An enriched environment increases the expression of fibronectin type Ⅲ domain-containing protein 5 and brain-derived neurotrophic factor in the cerebral cortex of the ischemic mouse brain

Many studies have shown that fibronectin type III domain-containing protein 5(FDNC5) and brain-derived neurotrophic factor(BDNF) play vital roles in plasticity after brain injury. An enriched environment refers to an environment that provides animals with multi-sensory stimulation and movement opportunities. An enriched environment has been shown to promote the regeneration of nerve cells, synapses, and blood vessels in the animal brain after cerebral ischemia;however, the exact mechanisms have not been clarified. This study aimed to determine whether an enriched environment could improve neurobehavioral functions after the experimental inducement of cerebral ischemia and whether neurobehavioral outcomes were associated with the expression of FDNC5 and BDNF. This study established ischemic mouse models using permanent middle cerebral artery occlusion(pMCAO) on the left side. On postoperative day 1, the mice were randomly assigned to either enriched environment or standard housing condition groups. Mice in the standard housing condition group were housed and fed under standard conditions. Mice in the enriched environment group were housed in a large cage, containing various toys, and fed with a standard diet. Sham-operated mice received the same procedure, but without artery occlusion, and were housed and fed under standard conditions. On postoperative days 7 and 14, a beam-walking test was used to assess coordination, balance, and spatial learning. On postoperative days 16–20, a Morris water maze test was used to assess spatial learning and memory. On postoperative day 15, the expression levels of FDNC5 and BDNF proteins in the ipsilateral cerebral cortex were analyzed by western blot assay. The results showed that compared with the standard housing condition group, the motor balance and coordination functions(based on beam-walking test scores 7 and 14 days after operation), spatial learning abilities(based on the spatial learning scores from the Morris water maze test 16–19 days after operation), and memory abilities(based on the memory scores of the Morris water maze test 20 days after operation) of the enriched environment group improved significantly. In addition, the expression levels of FDNC5 and BDNF proteins in the ipsilateral cerebral cortex increased in the enriched environment group compared with those in the standard housing condition group. Furthermore, the Pearson correlation coefficient showed that neurobehavioral functions were positively associated with the expression levels of FDNC5 and BDNF(r = 0.587 and r = 0.840, respectively). These findings suggest that an enriched environment upregulates FDNC5 protein expression in the ipsilateral cerebral cortex after cerebral ischemia, which then activates BDNF protein expression, improving neurological function. BDNF protein expression was positively correlated with improved neurological function. The experimental protocols were approved by the Institutional Animal Care and Use Committee of Fudan University, China(approval Nos. 20160858 A232, 20160860 A234) on February 24, 2016.

An enriched environment improves cognitive performance in mice from the senescence-accelerated prone mouse 8 strain Role of upregulated neurotrophic factor expression in the hippocampus

In this study,we examined 3-month-old female mice from the senescence-accelerated prone mouse 8 strain and age-matched homologous normal aging female mice from the senescence accelerated-resistant mouse 1 strain.Mice from each strain were housed in an enriched environment（including a platform,running wheels,tunnel,and some toys）or a standard environment for 3 months.The mice housed in the enriched environment exhibited shorter escape latencies and a greater percentage of time in the target quadrant in the Morris water maze test,and they exhibited reduced errors and longer latencies in step-down avoidance experiments compared with mice housed in the standard environment.Correspondently,brain-derived neurotrophic factor mRNA and protein ex- pression in the hippocampus was significantly higher in mice housed in the enriched environment compared with those housed in the standard environment,and the level of hippocampal brain-derived neurotrophic factor protein was positively correlated with the learning and memory abilities of mice from the senescence-accelerated prone mouse 8 strain.These results suggest that an enriched environment improved cognitive performance in mice form the senescence-accelerated prone mouse 8 strain by increasing brain-derived neurotrophic factor expression in the hippocampus.

