The role of nitric oxide in passive avoidance learning

Telegdy, Gyula; Kokavszky, R.

doi:10.1016/s0028-3908(97)00154-8

Cited by 46 publications

(20 citation statements)

References 16 publications

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“…Nitric-oxide synthase is widespread in the nervous system and NO is thought to play important roles in activity-dependent synaptic plasticity as well as a variety of forms of learning and memory (Watanabe et al, 1995;Hawkins et al, 1996;Teledgy and Kokavszky, 1997;Prast and Philippu, 2001). In general, the relation between synaptic plasticity and various forms of learning has been investigated by inhibiting synaptic plasticity in a living animal and examine the consequences on later retention behavior.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Long-Term Potentiation by a Potent Nitric Oxide-Guanylyl Cyclase Activator, 3-(5-Hydroxymethyl-2-furyl)-1-benzyl-indazole

Chien

Liang²,

Teng³

et al. 2003

Mol Pharmacol

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Nitric oxide (NO) is known to affect synaptic plasticity in various regions of the brain via the cGMP-cGMP-dependent protein kinase (PKG) pathway. We found that a novel compound 3-(5-hydroxymethyl-2-furyl)-1-benzyl-indazole (YC-1), a drug known to modulate the response of soluble guanylyl cyclase to NO, greatly potentiates long-term potentiation (LTP). This compound markedly enhanced the induction of LTP in rat hippocampal and amygdala slices by weak tetanic stimulation. The potentiation of LTP by YC-1 was greatly reduced by NO synthase inhibitor N G -nitro-L-arginine-methylester, guanylyl cyclase inhibitor 1 H-[1,2,4]-oxadiazolo(4,3-a)-quinoxalin-1-one, and PKG inhibitor (9S,10R,12R)-2,3,9,10,11,12, hexahydro-10-methoxy-2,9-dimethyl-1-ox0 -9.12-epoxy-1H-diindolo[1,2,3-fg:3Ј,2Ј,1Ј-kl]pyrrolo[3,4-I][1,6]benzodiazocine-10-carboxylic acid methyl ester (KT5823). In addition, mitogen-activated protein kinase kinase inhibitor 2Ј-amino-3Ј-methoxyflavone (PD98059) also markedly inhibited LTP potentiating action of YC-1. Intracellular increase of Ca 2ϩ concentration derived from N-methyl-D-aspartate and glutamate metabotropic receptors contributes to the potentiating action of YC-1. Concurrent perfusion of YC-1 and NO donor sodium nitroprusside for a short time period resulted in the induction of LTP by stimuli at a frequency as low as 0.02 Hz. Incubation of unstimulated hippocampal slices with YC-1 plus nitroprusside increased the immunofluorescence of phosphoextracellular signal-regulated kinase (ERK) and phospho-cAMP response element binding protein (CREB). Furthermore, the Western blot shows that the phosphorylation of ERKs 1 and 2 and CREB of unstimulated hippocampal slices was increased by YC-1 plus nitroprusside, which was inhibited by KT5823. The NO-cGMP-PKG-ERK signaling pathway thus plays important role in the potentiation of LTP by YC-1.Learning and memory are two of the most intensively studied subjects in neuroscience. Various approaches have been used to understand the underlying cellular and molecular mechanisms. Long-term potentiation (LTP) has been identified as a potential synaptic mechanism in several regions of the brain involved in learning and memory (Abel and Lattal, 2001;Schafe et al., 2001). Schaffer collateral inputs to pyramidal neurons in the hippocampus CA1 region exhibit a form of LTP that critically depends on N-methyl-D-aspartate (NMDA) receptor-mediated Ca 2ϩ influx into the postsynaptic cell (Tsien et al., 1996). It has been suggested that nitric oxide (NO), generated postsynaptically by Ca 2ϩ -calmodulindependent NO synthase (NOS), acts as a retrograde messenger (Son et al., 1996;Wilson et al., 1997). A major target of NO is soluble guanylyl cyclase (sGC), which generates the intracellular second messenger cGMP. Consistent with a functional role of cGMP in the expression of LTP, sGC inhibitors suppress LTP (Zhuo et al., 1994), and membrane-permeable dibutyryl-cGMP partially reverses reduction of LTP by an NOS inhibitor (Haley et al., 1992). It is well known that GMP regulates th...

