Eastern Equine Encephalitis Virus (EEEV) is the most pathogenic arbovirus endemic to the United States. EEEV primarily infects birds but can be fatal to humans, horses, and some other mammals. Although EEEV transmission occurs in the Northeastern, Southeastern, and Midwestern United States, the largest number of horse and human cases have been reported in Florida, the only state where transmission occurs year round. Currently, a GIS-based risk index (RI) model is used to map EEE transmission risk to horses in Florida. This study validates that RI model using a 5-yr dataset of horse cases in Florida. RI values were similar between summer (N = 152, x¯ = 0.59) and winter (N = 25, x¯ = 0.66) cases, suggesting the model is effective for mapping risk during both transmission seasons. These risk values were larger and remained similar when a 100-m buffer was applied to the case locations to account for modest spatial errors in case reporting (summer x¯ = 0.73, winter x¯ = 0.77). In both comparisons, RI values for summer and winter cases were higher than expected at random in the Panhandle, North, and Central regions of the state, although the analysis was inconclusive in the South, where only two cases were observed. This suggests the RI map could be used to target EEEV surveillance, prevention, and control efforts in both transmission seasons in Florida.
Background Small conductance, calcium-activated (SK3) potassium channels control the intrinsic excitability of dopaminergic neurons (DN) in the midbrain and modulate their susceptibility to toxic insults during development. Methods We evaluated the age-dependency of the neuroprotective effect of an SK3 agonist, 1-Ethyl-1,3-dihydro-2H-benzimidazol-2-one (1-EBIO), on Amino-3-hydroxy-5-methylisoxazole-4propionic acid (AMPA) excitotoxicity to DN in ventral mesencephalon (VM) organotypic cultures. Results Most tyrosine hydroxylase (TH)+ neurons were also SK3+; SK3+/TH-cells (DN+) were common at each developmental stage but more prominently at day in vitro (DIV) 8. Young DN+ neurons were small bipolar and fusiform, whereas mature ones were large and multipolar. Exposure of organotypic cultures to AMPA (100 μm, 16 h) had no effect on the survival of DN+ at DIV 8, but caused significant toxicity at DIV 15 (n = 15, p = 0.005) and DIV 22 (n = 15, p<0.001). These results indicate that susceptibility of DN to AMPA excitotoxicity is developmental stage-dependent in embryonic VM organotypic cultures. Immature DN+ (small, bipolar) were increased after AMPA (100 μm, 16 h) at DIV 8, at the expense of the number of differentiated (large, multipolar) DN+ (p = 0.039). This effect was larger at DIV 15 (p<<<0.0001) and at DIV 22 (p<<<0.0001). At DIV 8, 30 μM 1-EBIO resulted in a large increase in DN+. At DIV 15, AMPA toxicity was prevented by exposure to 30 μM, but not
calcium-activated potassium channel 3 also known as K Ca 2.3; DIV: days in vitro; DN: dopaminergic neurons. AbstractWe evaluated the age-dependency of the neuroprotective effect of an small-conductance calcium activated potassium channel 3 (SK3) agonist, 1-EBIO, on AMPA excitoxicity to dopaminergic neurons (DN) in organotypic cultures. Most TH+ neurons were also SK3+. SK3+/TH-cells (DN+) were common at each developmental stage but more prominently at day in vitro (DIV) 8. Young DN+ neurons were small bipolar and fusiform, whereas mature ones were large and multipolar. Exposure of organotypic cultures to AMPA (100 μm, 16 h) had no effect on the survival of DN+ at DIV 8, but caused significant toxicity at DIV 15 (n=15, p=0.005) and DIV 22 (n=15, p<<0.001). These results indicate that susceptibility of DN to AMPA excitotoxicity is developmental stage-dependent in embryonic VM organotypic cultures. Immature DN+ (small, bipolar) were increased after AMPA (100 μm, 16 h) at DIV 8, at the expense of the number of differentiated (large, multipolar) DN+ (p=0.039). This effect was larger at DIV 15 (p<<<0.0001) and at DIV 22 (p<<<0.0001). At DIV 8, 30 μM 1-EBIO resulted in a large increase in DN+. At DIV 15, AMPA toxicity was prevented by exposure to 30 μM, but not 100 μM 1-EBIO. At DIV 22, excitotoxicity was unaffected by 30 μM 1-EBIO, and partially reduced by 100 μM 1-EBIO. The effects of the SK3. channel agonist 1-EBIO on the survival of SK3.-expressing dopaminergic neurons were concentrationdependent and influenced by neuronal developmental stage.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.