Effects of Apoaequorin on Trace Fear Learning and Cytokine Expression in Adult and Aged Rats
Mentor 1
James Moyer
Location
Union Wisconsin Room
Start Date
29-4-2016 1:30 PM
End Date
29-4-2016 3:30 PM
Description
The hippocampus is well-recognized for its role in learning and memory. However, this region of the brain can be susceptible to aging-related dysfunction, resulting in cognitive decline. Our lab has used acquisition and extinction of hippocampus-dependent trace fear conditioning to study cognitive decline in aged rats. In the present study, two specific possible processes contributing to behavioral deficits seen in trace fear learning have been identified: 1) calcium (Ca2+) dysregulation and 2) poorly modulated cytokine expression. Previous data from our lab suggests that an intrahippocampal infusion of the Ca2+-binding protein (CaBP) apoaequorin (AQ) protects neurons from a subsequent ischemic insult, a process characterized by calcium-induced excitotoxicity. The intrahippocampal infusion of AQ also alters expression of several cytokines and chemokines, including the anti-inflammatory cytokine interleukin-10 (IL-10) and the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα). Thus, the neuroprotective effects of AQ may also involve a neuroimmunomodulatory component. However, the effects of AQ on trace fear memory as well as cytokine expression in aged animals has yet to be investigated. Thus, in the current study adult and aged rats will receive intrahippocampal infusions of AQ (or vehicle) to assess whether AQ impacts trace fear conditioning, after which the hippocampus will be processed for Western blot analyses of IL-10 and TNFα protein expression. These data will shed light on the possibility that AQ administration may have differential effects on aged animals.
Effects of Apoaequorin on Trace Fear Learning and Cytokine Expression in Adult and Aged Rats
Union Wisconsin Room
The hippocampus is well-recognized for its role in learning and memory. However, this region of the brain can be susceptible to aging-related dysfunction, resulting in cognitive decline. Our lab has used acquisition and extinction of hippocampus-dependent trace fear conditioning to study cognitive decline in aged rats. In the present study, two specific possible processes contributing to behavioral deficits seen in trace fear learning have been identified: 1) calcium (Ca2+) dysregulation and 2) poorly modulated cytokine expression. Previous data from our lab suggests that an intrahippocampal infusion of the Ca2+-binding protein (CaBP) apoaequorin (AQ) protects neurons from a subsequent ischemic insult, a process characterized by calcium-induced excitotoxicity. The intrahippocampal infusion of AQ also alters expression of several cytokines and chemokines, including the anti-inflammatory cytokine interleukin-10 (IL-10) and the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα). Thus, the neuroprotective effects of AQ may also involve a neuroimmunomodulatory component. However, the effects of AQ on trace fear memory as well as cytokine expression in aged animals has yet to be investigated. Thus, in the current study adult and aged rats will receive intrahippocampal infusions of AQ (or vehicle) to assess whether AQ impacts trace fear conditioning, after which the hippocampus will be processed for Western blot analyses of IL-10 and TNFα protein expression. These data will shed light on the possibility that AQ administration may have differential effects on aged animals.