An enriched environment reduces hippocampal inflammatory response and improves cognitive function in a mouse model of stroke

An enriched environment is used as a behavio ral intervention therapy that applies sensory,motor,and social stimulation,and has been used in basic and clinical research of va rious neurological diseases.In this study,we established mouse models of photothrombotic stroke and,24 hours later,raised them in a standard,enriched,or isolated environment for 4 weeks.Compared with the mice raised in a standard environment,the cognitive function of mice raised in an enriched environment was better and the pathological damage in the hippocampal CA1 region was remarkably alleviated.Furthermore,protein expression levels of tumor necrosis factor receptor-associated factor 6,nuclear factorκB p65,interleukin-6,and tumor necrosis factorα,and the mRNA expression level of tumor necrosis factor receptor-associated factor 6 were greatly lower,while the expression level of miR-146a-5p was higher.Compared with the mice raised in a standard environment,changes in these indices in mice raised in an isolated environment were opposite to mice raised in an enriched environment.These findings suggest that different living environments affect the hippocampal inflammatory response and cognitive function in a mouse model of stro ke.An enriched environment can improve cognitive function following stroke through up-regulation of miR-146a-5p expression and a reduction in the inflammatory response.

A novel viewpoint in glaucoma therapeutics: enriched environment

Glaucoma is one of the world’s most frequent visual impairment causes and leads to selective damage to retinal ganglion cells and their axons.Despite glaucoma’s most accepted risk factor is increased intraocular pressure(IOP),the mechanisms behind the disease have not been fully elucidated.To date,IOP lowering remains the gold standard;however,glaucoma patients may still lose vision regardless of effective IOP management.Therefore,the exclusive IOP control apparently is not enough to stop the disease progression,and developing new resources to protect the retina and optic nerve against glaucoma is a goal of vast clinical importance.Besides pharmacological treatments,environmental conditions have been shown to prevent neurodegeneration in the central nervous system.In this review,we discuss current concepts on key pathogenic mechanisms involved in glaucoma,the effect of enriched environment on these mechanisms in different experimental models,as well as recent evidence supporting the preventive and therapeutic effect of enriched environment exposure against experimental glaucomatous damage.Finally,we postulate that stimulating vision may become a non-invasive and rehabilitative therapy that could be eventually translated to the human disease,preventing glaucoma-induced terrible sequelae resulting in permanent visual disability.

The Effects of the Enriched Environment on Sympathetic Skin Response in Pentylenetetrazol-Kindled Rats

Epilepsy is a neurodegenerative disease that interrupts the normal electrical activity of the brain and promotes abnormal wiring in this organ.Epileptic seizures are often associated with significant changes in the functioning of the autonomic nervous system(ANS).

Three-phase Enriched Environment Improves Post-stroke Gait Dysfunction via Facilitating Neuronal Plasticity in the Bilateral Sensorimotor Cortex:A Multimodal MRI/PET Analysis in Rats

The three-phase Enriched Environment(EE)paradigm has been shown to promote post-stroke functional improvement,but the neuronal mechanisms are still unclear.In this study,we applied a multimodal neuroimaging protocol combining magnetic resonance imaging(MRI)and positron emission tomography(PET)to examine the effects of post-ischemic EE treatment on structural and functional neuroplasticity in the bilateral sensorimotor cortex.Rats were subjected to permanent middle cerebral artery occlusion.The motor function of the rats was examined using the DigiGait test.MRI was applied to investigate the EE-induced structural modifications of the bilateral sensorimotor cortex.[^(18)F]-fluorodeoxyglucose PET was used to detect glucose metabolism.Blood oxygen level-dependent(BOLD)-functional MRI(fMRI)was used to identify the regional brain activity and functional connectivity(FC).In addition,the expression of neuroplasticity-related signaling pathways including neurotrophic factors(BDNF/CREB),axonal guidance proteins(Robo1/Slit2),and axonal growth-inhibitory proteins(NogoA/NgR)as well as downstream proteins(RhoA/ROCK)in the bilateral sensorimotor cortex were measured by Western blots.Our results showed the three-phase EE improved the walking ability.Structural T2 mapping imaging and diffusion tensor imaging demonstrated that EE benefited structure integrity in the bilateral sensorimotor cortex.PET-MRI fused images showed improved glucose metabolism in the corresponding regions after EE intervention.Specifically,the BOLD-based amplitude of low-frequency fluctuations showed that EE increased spontaneous activity in the bilateral motor cortex and ipsilateral sensory cortex.In addition,FC results showed increased sensorimotor connectivity in the ipsilateral hemisphere and increased interhemispheric motor cortical connectivity and motor cortical-thalamic connectivity following EE intervention.In addition,a strong correlation was found between increased functional connectivity and improved motor performance of limbs.Specifically,EE regulated the expression of neuroplasticity-related signaling,involving BDNF/CREB,Slit2/Robo1,as well as the axonal growth–inhibitory pathways Nogo-A/Nogo receptor and RhoA/ROCK in the bilateral sensorimotor cortex.Our results indicated that the three-phase enriched environment paradigm enhances neuronal plasticity of the bilateral sensorimotor cortex and consequently ameliorates post-stroke gait deficits.These findings might provide some new clues for the development of EE and thus facilitate the clinical translation of EE.

