Effect of prenatal pentylenetetrazol-induced kindling on learning and memory of male offspring

Pourmotabbed, Ali; Nedaei, Seyed Ershad; Cheraghi, Maria; Moradian, Seyed Tayeb; Touhidi, A; Aeinfar, Mehrnoush; Seyfi, Z.; Pourmotabbed, Tayebeh

doi:10.1016/j.neuroscience.2010.11.001

Cited by 32 publications

(14 citation statements)

References 48 publications

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“…In contrast, benzodiazepine receptor antagonists, such as flumazenil [34] and CGS 8216 [36], attenuate amnesia induced by various benzodiazepines. Similar results were obtained by β-carboline, such as FG7142 [37], beta-CCM, [30,38,39], NO [40], and harmine [42]. It has been demonstrated that NO reversed anterograde amnesia-induced by brotizolam in rats.…”

Section: Discussionsupporting

confidence: 73%

“…The capability of a Benzodiazepine receptor inverse agonist to enhance acquisition and/or consolidation processes has been established in several different memory tasks [30][31][32]4]. The dose of β-carboline required for enhancing memory is usually lower than the dose required for eliciting anxiogenic actions [5,26] and this rule was replicated in our study.…”

Section: Discussionsupporting

confidence: 72%

See 1 more Smart Citation

Low and high doses of Norharmane respectively improve and impair learning and memory in streptozotocin-induced rat model of sporadic alzheimer’s disease

Hossein¹,

Charmchi²,

Behnaz³

2017

Alzheimers Dement Cogn Neurol

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Section: Discussionsupporting

confidence: 73%

Section: Discussionsupporting

confidence: 72%

Low and high doses of Norharmane respectively improve and impair learning and memory in streptozotocin-induced rat model of sporadic alzheimer’s disease

Hossein¹,

Charmchi²,

Behnaz³

2017

Alzheimers Dement Cogn Neurol

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“…In fact, it has been reported that hippocampal activity and synaptic reorganization get impaired following reduction of PSA-NCAM expression [51]. PTZ-induced seizures during pregnancy cause intensive cognition impairment, learning/memory deficits, neurodegeneration, and also neurodevelopmental impairments in offspring during the postnatal period [9,36]. Indeed, it has been shown that maternal seizures could cause an imbalance between excitatory and inhibitory interneurons, as well as impaired neuronal migration in the rat offspring hippocampi, and probably induce abnormalities in the structure and function of the hippocampus [6,15].…”

Section: Discussionmentioning

confidence: 99%

“…A recent study has shown that maternal seizures during pregnancy cause severe cognitive disturbances and decrease in learning and memory in the offspring [9]. In addition, it seems that some of the learning and memory disorders in adolescence and adulthood are probably due to neurogenesis impairment, neuronal migration failure, impaired hippocampal maturation, and neurodegeneration during the embryonic period [9-11]. …”

Section: Introductionmentioning

confidence: 99%

The effect of PTZ-induced epileptic seizures on hippocampal expression of PSA-NCAM in offspring born to kindled rats

et al. 2012

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BackgroundMaternal epileptic seizures during pregnancy can affect the hippocampal neurons in the offspring. The polysialylated neural cell adhesion molecule (PSA-NCAM), which is expressed in the developing central nervous system, may play important roles in neuronal migration, synaptogenesis, and axonal outgrowth. This study was designed to assess the effects of kindling either with or without maternal seizures on hippocampal PSA-NCAM expression in rat offspring.MethodsForty timed-pregnant Wistar rats were divided into four groups: A) Kind+/Seiz+, pregnant kindled (induced two weeks prior to pregnancy) rats that received repeated intraperitoneal (i.p.) pentylenetetrazol, PTZ injections on gestational days (GD) 14-19; B) Kind-/Seiz+, pregnant non-kindled rats that received PTZ injections on GD14-GD19; C) Kind+/Seiz-, pregnant kindled rats that did not receive any PTZ injections; and D) Kind-/Seiz-, the sham controls. Following birth, the pups were sacrificed on PD1 and PD14, and PSA-NCAM expression and localization in neonates’ hippocampi were analyzed by Western blots and immunohistochemistry.ResultsOur data show a significant down regulation of hippocampal PSA-NCAM expression in the offspring of Kind+/Seiz+ (p = 0.001) and Kind-/Seiz+ (p = 0.001) groups compared to the sham control group. The PSA-NCAM immunoreactivity was markedly decreased in all parts of the hippocampus, especially in the CA3 region, in Kind+/Seiz+ (p = 0.007) and Kind-/Seiz+ (p = 0.007) group’s newborns on both PD1 and 14.ConclusionOur findings demonstrate that maternal seizures but not kindling influence the expression of PSA-NCAM in the offspring’s hippocampi, which may be considered as a factor for learning/memory and cognitive impairments reported in children born to epileptic mothers.

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“…It causes neuroinflammation and oxidative stress, which affects cognition. In addition, PTZ has been observed to cause amnesia in animal models (Oscós-Alvarado and de Muñoz, 1981; Pourmotabbed et al, 2011; dos Santos Branco et al, 2013). It is also known to modulate glutamate receptors.…”

Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Jakaria

Park

Haque

et al. 2018

Front. Mol. Neurosci.

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Glutamate receptors play a crucial role in the central nervous system and are implicated in different brain disorders. They play a significant role in the pathogenesis of neurodegenerative diseases (NDDs) such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Although many studies on NDDs have been conducted, their exact pathophysiological characteristics are still not fully understood. In in vivo and in vitro models of neurotoxic-induced NDDs, neurotoxic agents are used to induce several neuronal injuries for the purpose of correlating them with the pathological characteristics of NDDs. Moreover, therapeutic drugs might be discovered based on the studies employing these models. In NDD models, different neurotoxic agents, namely, kainic acid, domoic acid, glutamate, β-N-Methylamino-L-alanine, amyloid beta, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 1-methyl-4-phenylpyridinium, rotenone, 3-Nitropropionic acid and methamphetamine can potently impair both ionotropic and metabotropic glutamate receptors, leading to the progression of toxicity. Many other neurotoxic agents mainly affect the functions of ionotropic glutamate receptors. We discuss particular neurotoxic agents that can act upon glutamate receptors so as to effectively mimic NDDs. The correlation of neurotoxic agent-induced disease characteristics with glutamate receptors would aid the discovery and development of therapeutic drugs for NDDs.

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Effect of prenatal pentylenetetrazol-induced kindling on learning and memory of male offspring

Cited by 32 publications

References 48 publications

Low and high doses of Norharmane respectively improve and impair learning and memory in streptozotocin-induced rat model of sporadic alzheimer’s disease

Low and high doses of Norharmane respectively improve and impair learning and memory in streptozotocin-induced rat model of sporadic alzheimer’s disease

The effect of PTZ-induced epileptic seizures on hippocampal expression of PSA-NCAM in offspring born to kindled rats

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

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