Effects of preweaning environmental enrichment on hippocampus-dependent learning and memory in developing rats

Lu, Chengqiu; Zhong, Ling; Yan, Chen‐Hua; Tian, Ying; Shen, Xiaoming

doi:10.1016/j.neulet.2016.12.053

Cited by 7 publications

(5 citation statements)

References 25 publications

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“…The rat pups were randomly assigned to either an EE or a standard environment (SE), for 3 h per day from P15 to P70. The EE was designed strictly based on its definition (Duran‐Carabali et al., 2018; Hebb, 1947; Lu et al., 2017). In detail, eight rat pups were placed together into an enriched plastic cage (60 cm high, 85 cm wide, and 110 cm long) containing various toys of different shapes, colors, and textures, for example, running wheels, tubes, wooden, and metal plates (Figure 1b).…”

Section: Methodsmentioning

confidence: 99%

“…Multiple studies have shown that animals living in EE exhibited increased dendritic spine length, synaptic size, and postsynaptic thickening, as well as increased dendritic branching (Diamond et al., 1964; Sager et al., 2018; Sale et al., 2014). In addition, other researches have indicated that EE had powerful effects on hippocampal LTP (Lu et al., 2017; X. M. Wang et al., 2019). Moreover, neurotrophic factors (X. M. Wang et al., 2019) and neurotransmitter systems related to synaptic plasticity, such as the glutamatergic and GABAergic systems, can also be modulated by EE (Murueta‐Goyena et al., 2018; Rampon et al., 2000).…”

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Enriched environment rescues neonatal pain induced cognitive deficits and the impaired hippocampal synaptic plasticity later in life

Min

Ling

Chen

et al. 2022

Developmental Neurobiology

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Although extensive and untreated pain that occurs during a critical developmental window may impair cognition later in life, environmental interventions early in life might promote cognition. However, the underlying mechanism is poorly understood. Our current study utilized a rat model of "repetitive needle pricks" from the day of birth (P0) to postnatal day 7 (P7) to mimic the painful experience of preterm neonates in the neonatal intensive care unit. Enriched environment (EE) during development period (from P15 to P70) was implemented as a nonpharmacological intervention approach. Electrophysiological recording, behavioral tests, and biochemical analysis were performed after the end of EE (between P71 and P80). The results showed neonatal repetitive pain resulted in a reduction in mechanical withdrawal thresholds by the von Frey test in P70 (p < .001). Furthermore, neonatal repetitive pain impaired spatial learning and memory (p < .05) and even led to dysfunction in fear memory (p < .01). In contrast, EE rescued neonatal pain-induced cognitive deficits and normalized hippocampal long-term potentiation in rats exposed to neonatal pain (p << .05). The beneficial effect of EE might be the improvements in hippocampal synaptic plasticity via upregulating neurotrophic factors and N-methyl-D-aspartate (NMDA) receptors in the hippocampus. Our findings provide evidence that early environmental intervention might be a safe strategy to overcome neurodevelopmental abnormalities in preterm infants who experienced multiple procedural painful events during the early critical period.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Enriched environment rescues neonatal pain induced cognitive deficits and the impaired hippocampal synaptic plasticity later in life

Min

Ling

Chen

et al. 2022

Developmental Neurobiology

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“…The fact that pre-weaning pups are largely unable to engage in voluntary physical activity has led to limitations in EE-related studies focusing on early intervention. But existing researches are enough to prove the positive role that early EE plays in neurodevelopment in which dendrite branches (Venable et al, 1989 ), neuronal differentiation ability (Pascual and Figueroa, 1996 ), exploration activities, learning and memory ability (Lu et al, 2017 ), and inhibitory to excitatory balance (Feng et al, 2021 ) in the hippocampus are improved observably. Especially in the visual system, early EE can not only promote the development of the visual cortex but also accelerate the development of the retina in terms of substantially no plasticity.…”

Section: The Effects Of Ee On Neurodevelopment In Brainmentioning

confidence: 99%

The role of enriched environment in neural development and repair

Yuan

Guo

Shen

et al. 2022

Front. Cell. Neurosci.

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In addition to genetic information, environmental factors play an important role in the structure and function of nervous system and the occurrence and development of some nervous system diseases. Enriched environment (EE) can not only promote normal neural development through enhancing neuroplasticity but also play a nerve repair role in restoring functional activities during CNS injury by morphological and cellular and molecular adaptations in the brain. Different stages of development after birth respond to the environment to varying degrees. Therefore, we systematically review the pro-developmental and anti-stress value of EE during pregnancy, pre-weaning, and “adolescence” and analyze the difference in the effects of EE and its sub-components, especially with physical exercise. In our exploration of potential mechanisms that promote neurodevelopment, we have found that not all sub-components exert maximum value throughout the developmental phase, such as animals that do not respond to physical activity before weaning, and that EE is not superior to its sub-components in all respects. EE affects the developing and adult brain, resulting in some neuroplastic changes in the microscopic and macroscopic anatomy, finally contributing to enhanced learning and memory capacity. These positive promoting influences are particularly prominent regarding neural repair after neurobiological disorders. Taking cerebral ischemia as an example, we analyzed the molecular mediators of EE promoting repair from various dimensions. We found that EE does not always lead to positive effects on nerve repair, such as infarct size. In view of the classic issues such as standardization and relativity of EE have been thoroughly discussed, we finally focus on analyzing the essentiality of the time window of EE action and clinical translation in order to devote to the future research direction of EE and rapid and reasonable clinical application.

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“…In particular, it has proven to enhance performance in several learning and memory tasks. It has been shown to overcome learning defects caused by different genetic and neurological alterations (Lu et al, 2017). Given the proven e cacy of EE housing across diverse animal models, and the shortage of studies examining the effects of EtOH intake using an intermittent voluntary intake paradigm in combination with noise exposure, it would be of interest to investigate whether housing in an EE can prevent the effects produced by both agents in adolescent animals housed in SC.…”

mentioning

confidence: 99%

Assessment of Hippocampal-Related Behavioral Changes in Adolescent Rats of both Sexes Following Voluntary Intermittent Ethanol Intake and Noise Exposure: A Putative Underlying Mechanism and Implementation of a Non-pharmacological Preventive Strategy

Buján,

D’Alessio,

Serra

et al. 2024

Neurotox Res

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Effects of preweaning environmental enrichment on hippocampus-dependent learning and memory in developing rats

Cited by 7 publications

References 25 publications

Enriched environment rescues neonatal pain induced cognitive deficits and the impaired hippocampal synaptic plasticity later in life

Enriched environment rescues neonatal pain induced cognitive deficits and the impaired hippocampal synaptic plasticity later in life

The role of enriched environment in neural development and repair

Assessment of Hippocampal-Related Behavioral Changes in Adolescent Rats of both Sexes Following Voluntary Intermittent Ethanol Intake and Noise Exposure: A Putative Underlying Mechanism and Implementation of a Non-pharmacological Preventive Strategy

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