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Disruption of calmodulin-dependent protein kinase II α/brain-derived neurotrophic factor (α-CaMKII/BDNF) signalling is associated with zinc deficiency-induced impairments in cognitive and synaptic plasticity.
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- Author(s): Yu, XiaoDan; Ren, TianHong; Yu, XiaoGang
- Source:
British Journal of Nutrition; 12/28/2013, Vol. 110 Issue 12, p2194-2200, 7p- Subject Terms:
ANALYSIS of variance; ANIMAL experimentation; CELLULAR signal transduction; CHEMILUMINESCENCE assay; COGNITION disorders; COMPARATIVE studies; DIETARY supplements; ELECTROPHYSIOLOGY; LACTATION; LEARNING; MEMORY in children; NEUROPLASTICITY; NUTRITION disorders; PEPTIDE hormones; PROBABILITY theory; PROTEIN kinases; RATS; RESEARCH funding; WESTERN immunoblotting; ZINC; DISEASE complications; CHILDREN; PREGNANCY - Source:
- Additional Information
- Abstract: Maternal dietary Zn deficiency during fetal development induces substantial cognitive dysfunctions in the resultant offspring. The mechanism underlying this effect is unclear. The present study evaluated whether the impairments caused by gestational and lactational Zn deficiency are mediated by the hippocampal calmodulin-dependent protein kinase II α (α-CaMKII)/brain-derived neurotrophic factor (BDNF) signalling pathway as well as whether they can be restored by postnatal Zn supplementation. Rats were randomly divided into four groups on the first day of pregnancy (n 12): control (CO) group; pair-fed (PF) group; Zn-deprived (ZD) group; orally Zn-supplemented group. The spatial memory of the offspring was tested at postnatal day 35 using the Morris water maze. Long-term potentiation (LTP) in the rat hippocampal medial perforant path–dentate gyrus pathway was evaluated simultaneously, and α-CaMKII and BDNF protein levels were examined by Western blot analysis. The results demonstrated that the ZD group exhibited a significantly longer latency period in the Morris water maze as well as a significantly decreased LTP amplitude compared with the CO and PF groups. α-CaMKII and BDNF protein expression in the hippocampus was significantly reduced in the ZD group. Postnatal Zn supplementation restored the cognitive dysfunction induced by gestational Zn deficiency but could not completely reverse the decreased LTP and α-CaMKII/BDNF protein levels. Our findings suggest that the α-CaMKII/BDNF signalling pathway may be involved in Zn deficiency-induced cognitive and synaptic impairments. [ABSTRACT FROM PUBLISHER]
- Abstract: Copyright of British Journal of Nutrition is the property of Cambridge University Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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