Protective Effect of Astaxanthin on Prenatal Bacterial Lipopolysaccharide Exposed Behavioral Deficits in Adult Mice

Here we describe long-lasting impacts on the microbiota-gut-brain (MGB) axis following administration of low-dose dextran sodium sulfate (DSS) to weaning mice (P21), including gut dysbiosis, colonic inflammation, and brain/behavioral deficits in adulthood (P56). Early-life DSS leads to acute colonic inflammation, similar to adult mice; however, it results in long-lasting deficits in the MGB axis in adulthood (P56), in contrast to the transient deficits seen in adult DSS. This model highlights the unique features of pediatric inflammatory bowel disease.

Download Full-text

Impaired Spatial Learning Memory after Isoflurane Anesthesia or Appendectomy in Aged Mice is Associated with Microglia Activation

Journal of Cell Death ◽

10.4137/jcd.s30596 ◽

2015 ◽

Vol 8 ◽

pp. JCD.S30596 ◽

Cited By ~ 22

Author(s):

Hui-Lin Wang ◽

Rui-Hua Ma ◽

Hao Fang ◽

Zhang-Gang Xue ◽

Qing-Wu Liao

Keyword(s):

Elderly Patients ◽

Spatial Learning ◽

Postoperative Cognitive Dysfunction ◽

Microglia Activation ◽

Behavioral Deficits ◽

Adult Mice ◽

Tnf Α ◽

Ifn Γ ◽

Common Problems ◽

Spatial Learning Memory

Postoperative cognitive dysfunction (POCD) has been one of the most common problems in elderly patients following surgery. But the specific mechanism of POCD is still not clear. To further understand the reason of these postoperative behavioral deficits, we evaluated the spatial learning memory of both adult (3 months) and aged (18 months) male mice, 3 or 28 days after isoflurane (Iso) exposure for two hours or appendectomy (App). Hippocampal microglia activation and IL-1β, TNF-α, and IFN-γ expression were also evaluated at day 3, day 14 and day 28 after Iso exposure or appendectomy. Results showed that spatial learning memory of aged, but not adult, mice was impaired after Iso exposure or appendectomy, accompanied with more hippocampal microglia activation and IL-1β, TNF-α, and IFN-γ overexpression. These findings suggest that the cognitive deficits of elderly patients who have undergone surgeries are quite possibly caused by hippocampal microglia overactivation and the subsequent inflammation.

Download Full-text

Protective Effect of Galanin on Behavioral Deficits in Experimental Traumatic Brain Injury

Journal of Neurotrauma ◽

10.1089/neu.1994.11.73 ◽

1994 ◽

Vol 11 (1) ◽

pp. 73-82 ◽

Cited By ~ 22

Author(s):

SHANLIANG LIU ◽

BRUCE G. LYETH ◽

ROBERT J. HAMM

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Protective Effect ◽

Behavioral Deficits ◽

Experimental Traumatic Brain Injury

Download Full-text

Sexual maturation protects against development of lung inflammation through estrogen

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00119.2015 ◽

2016 ◽

Vol 310 (2) ◽

pp. L166-L174 ◽

Cited By ~ 15

Author(s):

Christina Draijer ◽

Machteld N. Hylkema ◽

Carian E. Boorsma ◽

Pieter A. Klok ◽

Patricia Robbe ◽

...

Keyword(s):

Protective Effect ◽

Sexual Maturation ◽

Lung Inflammation ◽

Underlying Mechanism ◽

Alveolar Epithelial Cells ◽

Asthma Prevalence ◽

Alveolar Epithelial ◽

Adult Mice ◽

Anti Inflammatory ◽

Sexually Mature

Increasing levels of estrogen and progesterone are suggested to play a role in the gender switch in asthma prevalence during puberty. We investigated whether the process of sexual maturation in mice affects the development of lung inflammation in adulthood and the contributing roles of estrogen and progesterone during this process. By inducing ovalbumin-induced lung inflammation in sexually mature and immature (ovariectomized before sexual maturation) adult mice, we showed that sexually immature adult mice developed more eosinophilic lung inflammation. This protective effect of “puberty” appears to be dependent on estrogen, as estrogen supplementation at the time of ovariectomy protected against development of lung inflammation in adulthood whereas progesterone supplementation did not. Investigating the underlying mechanism of estrogen-mediated protection, we found that estrogen-treated mice had higher expression of the anti-inflammatory mediator secretory leukoprotease inhibitor (SLPI) and lower expression of the proasthmatic cytokine IL-33 in parenchymal lung tissue and that their expressions colocalized with type II alveolar epithelial cells (AECII). Treating AECII directly with SLPI significantly inhibited IL-33 production upon stimulation with ATP. Our data suggest that estrogen during puberty has a protective effect on asthma development, which is accompanied by induction of anti-inflammatory SLPI production and inhibition of proinflammatory IL-33 production by AECII.

Download Full-text

Environmental Enrichment Rescues Social Behavioral Deficits and Synaptic Abnormalities in Pten Haploinsufficient Mice

Genes ◽

10.3390/genes12091366 ◽

2021 ◽

Vol 12 (9) ◽

pp. 1366

Author(s):

Amy E. Clipperton-Allen ◽

Angela Zhang ◽

Ori S. Cohen ◽

Damon Theron Page

Keyword(s):

Synaptic Plasticity ◽

Environmental Enrichment ◽

Repetitive Behavior ◽

Synaptic Proteins ◽

Protein Abundance ◽

Synaptic Protein ◽

Wild Type ◽

Neuronal Connectivity ◽

Behavioral Deficits ◽

Adult Mice

Pten germline haploinsufficient (Pten+/−) mice, which model macrocephaly/autism syndrome, show social and repetitive behavior deficits, early brain overgrowth, and cortical–subcortical hyperconnectivity. Previous work indicated that altered neuronal connectivity may be a substrate for behavioral deficits. We hypothesized that exposing Pten+/− mice to environmental enrichment after brain overgrowth has occurred may facilitate adaptation to abnormal “hard-wired” connectivity through enhancing synaptic plasticity. Thus, we reared Pten+/− mice and their wild-type littermates from weaning under either standard (4–5 mice per standard-sized cage, containing only bedding and nestlet) or enriched (9–10 mice per large-sized cage, containing objects for exploration and a running wheel, plus bedding and nestlet) conditions. Adult mice were tested on social and non-social assays in which Pten+/− mice display deficits. Environmental enrichment rescued sex-specific deficits in social behavior in Pten+/− mice and partially rescued increased repetitive behavior in Pten+/− males. We found that Pten+/− mice show increased excitatory and decreased inhibitory pre-synaptic proteins; this phenotype was also rescued by environmental enrichment. Together, our results indicate that environmental enrichment can rescue social behavioral deficits in Pten+/− mice, possibly through normalizing the excitatory synaptic protein abundance.

Download Full-text