Environmental enrichment in combination with Bifidobacterium breve HNXY26M4 intervention amplifies neuroprotective benefits in a mouse model of Alzheimer's disease by modulating glutamine metabolism of the gut microbiome

The gut microbiota-brain axis has emerged as a novel target for Alzheimer's disease(AD),a neurodegenerative disease characterised by behavioural and cognitive impairment.However,most previous microbiome-based intervention studies have focused on single factors and yielded only modest cognitive improvements.Here,we proposed a multidomain intervention strategy that combined Bifidobacterium breve treatment with environmental enrichment(EE)training.In this study,we found that compared with EE or B.breve treatment alone,B.breve intervention combined with EE amplified its neuroprotective effects on AD mice,as reflected by improved cognition,inhibited neuroinflammation and enhanced synaptic function.Moreover,using microbiome and metabolome profiling,we found that the combination of B.breve and EE treatment restored AD-related gut microbiota dysbiosis and reversed microbial metabolite changes.Finally,by integrating behavioural and neurological data with metabolomic profiles,we revealed that the underlying mechanism may involve the modulation of microbiota-derived glutamine metabolism via gut-brain interactions.Collectively,combined B.breve intervention with EE treatment can alleviate AD-related cognitive impairment and improve brain function by regulating glutamine metabolism of the gut microbiome.Our findings provide a promising multidomain intervention strategy,with a combination of dietary microbiome-based and lifestyle-targeted interventions,to promote brain function and delay the progression of AD.

Molecular mechanisms underlying the neuroprotection of environmental enrichment in Parkinson’s disease

Parkinson’s disease is the most common movement disorder,affecting about 1%of the population over the age of 60 years.Parkinson’s disease is characterized clinically by resting tremor,bradykinesia,rigidity and postural instability,as a result of the progressive loss of nigrostriatal dopaminergic neurons.In addition to this neuronal cell loss,Parkinson’s disease is characterized by the accumulation of intracellular protein aggregates,Lewy bodies and Lewy neurites,composed primarily of the proteinα-synuclein.Although it was first described almost 200 years ago,there are no disease-modifying drugs to treat patients with Parkinson’s disease.In addition to conventional therapies,non-pharmacological treatment strategies are under investigation in patients and animal models of neurodegenerative disorders.Among such strategies,environmental enrichment,comprising physical exercise,cognitive stimulus,and social interactions,has been assessed in preclinical models of Parkinson’s disease.Environmental enrichment can cause structural and functional changes in the brain and promote neurogenesis and dendritic growth by modifying gene expression,enhancing the expression of neurotrophic factors and modulating neurotransmission.In this review article,we focus on the current knowledge about the molecular mechanisms underlying environmental enrichment neuroprotection in Parkinson’s disease,highlighting its influence on the dopaminergic,cholinergic,glutamatergic and GABAergic systems,as well as the involvement of neurotrophic factors.We describe experimental pre-clinical data showing how environmental enrichment can act as a modulator in a neurochemical and behavioral context in different animal models of Parkinson’s disease,highlighting the potential of environmental enrichment as an additional strategy in the management and prevention of this complex disease.

