Stress during first gestation of ewes impairs memory and learning of male offspring

Henrique, Fábio Luís; Zanella, Adroaldo José; Bezerra, Helena Viel Alves; Polato, Heloise Zavatieri; Fernandes, Arícia Christofaro; Hooper, Henrique Barbosa; Pulido-Rodríguez, Lina Fernanda; Titto, Evaldo Antônio Lencioni; Pereira, Alfredo Manuel Franco; Titto, Cristiane Gonçalves

doi:10.1007/s11259-021-09805-3

Cited by 2 publications

(2 citation statements)

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“…Pro-inflammatory mediators cross the dysfunctional placental and blood–brain barriers to enter the fetal blood circulation and brain, thereby elevating concentrations of cytokines in fetuses during and after LPS-induced MIA ( Simões et al, 2018 ; Cadaret et al, 2019 ). In addition, fetuses in utero trigger their own inflammatory response and promote the production of inflammatory cytokines after MIA ( Elovitz et al, 2011 ; Henrique et al, 2021 ). These changes have the capacity to modulate fetal neurodevelopmental trajectories, thereby impairing cognitive performance in adult offspring ( Henrique et al, 2021 ; Guma et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, fetuses in utero trigger their own inflammatory response and promote the production of inflammatory cytokines after MIA ( Elovitz et al, 2011 ; Henrique et al, 2021 ). These changes have the capacity to modulate fetal neurodevelopmental trajectories, thereby impairing cognitive performance in adult offspring ( Henrique et al, 2021 ; Guma et al, 2022 ). However, only a limited number of studies have investigated the age-associated cognitive consequences of prenatal MIA exposure in these offspring, especially after midlife.…”

Section: Introductionmentioning

confidence: 99%

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Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Zhang²,

Li³

et al. 2022

Front. Aging Neurosci.

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IntroductionResearch suggests that prenatal inflammatory exposure could accelerate age-related cognitive decline that may be resulted from neuroinflammation and synaptic dysfunction during aging. Environmental enrichment (EE) may mitigate the cognitive and synaptic deficits. Neurite growth-promoting factor 2 (NGPF2) and postsynaptic density protein 95 (PSD-95) play critical roles in neuroinflammation and synaptic function, respectively.MethodsWe examined whether this adversity and EE exposure can cause alterations in Ngpf2 and Psd-95 expression. In this study, CD-1 mice received intraperitoneal injection of lipopolysaccharide (50 μg/kg) or normal saline from gestational days 15–17. After weaning, half of the male offspring under each treatment were exposed to EE. The Morris water maze was used to assess spatial learning and memory at 3 and 15 months of age, whereas quantitative real-time polymerase chain reaction and Western blotting were used to measure hippocampal mRNA and protein levels of NGPF2 and PSD-95, respectively. Meanwhile, serum levels of IL-6, IL-1β, and TNF-α were determined by enzyme-linked immunosorbent assay.ResultsThe results showed that aged mice exhibited poor spatial learning and memory ability, elevated NGPF2 mRNA and protein levels, and decreased PSD-95 mRNA and protein levels relative to their young counterparts during natural aging. Embryonic inflammatory exposure accelerated age-related changes in spatial cognition, and in Ngpf2 and Psd-95 expression. Additionally, the levels of Ngpf2 and Psd-95 products were significantly positively and negatively correlated with cognitive dysfunction, respectively, particularly in prenatal inflammation-exposed aged mice. Changes in serum levels of IL-6, IL-1β, and TNF-α reflective of systemic inflammation and their correlation with cognitive decline during accelerated aging were similar to those of hippocampal NGPF2. EE exposure could partially restore the accelerated decline in age-related cognitive function and in Psd-95 expression, especially in aged mice.DiscussionOverall, the aggravated cognitive disabilities in aged mice may be related to the alterations in Ngpf2 and Psd-95 expression and in systemic state of inflammation due to prenatal inflammatory exposure, and long-term EE exposure may ameliorate this cognitive impairment by upregulating Psd-95 expression.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Zhang²,

Li³

et al. 2022

Front. Aging Neurosci.

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Pathophysiology of Fever and Application of Infrared Thermography (IRT) in the Detection of Sick Domestic Animals: Recent Advances

Mota-Rojas

Wang

Titto

et al. 2021

Animals

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Body-temperature elevations are multifactorial in origin and classified as hyperthermia as a rise in temperature due to alterations in the thermoregulation mechanism; the body loses the ability to control or regulate body temperature. In contrast, fever is a controlled state, since the body adjusts its stable temperature range to increase body temperature without losing the thermoregulation capacity. Fever refers to an acute phase response that confers a survival benefit on the body, raising core body temperature during infection or systemic inflammation processes to reduce the survival and proliferation of infectious pathogens by altering temperature, restriction of essential nutrients, and the activation of an immune reaction. However, once the infection resolves, the febrile response must be tightly regulated to avoid excessive tissue damage. During fever, neurological, endocrine, immunological, and metabolic changes occur that cause an increase in the stable temperature range, which allows the core body temperature to be considerably increased to stop the invasion of the offending agent and restrict the damage to the organism. There are different metabolic mechanisms of thermoregulation in the febrile response at the central and peripheral levels and cellular events. In response to cold or heat, the brain triggers thermoregulatory responses to coping with changes in body temperature, including autonomic effectors, such as thermogenesis, vasodilation, sweating, and behavioral mechanisms, that trigger flexible, goal-oriented actions, such as seeking heat or cold, nest building, and postural extension. Infrared thermography (IRT) has proven to be a reliable method for the early detection of pathologies affecting animal health and welfare that represent economic losses for farmers. However, the standardization of protocols for IRT use is still needed. Together with the complete understanding of the physiological and behavioral responses involved in the febrile process, it is possible to have timely solutions to serious problem situations. For this reason, the present review aims to analyze the new findings in pathophysiological mechanisms of the febrile process, the heat-loss mechanisms in an animal with fever, thermoregulation, the adverse effects of fever, and recent scientific findings related to different pathologies in farm animals through the use of IRT.

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Stress during first gestation of ewes impairs memory and learning of male offspring

Cited by 2 publications

References 53 publications

Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Pathophysiology of Fever and Application of Infrared Thermography (IRT) in the Detection of Sick Domestic Animals: Recent Advances

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