). Disruption of prepulse inhibition involves defici...

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Inhibition of nitric oxide synthesis impairs two different forms of learning

Cited by 226 publications

References 0 publications

Neonatal Nonhandling andIn UteroPrenatal Stress Reduce the Density of NADPH-Diaphorase-Reactive Neurons in the Fascia Dentata and Ammon’s Horn of Rats

Neonatal Nonhandling andIn UteroPrenatal Stress Reduce the Density of NADPH-Diaphorase-Reactive Neurons in the Fascia Dentata and Ammon’s Horn of Rats

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

Nitric Oxide Synthase Inhibitors Attenuate Phencyclidine-Induced Disruption of Prepulse Inhibition

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