Environmental Enrichment and Its Effect on the Welfare of Two Asian Elephants in Africam Safari Wildlife Conservation Park (Puebla, Mexico)

Animal welfare is important in zoos to maintain the physical well-being and psychological health of individuals. An animal is considered to have welfare if it has good nutrition and also expresses its innate behavior, including sensations and feelings experienced as a result of physical health. The objective of this study was to evaluate the effect of environmental enrichment on the behaviors of two Asian elephants in a wildlife conservation park. The behavior of two Asian elephants, a 46-year-old male and a 59-year-old female, was observed. Behavior was measured by quantifying the frequency, latency, and duration of behavioral actions. Measurements were done with ad libitum sampling during 5 days of testing, then observations were recorded with focal sampling for 25 days with environmental enrichment and 25 days without enrichment. Data were analyzed with the Chi-square statistical test using the statistical program SPSS 20, observing significant differences (P the application of environmental enrichment. The frequency of maintenance behaviors was higher when environmental enrichment was provided, and the frequency of social conducts (affiliative and agonistic) decreased. In fact, the behaviors most frequently presented by elephants with and without environmental enrichment were definitely maintenance behaviors. The environmental enrichment program helped to reduce the duration of abnormal behaviors and increase the frequency of typical behaviors of the species. It also increased independent movements within the exhibition area and helped to know each of the elephants individually in order to apply each enrichment combination according to their needs.

Targeting epigenetic mechanisms in amyloid-β-mediated Alzheimer’s pathophysiology:unveiling therapeutic potential

Alzheimer’s disease is a prominent chronic neurodegenerative condition characterized by a gradual decline in memory leading to dementia.Growing evidence suggests that Alzheimer’s disease is associated with accumulating various amyloid-βoligomers in the brain,influenced by complex genetic and environmental factors.The memory and cognitive deficits observed during the prodromal and mild cognitive impairment phases of Alzheimer’s disease are believed to primarily result from synaptic dysfunction.Throughout life,environmental factors can lead to enduring changes in gene expression and the emergence of brain disorders.These changes,known as epigenetic modifications,also play a crucial role in regulating the formation of synapses and their adaptability in response to neuronal activity.In this context,we highlight recent advances in understanding the roles played by key components of the epigenetic machinery,specifically DNA methylation,histone modification,and microRNAs,in the development of Alzheimer’s disease,synaptic function,and activity-dependent synaptic plasticity.Moreover,we explore various strategies,including enriched environments,exposure to non-invasive brain stimulation,and the use of pharmacological agents,aimed at improving synaptic function and enhancing long-term potentiation,a process integral to epigenetic mechanisms.Lastly,we deliberate on the development of effective epigenetic agents and safe therapeutic approaches for managing Alzheimer’s disease.We suggest that addressing Alzheimer’s disease may require distinct tailored epigenetic drugs targeting different disease stages or pathways rather than relying on a single drug.

Postischemic Housing Environment on Cerebral Metabolism and Neuron Apoptosis after Focal Cerebral Ischemia in Rats

The purpose of this study was to evaluate the roles of different housing environments in neurological function, cerebral metabolism, cerebral infarction and neuron apoptosis after focal cerebral ischemia. Twenty-eight Sprague-Dawley rats were divided into control group （CG） and cerebral ischemia group, and the latter was further divided into subgroups of different housing conditions： standard environment （SE） subgroup, individual living environment （IE） subgroup, and enriched environment （EE） subgroup. Focal cerebral ischemia was induced by the middle cerebral artery occlusion （MCAO）. Beam walking test was used to quantify the changes of overall motor function. Cerebral infarction and cerebral metabolism were studied by in vivo magnetic resonance imaging and 1H-magnetic resonance spectra, respectively. Neuron necrosis and apoptosis were detected by hematoxylin-eosin and TUNEL staining methods, respectively. The results showed that performance on the beam-walk test was improved in EE subgroup when compared to SE subgroup and IE subgroup. Cerebral infarct volume in IE subgroup was significantly larger than that in SE subgroup （P〈0.05） and EE subgroup （P〈0.05） on day 14 after MCAO. NAA/Cr and Cho/Cr ratios were lower in MCAO groups under different housing conditions as compared to those in CG （P〈0.05）. NAA/Cr ratio was lower in IE subgroup （P〈0.05） and higher in EE subgroup （P〈0.05） than that in SE subgroup. NAA/ Cr ratio in EE was significantly higher than that in IE subgroup （P〈0.05）. Cho/Cr ratio was decreased in MCAO groups as compared to that in CG （P〈0.05）. A significant decrease in normal neurons in cerebral cortex was observed in MCAO groups as compared to CG （P〈0.05）. The amount of normal neurons was less in IE subgroup （P〈0.05）, and more in EE subgroup （P〈0.05） than that in SE subgroup after MCAO. The amotmt of normal neurons in EE subgroup was significantly more than that in IE subgroup after MCAO （P〈0.05）. The ratio of TUNEL-positive neurons in EE was significantly lower than that in SE subgroup （P〈0.05） and IE subgroup （P〈0.05）. Correlation analysis showed that the beam walking test was negatively correlated with NAA/Cr ratio （P〈0.05）. Cerebral infarct volume was negatively correlated with both NAA/Cr ratio （P〈0.01） and Cho/Cr ratio （P〈0.01）. The amount of normal cortical neurons was positively correlated with both NAA/Cr ratio （P〈0.0I） and Cho/Cr ratio （P〈0.05）. The TUNEL-positive neurons showed a negative correlation with both NAA/Cr ratio （P〈0.01） and Cho/Cr ratio （P〈0.01）. This study goes further to show that EE may improve neurological functional deficit and cerebral metabolism, decrease cerebral infarct volume, neuron necrosis and apoptosis, while IE may aggravate brain damage after MCAO.

