HuanHuan Fu1, WeiWei Chen1, HongPing Yu2, ZhenZhen Wei1, XiaoDan Yu3. 1. MOE-Shanghai Key Lab of Children Environmental Health, XinHua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. 2. Department of Epidemiology, School of Public Health, Guilin Medical University, Guangxi, China. 3. MOE-Shanghai Key Lab of Children Environmental Health, XinHua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: xd_yu2003@126.com.
Abstract
BACKGROUND: The effects and mechanisms of preweaning Manganese (Mn) exposure on cognitive dysfunction remain unclear. OBJECTIVE: This study evaluated the effects of preweaning Mn exposure on spatial learning and memory as well as the protein expression of CaMKIIα and p-CaMKIIα. METHODS: We treated neonate rats with Mn(2+) doses of 0 (control group), 10, 20 and 30mg of Mn(2+) per kg body weight (Mn-exposed groups) over postnatal day (PND) 1-21 by intraperitoneal injection. The ability of spatial learning and memory was tested on PND 22 using the Morris water maze (MWM), while the protein expressions of CaMKIIα and p-CaMKIIα in the hippocampus were evaluated by Western blotting. The levels of Mn in the blood and hippocampus were measured by inductively coupled plasma-mass spectrometry (ICP-MS). RESULTS: The rats in Mn-exposed groups showed a significant delay in spatial learning ability on the third day of the MWM without dose-dependent differences, but there was no effect on the spatial memory ability. p-CaMKIIα, but not CaMKIIα protein expression significantly reduced in the Mn-exposed group. CONCLUSION: These findings suggested that the inhibition of p-CaMKIIα could be one of the mechanisms involved in the occurrence of Mn-induced cognitive impairments.
BACKGROUND: The effects and mechanisms of preweaning Manganese (Mn) exposure on cognitive dysfunction remain unclear. OBJECTIVE: This study evaluated the effects of preweaning Mn exposure on spatial learning and memory as well as the protein expression of CaMKIIα and p-CaMKIIα. METHODS: We treated neonate rats with Mn(2+) doses of 0 (control group), 10, 20 and 30mg of Mn(2+) per kg body weight (Mn-exposed groups) over postnatal day (PND) 1-21 by intraperitoneal injection. The ability of spatial learning and memory was tested on PND 22 using the Morris water maze (MWM), while the protein expressions of CaMKIIα and p-CaMKIIα in the hippocampus were evaluated by Western blotting. The levels of Mn in the blood and hippocampus were measured by inductively coupled plasma-mass spectrometry (ICP-MS). RESULTS: The rats in Mn-exposed groups showed a significant delay in spatial learning ability on the third day of the MWM without dose-dependent differences, but there was no effect on the spatial memory ability. p-CaMKIIα, but not CaMKIIα protein expression significantly reduced in the Mn-exposed group. CONCLUSION: These findings suggested that the inhibition of p-CaMKIIα could be one of the mechanisms involved in the occurrence of Mn-induced cognitive impairments.