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Section: Discussionmentioning

confidence: 99%

Enhancement of Long-Term Potentiation by a Potent Nitric Oxide-Guanylyl Cyclase Activator, 3-(5-Hydroxymethyl-2-furyl)-1-benzyl-indazole

Chien

Liang²,

Teng³

et al. 2003

Mol Pharmacol

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“…Studies have shown that post-training administration of NO synthase (NOS) inhibitors could impair the consolidation of memory in different paradigms [13,14] . However, posttraining administration of L -arginine can facilitate mem-ory formation and reverses the memory-impairing effects of the NOS inhibitor [15] .…”

Section: Introductionmentioning

confidence: 99%

Morphine State-Dependent Learning Sensitization and Interaction with Nitric Oxide

et al. 2006

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In the present study, the effects of nitric oxide (NO) precursor L-arginine and L-NAME, a potent inhibitor of NO synthase (NOS), on the expression of sensitization of morphine were investigated. Pre-training administration of morphine (5 mg/kg) impaired memory retrieval compared to pre-training saline-treated animals. Amnesia due to pre-training morphine (5 mg/kg) was restored by pre-test morphine (5 mg/kg).The retrieval impairment was also inhibited in mice which had received once-daily injections of morphine (20 and 30 mg/kg, s.c.) for 3 days, followed by 5 days of no drug treatment before training (in order to induce morphine sensitization). Administration of L-arginine (60 mg/kg/day – 3 days) or L-NAME (20 mg/kg/day – 3 days) before training did not alter morphine state dependency. During acquisition of sensitization, administration of L-arginine (60 mg/kg) 20 min before morphine (10 mg/kg/day, for 3 days) increased, while injection of L-NAME (20 mg/kg) 20 min before morphine (30 mg/kg/day, for 3 days) decreased morphine state dependency. It is concluded that NO is involved in the morphine-induced sensitization.

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“…Reportedly, NO was not involved in retrieval formation in olfactory memory task in the adult sheep (Kendrick et al 1997), in the newborn rat (Samana and Boehm 1999), and in a passive avoidance test in the mouse (Telegdy and Kokavszky 1997). In contrast, involvement of NO in the retrieval of information was reported in inhibitory memory tasks performed in the newborn rat (Myslivecek et al 1996) and in the adult rat (Sudha et al 2001).…”

Section: Discussionmentioning

confidence: 88%

“…The involvement of NO in acquisition (Bohme et al 1993;Bernabeu et al 1995;Cobb et al 1995;Kendrick et al 1997;Telegdy and Kokavszky 1997) and storage formation is widely documented (Bernabeu et al 1995;Huang and Lee 1995;Prikaerts et al 1997;Telegdy and Kokavszky 1997;Blokland et al 1998), whereas the role of NO in the retrieval of information has yet to be clarified. Reportedly, NO was not involved in retrieval formation in olfactory memory task in the adult sheep (Kendrick et al 1997), in the newborn rat (Samana and Boehm 1999), and in a passive avoidance test in the mouse (Telegdy and Kokavszky 1997).…”

Section: Discussionmentioning

confidence: 99%

Effects of the nitric oxide donor molsidomine on different memory components as assessed in the object-recognition task in the rat

et al. 2002

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The role of nitric oxide in passive avoidance learning

Cited by 46 publications

References 16 publications

Enhancement of Long-Term Potentiation by a Potent Nitric Oxide-Guanylyl Cyclase Activator, 3-(5-Hydroxymethyl-2-furyl)-1-benzyl-indazole

Enhancement of Long-Term Potentiation by a Potent Nitric Oxide-Guanylyl Cyclase Activator, 3-(5-Hydroxymethyl-2-furyl)-1-benzyl-indazole

Morphine State-Dependent Learning Sensitization and Interaction with Nitric Oxide

Effects of the nitric oxide donor molsidomine on different memory components as assessed in the object-recognition task in the rat

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