Does the provision of live black soldier fly and yellow mealworm larvae improve Muscovy duck welfare?

Background The provision of environmental enrichments to Muscovy ducks could reduce the expression of the aggressive behaviors.The aim of the present study was to evaluate the effects of black soldier fly(BSF)and yellow mealworm(YM)live larva provision on Muscovy duck performance,excreta corticosterone metabolites(ECM),behavior,and blood parameters.Methods A total of 1263-day-old female Muscovy ducklings were allotted to 18 pens(6 replicates/treatment,7 birds/pen)and assigned to 3 experimental treatments:a control group fed commercial feed,and two experimental treatments fed commercial feed plus the 5%(based on the expected daily feed intake,as fed basis)of BSF and YM live larvae(BSF and YM groups,respectively).A two-phase feeding program was applied:starter(from 3 to 31 days of age)and grower-finisher(from 32 to 55 days of age).The live weight,average daily gain,average daily feed intake,and feed conversion ratio were calculated.Larva consumption times were collected,and video recordings were performed during 3 periods(P)each day:the hour before(P1),during(P2),and after(P3)the larva administration.ECM were evaluated at 3,31,and 55-day-old.Finally,the total red and white blood cell counts,serum proteins,lipids,and liver and renal function serum enzymes were evaluated on 12 birds/treatment.Results The experimental treatment did not affect the growth performance of the birds(P>0.05).Larva consumption times were always similar between the two insect species,except at 14–18 days of age,were BSF larvae were consumed faster than YM larvae(P<0.001).The birds showed less walking activity during P2,and preening behavior increased in YM birds during P3.The C birds increased the attack behavior over the weeks(P<0.05).During weeks 1–3 the YM group reduced the attack frequency(P1>P3;P<0.05).Finally,the provision of live BSF and YM larvae significantly reduced the ECM at 55 days of age and the heterophil to lymphocyte ratio(P<0.05).Conclusions Live BSF and YM larva supplementation in Muscovy duck improves duck welfare,without impairing birds'growth performance.

Influence of environmental enrichment on hippocampal synapses in adolescent offspring of mothers exposed to prenatal stress

Environmental enrichment attenuates hippocampal synaptic injury induced by prenatal stress in offspring. However, the influence of hippocampal synaptic changes and regional differences in prenatal stress remains poorly understood. The present study induced stress in Sprague Dawley rats, which were at gestational age 13-19 days. Following weaning, the offspring were raised in an enriched environment to establish models of stress ＋ enriched environment. Dendritic spine density and synaptophysin expression were detected in hippocampal neurons using Golgi staining and western blot analysis, respectively. Results showed that enriched environment increased dendritic spine density of apical dendrites in CA1 pyramidal cells and basal dendrites of granular cells in the outer layer of the dentate gyrus. In addition, hippocampal synaptophysin expression increased and the effects of prenatal stress on neuronal dendritic spines were reversed in adolescence.

