Mitigation of postnatal ethanol-induced neuroinflammation ameliorates trace fear memory deficits in juvenile rats

Histamine 2/3 receptor agonists alleviate perioperative neurocognitive disorders by inhibiting microglia activation through the PI3K/AKT/FoxO1 pathway in aged rats

“…These results could be supported by a mouse model with a disrupted H3 receptor (H3RKO), in which more severe disease and neuroinflammation developed compared with those of wild-type animals [ 42 ]. Current studies indicate that neuroinflammation plays a vital role in the pathogenesis of several disorders and can induce cognitive decline [ 43 – 45 ]. Thus, we further examined the cognitive function of the rats and discovered that rats that underwent exploratory laparotomy experienced serious cognitive declines in trace fear conditioning, while those that were pretreated with the H2R/H3R agonists in the lateral ventricles did not show obvious cognitive differences.…”

Neonatal ethanol exposure impairs long-term context memory formation and prefrontal immediate early gene expression in adolescent rats

“…Sensitivity of CA1 pyramidal neurons is at its peak during this third-trimester equivalent period, with no additional decreases when combined with first and second trimester-equivalent exposure [26]. During this period of cell loss, there is also a stark increase in neuroinflammation, cytokine production (e.g., increased interleukin 1 beta and tumor necrosis factor), DNA methyltransferase activity, and global DNA methylation in the hippocampus in ethanolexposed rats [28,30,65,66]. Increased DNA methylation generally results in a restrictive state for gene expression and thus could have a negative impact on experience-dependent plasticity [30].…”

“…Animal model research has focused on ethanol-induced alterations in hippocampal neuroanatomy and function, and impaired performance in "hippocampal-dependent" behavioral paradigms. For example, ethanol-induced behavioral impairments are seen in spatial navigation in the Morris water maze [25,[69][70][71][72][73], spatial alternation learning in the T-Maze [74,75], delay and trace eyeblink conditioning [56,[76][77][78], in addition to contextual and trace fear conditioning [24,27,80,81,28,29,[37][38][39]51,65,79]. Although deficits are largely attributed to the hippocampus, the medial prefrontal cortex is also required or engaged in the behavioral paradigms in which neonatal alcohol exposure has the most disruptive effects.…”

“…Although deficits are largely attributed to the hippocampus, the medial prefrontal cortex is also required or engaged in the behavioral paradigms in which neonatal alcohol exposure has the most disruptive effects. For example, PD4-9 ethanol exposure severely disrupts trace fear conditioning to a tone CS and to the background context in which the tone is presented [28,29,51,65,[79][80][81]. Successful acquisition and consolidation of a long-term trace fear conditioning memory generally depends on activity and NMDAR plasticity in the medial prefrontal cortex and dorsal hippocampus, and, in some cases, the ventral hippocampus [82][83][84][85][86][87].…”

Sex Differences in Context-Driven Reinstatement of Methamphetamine Seeking Is Associated with Distinct Neuroadaptations in the Dentate Gyrus<strong> </strong>

“…These findings suggest that changes in the density of axons of mature GCNs are perhaps influenced to a greater extent in females than males, and in males are compensatory to the effects on mature progenitors. It is also evident that newly born progenitors contribute to neuroimmune responses in the DG (Klaus et al, 2016;Marshall et al, 2016;Peng et al, 2017;Goodfellow et al, 2018). Furthermore, high doses of methamphetamine experience is associated with microglial activation in the DG (Buchanan et al, 2010).…”