Nifedipine blocks retention of a visual discrimination task in chicks

Deyo, Richard A.; Nix, Dorothy A.; Parker, Timothy W.

doi:10.1016/0163-1047(92)90262-3

Cited by 16 publications

(5 citation statements)

References 11 publications

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“…It was previously reported that acute systemic administration of the L-type VDCC antagonist nimodipine, in the low mg/kg dose range, induces a marked impairment of learning on a variety of behavioural tests in mice, including spontaneous alternation in the Y-maze, step-down type passive avoidance, and place learning in a water-maze (Maurice et al, 1995), and on the two-way active avoidance test in rats (Nikolaev and Kaczmarek, 1994). These observations were in accordance with several previous reports using other dihydropyridine VDCC blockers, including the one by Deyo et al (1992), who described a blocking effect on the retention of a visual discrimination task in chicks by nifedipine, administered i.c.v. 5 min before training.…”

Section: Discussionsupporting

confidence: 92%

“…The implication of Ca 2~ fluxes in memory processes is suggested by several direct experiments. Acute administration of nifedipine, a dihydropyridine VDCC antagonist, blocked retention of a visual discrimination task in chicks (Deyo et al, 1992). Low doses, in the ]g/kg dose range, of nimodipine, another dihydropyridine highly efficient as an L-type VDCC antagonist (Hoffmeister et al, 1982;Meyer et al, 1983;Scriabine et al, 1989), disrupted a two-way active avoidance behaviour in young adult rats (Nikolaev and Kaczmarek, 1994), and induced impairments of spontaneous alternation behaviour, of step-down passive avoidance, and of place learning in a water-maze, in mice (Maurice et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

Maurice

Parish

et al. 1995

J. Neural Transmission

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The high selectivity of the phencyclidine derivative PRE-084 for sigma (sigma) sites is demonstrated. We previously reported that this compound is able to markedly attenuate the impairment of learning induced in mice by the non-competitive NMDA antagonist MK-801, and the cholinergic nicotinic antagonist mecamylamine. In this study, we examined the effect of PRE-084 on the impairment of learning induced by acute administration of the calcium channel antagonist nimodipine. Nimodipine (0.3 mg/kg i.p.) impaired the spontaneous alternation behaviour in a Y-maze, decreased the step-down latency (SDL) in a passive avoidance task, and altered place learning and retention in a water-maze paradigm, with no marked effect on the motility observed using an open-field test. Preadministration of PRE-084 resulted in an attenuation of the impairment of alternation, in the 0.3-1 mg/kg s.c. range, in a marked increase in SDL, at 1-3 mg/kg, and improved place learning and retention in the water-maze, at 1 mg/kg. The effects on alternation behaviour and passive avoidance were completely prevented by co-administration of the purported sigma antagonist BMY-14802 (10 mg/kg i.p.), implicating the sigma sites. These results confirm the beneficial effect of the sigma ligand PRE-084 on pharmacological models of learning impairments, and indicate that sigma sites may modulate Ca2+ fluxes through VDCC, which may in turn bear some as yet unknown relationship to the previously described interaction with neurotransmitter systems.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

Maurice

Parish

et al. 1995

J. Neural Transmission

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“…This LTP depends, instead, on LVGCCs, because it can be blocked by nifedipine. Consistent with this, few previous reports indicate a clear dependence of learning on LVGCCs (Lee and Lin, 1991;Deyo et al, 1992;Borroni et al, 2000). To the contrary, many studies indicate that LVGCC blockade promotes learning rather than blocking it (Disterhoft et al, 1993;Vetulani et al, 1993;Fulga and Stroescu, 1997;Quevedo et al, 1998;Quartermain et al, 2001).…”

Section: Discussionsupporting

confidence: 57%

L-Type Voltage-Gated Calcium Channels Are Required for Extinction, But Not for Acquisition or Expression, of Conditional Fear in Mice

Blouin²,

2002

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It has been shown recently that extinction of conditional fear does not depend acutely on NMDA-type glutamate receptors, although other evidence has led to the hypothesis that L-type voltage-gated calcium channels (LVGCCs) play a role in conditional fear. We therefore tested the role of LVGCCs in the acquisition, expression, and extinction of conditional fear of cue and context in mice. Using systemic injections of two LVGCC inhibitors, nifedipine and nimodipine, which both effectively cross the blood-brain barrier, we show that LVGCCs are essential for the extinction, but not for the acquisition or expression, of conditional fear in mice.

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“…For instance, nimodipine administration enhanced memory performance in young chicks at low doses, while it induced an amnesic effect at high doses in a visual discrimination task (Deyo et al ., ). Nifedipine also impaired retention in the same task (Deyo et al ., ). Nimodipine administration was shown to improve spatial working memory in the eight‐arm radial maze in young rats (Levy et al ., ).…”

Section: Discussionmentioning

confidence: 97%

Sex‐dependent modulation of age‐related cognitive decline by the L‐type calcium channel gene Cacna1c (Ca_v1.2)

Zanos

Bhat

Terrillion

et al. 2015

Eur J of Neuroscience

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Increased calcium influx through L-type voltage-gated calcium channels (L-VGCC) has been implicated in the neuronal dysfunction underlying age-related memory declines. In the present study we sought to test the specific role of Cacna1c (which encodes Cav1.2) in modulating age-related memory dysfunction. Short-term, spatial, and contextual/emotional memory was evaluated in young and aged, wild-type as well as mice with one functional copy of Cacna1c (haploinsufficient), using the novel object recognition, Y-maze, and passive avoidance tasks respectively. Hippocampal expression of Cacna1c mRNA was measured by quantitative polymerase chain reaction (qPCR). Aging was associated with object recognition and contextual/emotional memory deficits and a significant increase in hippocampal Cacna1c mRNA expression. Cacna1c haploinsufficiency was associated with decreased Cacna1c mRNA expression in both young and old animals. However, haploinsufficient mice did not manifest an age-related increase in expression of this gene. Behaviorally, Cacna1c haploinsufficiency prevented object recognition deficits during aging in both male and female mice. A significant correlation between higher Cacna1c levels and decreased object recognition performance was observed in both sexes. We have also observed a sex-dependent protective role of decreased Cacna1c levels in contextual/emotional memory loss, specifically in male mice. These data provide evidence for an association between increased hippocampal Cacna1c expression and age-related cognitive decline. Additionally, they indicate an interaction between the Cacna1c gene and sex in the modulation of age-related contextual memory declines.

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Nifedipine blocks retention of a visual discrimination task in chicks

Cited by 16 publications

References 11 publications

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

L-Type Voltage-Gated Calcium Channels Are Required for Extinction, But Not for Acquisition or Expression, of Conditional Fear in Mice

Sex‐dependent modulation of age‐related cognitive decline by the L‐type calcium channel gene Cacna1c (Ca_v1.2)

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Nifedipine blocks retention of a visual discrimination task in chicks

Cited by 16 publications

References 11 publications

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

L-Type Voltage-Gated Calcium Channels Are Required for Extinction, But Not for Acquisition or Expression, of Conditional Fear in Mice

Sex‐dependent modulation of age‐related cognitive decline by the L‐type calcium channel gene Cacna1c (Cav1.2)

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Product

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Sex‐dependent modulation of age‐related cognitive decline by the L‐type calcium channel gene Cacna1c (Ca_v1.2)