Environmental enrichment combined with fasudil promotes motor function recovery and axonal regeneration after stroke

Fasudil,a Rho-associated protein kinase(ROCK)inhibitor,has a protective effect on the central nervous system.In addition,environmental enrichment is a promising technique for inducing the recovery of motor impairments in ischemic stroke models.The present study aimed to explore whether environmental enrichment combined with fasudil can facilitate motor function recovery and induce cortical axonal regeneration after stroke.First,a mouse model of ischemic cerebral stroke was established by photochemical embolization of the left sensorimotor cortex.Fasudil solution(10 mg/kg per day)was injected intraperitoneally for 21 days after the photothrombotic stroke.An environmental enrichment intervention was performed on days 7-21 after the photothrombotic stroke.The results revealed that environmental enrichment combined with fasudil improved motor function,increased growth-associated protein 43 expression in the infarcted cerebral cortex,promoted axonal regeneration on the contralateral side,and downregulated ROCK,p-LIM domain kinase(LIMK)1,and p-cofilin expression.The combined intervention was superior to monotherapy.These findings suggest that environmental enrichment combined with fasudil treatment promotes motor recovery after stroke,at least partly by stimulating axonal regeneration.The underlying mechanism might involve ROCK/LIMK1/cofilin pathway regulation.This study was approved by the Institutional Animal Care and Use Committee of Fudan University,China(approval No.20160858A232)on February 24,2016.

Memantine combined with environmental enrichment improves spatial memory and alleviates Alzheimer's disease-like pathology in senescence-accelerated prone-8(SAMP8) mice

Memantine is a N-methyl-D-aspartate (NMDA) receptor antagonist approved for the treatment of moderate to severe Alzheimer's disease (AD). Environmental enrichment (EE) has shown significant beneficial effects on func- tional improvement in AD. In this study, we sought to determine whether combining these two distinct therapies would yield greater benefit than either drug used alone. We investigated the effect of memantine combined with EE on spatial learning and memory and AD-like pathology in a widely used AD model, the senescence-accelerated prone mice (SAMP8). The SAMP8 mice were randomly assigned to enriched housing (EH) or standard housing (SH), where either memantine (20 mg/kg) or saline was given by gastric lavage once daily continuously for eight weeks. Our results showed that, when provided separately, memantine and EE significantly improved spatial learning and memory by shortening escape latencies and increasing the frequency of entrance into the target quadrant. When combined, memantine and EE showed additive effect on learning and memory as evidenced by significant shorter escape latencies and higher frequency of target entrance than either drug alone. Consistent with the behavior results, pathological studies showed that both memantine and EE significantly reduced hippocampal CA1 neurofibrilliary tangles (NFTs) as well as amyloid beta precursor protein (APP) levels. Combining both therapies synergistically lessened NFTs and APP expression compared to either drug alone in SAMP8 mice, indicating that the combination of memantine with EE could offer a novel and efficient therapeutic strategy for the treatment of AD.

Impact of Vertically-Suspended Environmental Enrichment and Two Densities of Fish on Circular Tank Velocity Profiles

Vertically-suspended environmental enrichment has been shown to produce improvements in fish growth during hatchery rearing in circular tanks. This study documented the effects of a novel suspended structure on the velocity profile of a 3.63-m diameter circular tank containing juvenile landlocked fall Chinook salmon (Oncorhynchus tshawytscha) at two different densities (9.0 and 34.3 kg/m3). The addition of vertically-suspended structure to the tank significantly decreased velocities at nearly every sampling point, with velocities typically dropping from 15 cm/s without structure to less than 6 cm/s when structure was present. Fish density also significantly impacted in-tank velocities, with an inverse relationship observed between the density of fish and water velocity. Significant interactions were present among the presence or absence of structure and fish density. When structure and fish were absent, the velocity at the edge of the tank was 15.63 cm/s, which was significantly higher than the 4.75 cm/s velocity when both structure and the lower fish density were added, which was in turn significantly higher than the 2.29 cm/s velocity observed with structure and higher fish density. Despite the potentially unique features of this study, vertically-suspended environmental enrichment and the presence of fish clearly alter circular tank water velocities, which may at least partially explain the improvements in fish rearing performance observed with the use of suspended structure.

