“…Previously, prenatal exposure to CA at the doses of 20 mg/kg and 40 mg/kg undoubtedly impaired spatial learning ability . 17, 35 Therefore, we only employed the dose of 20 mg/kg in the following tests.Figure 1.ACh levels in the hippocampus and performance in the Y-maze task (A) The expression of ACh is reduced following prenatal CA exposure. #, p < .05, vs. CA (20); %, p < .05, vs. others.…”
Section: Resultsmentioning
confidence: 99%
“…The doses of CA were used according to the doses used by the previous studies. 12,17,35 Each litter was standardized on the day after birth to 8–13 pups, with the similar number of males and females. Since the sex-specific effect of CA in the CNS has not yet well been defined, only male offspring were selected for this study.…”
Section: Methodsmentioning
confidence: 99%
“…Previously, prenatal exposure to CA at the doses of 20 mg/kg and 40 mg/kg undoubtedly impaired spatial learning ability . 17,35 Therefore, we only employed the dose of 20 mg/kg in the following tests.…”
Section: The Ach Levels In the Ca Groupsmentioning
confidence: 99%
“…33,34 More importantly, prenatal CA exposure compromises learning and memory encoding by functionally disrupting synaptic transmission. 17,35 Meanwhile, intrahippocampal infusion with ACh could mitigate the weakened neural information flow (NIF) induced by prenatal melamine treatment. 15 Little is known about whether prenatal CA exposure influences ACh expression or whether this change is sufficient to obstruct hippocampal NIF.…”
Cyanuric acid (CA) is reported to induce nephrotoxicity but its toxic effect is not fully known. Prenatal CA exposure causes neurodevelopmental deficits and abnormal behavior in spatial learning ability. Dysfunction of the acetyl-cholinergic system in neural information processing is correlated with spatial learning impairment and was found in the previous reports of CA structural analogue melamine. To further investigate the neurotoxic effects and the potential mechanism, the acetylcholine (ACh) level was detected in the rats which were exposed to CA during the whole of gestation. Local field potentials (LFPs) were recorded when rats infused with ACh or cholinergic receptor agonist into hippocampal CA3 or CA1 region were trained in the Y-maze task. We found the expression of ACh in the hippocampus was significantly reduced in dose-dependent manners. Intra-hippocampal infusion of ACh into the CA1 but not the CA3 region could effectively mitigate learning deficits induced by CA exposure. However, activation of cholinergic receptors did not rescue the learning impairments. In the LFP recording, we found that the hippocampal ACh infusions could enhance the values of phase synchronization between CA3 and CA1 regions in theta and alpha oscillations. Meanwhile, the reduction in the coupling directional index and the strength of CA3 driving CA1 in the CA-treated groups was also reversed by the ACh infusions. Our findings are consistent with the hypothesis and provide the first evidence that prenatal CA exposure induced spatial learning defect is attributed to the weakened ACh-mediated neuronal coupling and NIF in the CA3-CA1 pathway.
“…Previously, prenatal exposure to CA at the doses of 20 mg/kg and 40 mg/kg undoubtedly impaired spatial learning ability . 17, 35 Therefore, we only employed the dose of 20 mg/kg in the following tests.Figure 1.ACh levels in the hippocampus and performance in the Y-maze task (A) The expression of ACh is reduced following prenatal CA exposure. #, p < .05, vs. CA (20); %, p < .05, vs. others.…”
Section: Resultsmentioning
confidence: 99%
“…The doses of CA were used according to the doses used by the previous studies. 12,17,35 Each litter was standardized on the day after birth to 8–13 pups, with the similar number of males and females. Since the sex-specific effect of CA in the CNS has not yet well been defined, only male offspring were selected for this study.…”
Section: Methodsmentioning
confidence: 99%
“…Previously, prenatal exposure to CA at the doses of 20 mg/kg and 40 mg/kg undoubtedly impaired spatial learning ability . 17,35 Therefore, we only employed the dose of 20 mg/kg in the following tests.…”
Section: The Ach Levels In the Ca Groupsmentioning
confidence: 99%
“…33,34 More importantly, prenatal CA exposure compromises learning and memory encoding by functionally disrupting synaptic transmission. 17,35 Meanwhile, intrahippocampal infusion with ACh could mitigate the weakened neural information flow (NIF) induced by prenatal melamine treatment. 15 Little is known about whether prenatal CA exposure influences ACh expression or whether this change is sufficient to obstruct hippocampal NIF.…”
