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Notably, postnatal CPF ameliorated the anxiety-like and the heightened HFD-seeking responses in adult apoE4 female mice, while caused them to gain weight steadily compared to control peers. In turn, an early-life transient exposure to CPF fostered the over-consumption of HFD during adulthood without affecting how much this reward was "wanted" or the total caloric intake. These data reveal a role for CPF towards fostering "unhealthy" dietary choices. We conclude that the APOE4 genotype modulates non-cognitive behaviours and we provide support for an APOE4-dependent cholinergic dysfunction. Intracerebroventricular (icv) administration of streptozotocin (STZ) has been used as a metabolic model of sporadic Alzheimer's disease (AD). Erythropoietin (EPO) possesses neuroprotective and memory-improving effects, which might be advantageous in treating different characteristics of AD. Nevertheless, the hematopoietic effect of EPO has hindered its application as a neuroprotective agent. Previous studies have shown that a new Epo derivative called carbamylated Erythropoietin-Fc (CEPO-Fc), yield noticeable neuroprotective effects without affecting hematopoiesis. In this study, the neuroprotective effects of CEPO-Fc on icv-STZ induced memory impairment and hippocampal apoptosis were examined. Adult male Wistar rats weighing 250-300 g were used. STZ was administered on days 1 and 3 (3 mg/kg in divided doses/icv), and CEPO-Fc was administered at the dose of 5000 IU/ip/daily during days 4-14. The animals were trained in Morris water maze during days 15-17, and the memory retention test was performed on the 18th day. Following behavioral studies, the animals were sacrificed and their hippocampi isolated to determine the amounts of cleaved caspase-3 (the landmark of apoptosis). The results showed that CEPO-Fc treatment at the dose of 5000 IU/kg/ip was able to prevent the learning and memory deficit induced by icv-STZ. Western blot analysis revealed that STZ prompted the cleavage of caspase-3 in the hippocampus while pretreatment with CEPO-Fc significantly reduced the cleavage of this protein. Collectively, our findings suggest that CEPO-Fc could restore STZ-induced learning and memory impairment as well as apoptosis in the hippocampal region in a rat model of sporadic AD induced by icv-STZ. We performed optogenetic inactivation of rats' entopeduncular nucleus (EP, homologous to primates' globus pallidus interna (GPi)) and investigated the therapeutic effect in a rat model of PD. 6-Hydroxydopamine (6-OHDA)-induced hemiparkinsonian rats were injected with either a virus for halorhodopsin expression that is used to inactivate GABAergic neurons or a control virus injection and received optic fiber insertion. All the rats were illuminated by 590 nm of light. Each rat was then subjected to sequential sessions of stepping tests under controlled illumination patterns. The stepping test is a reliable evaluation method for forelimb akinesia. The number of adjusting steps was significantly higher in experimental (optogene with reporter gene expression) (5Hz - 10ms 15.7 ± 1.9, 5Hz - 100ms 16.0 ± 1.8, continuous 21.6 ± 1.9) than control rats (reporter gene expression) (5Hz-10ms 1.9 ± 1.1, 5Hz-100ms 2.6 ± 1.0, continuous 2.5 ± 1.2) (p less then 0.001). Continuous EP illumination showed a significantly higher improvement of forelimb akinesia than other illumination patterns (p less then 0.01). Optogene expression in the GABAergic neurons of the EP was confirmed by immunohistochemistry. Optogenetic inhibition of EP was effective to improve contralateral forelimb akinesia. However, further studies using prolonged illumination are needed to investigate the best illumination pattern for optogenetic stimulation. V.Chronic social defeat stress (CSDS) has been found to produce different impacts on anxiety-like behaviors, spatial cognitive function and memory in rodents with different susceptibilities. However, the impacts of chronic social defeat on social behaviors in adult male mice with different susceptibilities to social defeat and the underlying mechanisms in the brain remain unclear. In the present study, we found that ten days of social defeat reduced the tendency of susceptible adult male C57 mice to approach an unfamiliar individual and increased their avoidance of an unfamiliar CD-1 mouse but had no effects on resilient individuals. In addition, CSDS enhanced anxiety-like behavior in susceptible animals, but produced no effects in the resilient group. Meanwhile, CSDS increased the number of corticotropin-releasing factor (CRF)-positive neurons in the paraventricular nucleus of the hypothalamus and CRF-R2-positive neurons in the accumbens nucleus shell in both resilient and susceptible animals. Selleck PTC-209 CSDS increased the number of CRF-R1-positive neurons and CRF-R1 mRNA expression in the prelimbic cortex (PrL) and the number of CRF-R2-positive neurons in the basolateral amygdala, but reduced the number of CRF-R2-positive neurons and mRNA expression in the PrL in susceptible animals. Therefore, the different effects of CSDS on sociability and anxiety-like behavior in mice with different susceptibilities may be associated with region- and type-specific alterations in CRF receptor levels. These findings help us understand the underlying mechanism by which social stress affects emotion and social behavior and provides an important basis for the treatment of disorders of social and emotional behavior caused by social stress. Calorie restriction (CR) is the most potent, non-pharmacological intervention to support metabolic health. The effects of calorie restriction exceed weight loss. Consistent throughout many studies, calorie restriction induces a reduction in energy expenditure that is larger than the loss of metabolic mass, i.e. fat-free mass and fat mass, can explain. Per prevailing theories of mammalian aging, this disproportionate reduction in metabolic rate, defined as metabolic adaptation, reduces oxidative damage and thereby delays age-associated declines in physiological function. The aim of this narrative review is to investigate the origins of CR-induced metabolic adaptation. From a physiological standpoint this likely relates to the composition of body weight loss, reductions in insulin secretion, thyroid and leptin concentrations, and increased mitochondrial energy efficiency. Behavioral factors including physical activity and eating behaviors likely also play a role, specifically to prevent weight regain. Future studies are required to understand the interindividual differences in the response to CR, e.