Lead exposure-induced cognitive impairment through RyR-modulating intracellular calcium signaling in aged rats

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

“…As Ca 2+ is indispensable for insulin and glucagon secretion, alterations in Ca 2+ homeostasis caused by DM can thus impact blood glucose [37]. Many studies suggest that Ca 2+ dysregulation could be a pivotal target of DM and might mediate the deleterious effects of DM on hippocampal function and behavior [10,38]. Moreover, accumulation of intracellular free Ca 2+ could also decrease the levels of Ca 2+ /calmodulin-dependent protein kinase II (CaMKII).…”

“…Moreover, accumulation of intracellular free Ca 2+ could also decrease the levels of Ca 2+ /calmodulin-dependent protein kinase II (CaMKII). As CaMKII regulated cAMP-response element binding protein (CREB) is involved in maintaining appropriate cognitive formation, disruption of calcium signaling by diabetic hyperglycemia can thus result in cognitive impairment [38] (Figure 1). Conversely, modulation of calcium-binding protein apoaequorin could have positive effects in treating cognitive dysfunction [39,40].…”

Sodium para-aminosalicylic acid ameliorates lead-induced hippocampal neuronal apoptosis by suppressing the activation of the IP3R-Ca2+-ASK1-p38 signaling pathway

“…In particular, the hippocampus, a brain region in the temporal lobe that is central to long-term memory formation, is a key target of Pb-induced effects ( Bakulski et al, 2020 ). Once Pb crosses the blood–brain barrier (BBB) and the blood-cerebrospinal fluid (CSF) barrier into the brain and accumulates in the hippocampus ( Ouyang et al, 2019 ), it may impair hippocampal structure and function. Although Pb affects the CNS of all ages of human and animals, the developing animals are particularly vulnerable to its toxicity, where it can disrupt cognitive and behavioral development, arresting children’s intellectual development, and culminating in cognitive and behavioral deficits ( Shadbegian et al, 2019 ; Reuben et al, 2020).…”

Developmental toxicity and neurotoxicity assessment of R-, S-, and RS-propylene glycol enantiomers in zebrafish (Danio rerio) larvae

“…Ryanodine receptors (RyRs) are calcium-dependent calcium release channels embedded in the sarcoplasmic/endoplasmic reticulum (SR/ER), which regulate calcium-dependent signal transduction in neurons or skeletal muscles (Frank et al, 2018;Tanaka et al, 2018). RyRs subunits contain a calciumbinding site that mediates calcium release and triggers intracellular calcium-induced calcium release, which is vital for muscle contraction (Ouyang et al, 2019;Wang et al, 2020b). RyRs have been characterized in many vertebrates including sh, birds, and amphibians (Darbandi & Franck, 2009;Murayama & Kurebayashi, 2011;Wang et al, 2020b).…”