Vertically-Suspended Environmental Enrichment Improves Growth of Landlocked Fall Chinook Salmon during Initial Hatchery Rearing

Environmental enrichment has been shown to improve juvenile salmonid growth during hatchery rearing. This study examined the effects of vertically-suspended environmental enrichment starting seven days after feed training and continuing for the next 32 days of landlocked fall Chinook salmon (Oncorhynchus tshawytscha) rearing. At the end of this experiment, final tank weights, gain, percent gain, and feed conversion ratio were all significantly improved in the tanks of salmon with environmental enrichment compared to barren tanks, with a nearly 25% improvement in feed conversion ratio. Individual salmon in tanks with environmental enrichment were significantly longer and weighed significantly more than salmon from tanks without enrichment. Specific growth rate was also significantly improved with the use of enrichment. The use of vertically-suspended environmental enrichment to improve growth and rearing efficiency is recommended during the initial rearing of landlocked fall Chinook salmon.

Environmental enrichment promotes neural remodeling in newborn rats with hypoxic-ischemic brain damage

We evaluated the effect of hypoxic-ischemic brain damage and treatment with early environmental enrichment intervention on development of newborn rats, as evaluated by light and electron microscopy and morphometry. Early intervention with environmental enrichment intelligence training attenuated brain edema and neuronal injury, promoted neuronal repair, and increased neuronal plasticity in the frontal lobe cortex of the newborn rats with hypoxic-ischemic brain damage.

Neuroprotection and recovery from early-life adversity: considerations for environmental enrichment

In the laboratory,environmental enrichment（EE）is used as a protocol to understand the functional,behavioral and molecular mechanisms that underlie neural plasticity（van Praag et al.,2000;Sale et al.,2014）.In addition,it is utilized to provide supplementary resources to animals in order to maintain their well-being and to preserve the scientific validity of the study at hand（see http：//www.nap.edu/catalog/12910/guide-for-thecare-and-use-of-laboratory-animals-eighth）.

Effect of differential rearing environments on nicotine-stimulated locomotor activity and nicotinic acetylcholine receptor subtypes

OBJECTIVE Individuals vary in sensitivity to the behavioral effects of nicotine,resulting in differences in their vulnerability to addiction.The role of rearing environment in determining individual sensitivity to nicotine is unclear.The neuropharmacological mechanisms mediating the effect of rearing environment on the actions of nicotine are also understood.Thus,the contribution of rearing environment in determining the sensitivity to the locomotor effects of nicotine and regulating α4β2*-and α7-nicotinic acetylcholine(n ACh) receptor expressionwas determined in rats reared in isolated(IC) or enriched(EC) conditions.METHODS To measure locomotor activity,adolescent rats(postnatal day 21-51)were injected with saline(1 mL·kg^(-1)) or nicotine(0.3 mg·kg^(-1)) subcutaneously,then placed in chamberswhere ambulatory activity was monitored for 30-min by computer for 14 daily sessions.α4β2*-andα7-n ACh receptor expression in the mesolimbic dopamine pathway was determined by quantitative autoradiography of [125 I]-epibatidine and [125 I]-bungarotoxinbinding,respectively,in 16 μmol·L^(-1) coronal sections.Values for receptor expression in fmol are ±s of 8 brains and compared by two-tailed,unpaired t-test with P<0.05 considered significant.RESULTS EC-rats are similarly sensitive as IC-rats to the locomotor effects of nicotine.[125 I]-epibatidine binding in the ventral tegmental area of EC-rats was reduced(2.8±0.3 fmo L) compared to IC-rats(4.0±0.4 fmo L);there was no difference in the nucleus accumbens.There was no difference between EC-and IC-rats in α7-n ACh receptor expression in the mesolimbic dopamine pathway.CONCLUSION Rearing environment differentially regulates n ACh receptor subtypes in EC and IC rats.These data suggest regulation of n ACh receptors by environmental factors may be a mechanism for the protective effect of enrichment against altered sensitivity to nicotine in genetically vulnerable individuals.The characterization of these mechanisms will aid in development of novel pharmacological tools mimicking the protection afforded by environmental enrichment in nicotine-sensitive individuals.