Protective effect of the calcium antagonist nimodipine on discrimination learning deficits and impaired retention behavior caused by prenatal nitrite exposure in rats

Nyakas, Csaba; Markel, E; Bohus, B.; Schuurman, T.; Luiten, P.G.M.

doi:10.1016/0166-4328(90)90025-a

Cited by 18 publications

(9 citation statements)

References 19 publications

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“…1976). In our previous studies (Nyakas et al, 1989(Nyakas et al, . 1990 we have shown that prenatal chronic hypoxia caused by nitrite intoxication also leads to a discrimination learning deficit in the offspring reaching adult age.…”

Section: Discussionmentioning

confidence: 86%

“…In our previous studies it has been demonstrated that prenatal chronic hypoxia induced by nitrite in rats results in an impaired discrimination learning ability, which is antagonized by concomitant treatment with nimodipine (Nyakas et al, 1989(Nyakas et al, , 1990. Nitrite is considered to act as a toxic substance causing hypoxia of an anaemic type (Gruener et nl., 1973nl., : Fahey et al, 1989Nyakas et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Impaired Learning and Abnormal Open‐field Behaviours of Rats After Early Postnatal Anoxia and the Beneficial Effect of the Calcium Antagonist Nimodipine

Nyakas

Markel²,

Schuurman

et al. 1991

Eur J of Neuroscience

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Perinatal anoxia/hypoxia is considered a serious risk factor for normal brain development. Anoxia induced by repeated asphyxia at 2 and 4 days after birth resulted in a transient hyperactivity in the small open-field, and a behavioural depression in adult open-field activity of male Wistar rats. The same treatment impaired adult learning behaviour in pole-jumping conditioned avoidance and appetitively motivated hole-board test situations. The calcium entry blocker nimodipine (in doses of 3 and 10 mg/kg) prevented the anoxia-induced changes in orientation motility in the open-field tests and almost fully antagonized the learning deficit in the hole-board test. The behavioural deficit seen during acquisition of the pole-jumping conditioned avoidance response was ameliorated to a lesser degree. The results indicate that the maintenance of calcium homeostasis during the early postnatal phase of brain development is crucial to prevent anoxia-induced behavioural abnormalities.

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Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Impaired Learning and Abnormal Open‐field Behaviours of Rats After Early Postnatal Anoxia and the Beneficial Effect of the Calcium Antagonist Nimodipine

Nyakas

Markel²,

Schuurman

et al. 1991

Eur J of Neuroscience

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“…Cytosolic neuronal Ca 2+ overload in vulnerable brain regions, like cortex and hippocampus elicited by the perinatal hypoxia [7,38], may well be responsible for the observed anatomical and behavioral effects. This hypothesis finds support in the finding that chronic perinatal administration of the L-type Ca 2+ channel antagonist nimodipine during hypoxia prevented both suppression of cholinergic and serotonergic innervation of cortex and hippocampus [26] as well as behavioral abnormalities [24,25]. The neuroprotective action of the Ca 2+ antagonist during perinatal hypoxia may be caused by a decreased Ca 2+ influx.…”

Section: Introductionmentioning

confidence: 72%

“…After delivery, the treatment was continued throughout the experiment. The selection of the single dose of the Ca 2+ antagonist was based on the results of previous immunocytochemical and behavioral studies performed in this laboratory [24][25][26].…”

Section: Treatmentmentioning

confidence: 99%

“…We recently reported that pre-and early-postnatal hypoxia transiently retarded the ingrowth of serotonergic and cholinergic fibers in neocortex and hippocampus [26]. The effects of such perinatal hypoxic events were also reflected in the impaired adult cognitive and motivational behaviors in which the above-mentioned neurotransmitter systems play a prominent role [24][25][26]. Cytosolic neuronal Ca 2+ overload in vulnerable brain regions, like cortex and hippocampus elicited by the perinatal hypoxia [7,38], may well be responsible for the observed anatomical and behavioral effects.…”

Section: Introductionmentioning

confidence: 99%

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Nimodipine accelerates the postnatal development of parvalbumin and S-100β immunoreactivity in the rat brain

Buwalda¹,

Naber

Nyakas

et al. 1994

Developmental Brain Research

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The effects of chronic maternal perinatal nimodipine treatment on the immunocytochemical distribution of the Ca(2+)-binding proteins parvalbumin (PV) and S-100 beta in neocortex and hippocampus were studied at the age of postnatal day (PD) 5, 7, 10, 14 and 20. The Ca2+ antagonist nimodipine (1000 ppm BAY e 9736 in daily food) was administered to pregnant rats starting at postconceptual day 11. The expression of PV exemplified in layer V of parietal and retrosplenial cortex and in all hippocampal layers of CA1 and CA3 was enhanced by more than two-fold in the offspring of nimodipine-treated dams at PD 10 compared with placebo-treated animals. The difference was no longer present at PD 14 and 20. Nimodipine administration also significantly increased the number of S-100 beta-immunopositive glial cells in upper neocortical layers I-III at PD 5 and 7. Again, the difference between nimodipine and placebo-treated animals disappeared after PD 10. The data indicate an accelerated development of PV and S-100 immunoreactivity in the postnatal forebrain as a result of perinatal blockade of the L-type Ca2+ current.

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Amiridine (NIK‐247) and cerebrocrast in the alleviation of cholinergic lesion‐induced learning deficit in male rats

Männistö

Kutepova

Leinonen

et al. 1993

Drug Development Research

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Learning of the male rats was impaired by injecting ethylcholine aziridiniurn (AF64A) bilaterally into the basal magnocellular nuclei of Meynert. The performance of the rats in a passive avoidance test and in a one-way active avoidance test was significantly improved by giving a novel acetylcholinesterase inhibitor, amiridine (NIK-247; 9-amino-2,3,5,6,7,8-hexahydro-lH-cyclopenta(b)-quinoline rnonohydrate hydrochloride) after each learning session but not when the drug was given before the sessions. Cerebrocrast, an antagonist of L-type calcium channels, was not effective in either case. Rather it worsened the learning results when given after the sessions of the active avoidance test. The conclusions in the passive avoidance test were hampered by the observed inconsistent effects of cholinotoxin. o 1993 Wiiey-Liss, inc.

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Protective effect of the calcium antagonist nimodipine on discrimination learning deficits and impaired retention behavior caused by prenatal nitrite exposure in rats

Cited by 18 publications

References 19 publications

Impaired Learning and Abnormal Open‐field Behaviours of Rats After Early Postnatal Anoxia and the Beneficial Effect of the Calcium Antagonist Nimodipine

Impaired Learning and Abnormal Open‐field Behaviours of Rats After Early Postnatal Anoxia and the Beneficial Effect of the Calcium Antagonist Nimodipine

Nimodipine accelerates the postnatal development of parvalbumin and S-100β immunoreactivity in the rat brain

Amiridine (NIK‐247) and cerebrocrast in the alleviation of cholinergic lesion‐induced learning deficit in male rats

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