Cyanuric acid (CA) is reported to induce nephrotoxicity but its toxic effect is not fully known. Prenatal CA exposure causes neurodevelopmental deficits and abnormal behavior in spatial learning ability. Dysfunction of the acetyl-cholinergic system in neural information processing is correlated with spatial learning impairment and was found in the previous reports of CA structural analogue melamine. To further investigate the neurotoxic effects and the potential mechanism, the acetylcholine (ACh) level was detected in the rats which were exposed to CA during the whole of gestation. Local field potentials (LFPs) were recorded when rats infused with ACh or cholinergic receptor agonist into hippocampal CA3 or CA1 region were trained in the Y-maze task. We found the expression of ACh in the hippocampus was significantly reduced in dose-dependent manners. Intra-hippocampal infusion of ACh into the CA1 but not the CA3 region could effectively mitigate learning deficits induced by CA exposure. However, activation of cholinergic receptors did not rescue the learning impairments. In the LFP recording, we found that the hippocampal ACh infusions could enhance the values of phase synchronization between CA3 and CA1 regions in theta and alpha oscillations. Meanwhile, the reduction in the coupling directional index and the strength of CA3 driving CA1 in the CA-treated groups was also reversed by the ACh infusions. Our findings are consistent with the hypothesis and provide the first evidence that prenatal CA exposure induced spatial learning defect is attributed to the weakened ACh-mediated neuronal coupling and NIF in the CA3-CA1 pathway.
“…The co-exposure severely impairs neuronal and synaptic functions, reducing the amplitude, decay time, and frequency of miniature excitatory postsynaptic currents (mEPSCs) without affecting miniature inhibitory postsynaptic currents (mIPSCs) ( 31 ). Prenatal exposure to cyanuric acid elevates alkaline phosphatase levels in the maternal placenta and fetal brains ( 32 ).…”
Section: Study On Health Risk and Control Standard Of Cyanuric Acid I...mentioning
Cyanuric acid is a widely used fine chemical intermediate that acts as a free chlorine buffer in swimming pool water, wherein it is often used as a stabilizer to maintain the germicidal efficacy of chlorinated disinfectants. However, it has also been associated with health risks. Herein, we introduced the sources and functions of cyanuric acid in swimming pool water, focusing on potential health risks associated with excessive concentration of the component and the current control standards worldwide. Also, the prevention and control measures were summarized in terms of physical chemistry, biodegradation, and ultraviolet radiation to provide a basis for the development of public health policies for swimming pool management.
Prenatal exposure to maternal infection increases the risk of offspring developing schizophrenia in adulthood. Current theories suggest that the consequences of MIA on mBDNF secretion may underlie the increased risk of cognitive disorder. There is little evidence for whether the expression of its precursor, proBDNF, is changed and how proBDNF-mediated signaling may involve in learning and memory. In this study, proBDNF levels were detected in the hippocampal CA1 and CA3 regions of male adult rats following MIA by prenatal polyI:C exposure. Behaviorally, learning and memory were assessed in contextual fear conditioning tasks. Local field potentials were recorded in the hippocampal CA3-CA1 pathway. The General Partial Directed Coherence approach was utilized to identify the directional alternation of neural information flow between CA3 and CA1 regions. EPSCs were recorded in CA1 pyramidal neurons to explore a possible mechanism involving the proBDNF-p75NTR signaling pathway. Results showed that the expression of proBDNF in the polyI:C-treated offspring was abnormally enhanced in both CA3 and CA1 regions. Meanwhile, the mBDNF expression was reduced in both hippocampal regions. Intra-hippocampal CA1 but not CA3 injection with anti-proBDNF antibody and p75NTR inhibitor TAT-Pep5 effectively mitigated the contextual memory deficits. Meanwhile, reductions in the phase synchronization between CA3 and CA1 and the coupling directional indexes from CA3 to CA1 were enhanced by the intra-CA1 infusions. Moreover, blocking proBDNF/p75NTR signaling could reverse the declined amplitude of EPSCs in CA1 pyramidal neurons, indicating the changes in postsynaptic information processing in the polyI:C-treated offspring. Therefore, the changes in hippocampal proBDNF activity in prenatal polyI:C exposure represent a potential mechanism involved in NIF disruption leading to contextual memory impairments.
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