Stress in puberty unmasks latent neuropathological consequences of prenatal immune activation in mice.
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Citations
Adolescence as a period of vulnerability and intervention in schizophrenia: Insights from the MAM model
Bridging Autism Spectrum Disorders and Schizophrenia through inflammation and biomarkers - pre-clinical and clinical investigations.
On place and time: microglia in embryonic and perinatal brain development
Multi-hit early life adversity affects gut microbiota, brain and behavior in a sex-dependent manner
Sexually dimorphic effects of prenatal exposure to lipopolysaccharide, and prenatal and postnatal exposure to propionic acid, on acoustic startle response and prepulse inhibition in adolescent rats: relevance to autism spectrum disorders.
References
Analysis of relative gene expression data using real-time quantitative pcr and the 2(-delta delta c(t)) method
The adolescent brain and age-related behavioral manifestations
The new stereological tools: disector, fractionator, nucleator and point-sampled intercepts and their use in pathological research and diagnosis
Why do many psychiatric disorders emerge during adolescence
Childhood Adversities Increase the Risk of Psychosis: A Meta-analysis of Patient-Control, Prospective- and Cross-sectional Cohort Studies
Related Papers (5)
Prenatal Infection and Schizophrenia: A Review of Epidemiologic and Translational Studies
Frequently Asked Questions (13)
Q2. What are the two environmental risk factors for developmental psychiatric disorders?
Prenatal maternal infection and postnatal ex-posure to psychological trauma are twoenvironmental risk factors for developmental psychiatric disorders, including autism, schizophrenia, and bipolar disorder (1–4).
Q3. What is the role of the CD200 receptor in neuron-microglia inhibitory signal?
Besides other signaling pairs, contact-dependent neuronmicroglia inhibitory signaling is governed by CD200-CD200 receptor (CD200R) and CD47CD172a interactions, in which CD200 and CD47 are primarily expressed by neurons, and CD200R and CD172a by microglia (23).
Q4. What is the role of the RNA in the induced immune response?
Prenatal immune activation was induced by the viral mimetic polyriboinosinicpolyribocytidilic acid [poly(I:C)], a synthetic analog of double-stranded RNA that induces a cytokineassociated, viral-like acute-phase response (14).
Q5. What is the meaning of the term “prenatal infection”?
The concept by which prenatal infection can “prime” the developing organism’s sensitivity to subsequent environmental challenges postnatally is consistent with other models demonstrating synergistic pathological effects between prenatal and postnatal insults, including prenatal exposure to air pollution and chronic high-fat diet consumption in adulthood (24).
Q6. What is the effect of stress on the behavior of adult mice?
(A) Adult mice subjected to peripubertal stress (S+) display enhanced anxiety-like behavior in the elevated plus maze test (as indexed by the reduced time spent on the open arms) compared with nonstressed (S-) offspring regardless of the prenatal conditions [CON, vehicle control; POL, poly(I:C)]; +P < 0.05, main effect of peripubertal stress.
Q7. What is the possible scenario for a prenatal environmental insult?
Another feasible scenario is that initial exposure to a prenatal environmental insult, such as infection, can render the offspring more vulnerable to the pathological effects of a second postnatal stimulus, such as stress (12, 13).
Q8. What is the effect of stress on microglia?
single or combined exposure to prenatal immune activation and peripubertal stress exert only a minimal long-term impact on microglia cells and induce no overt changes in the central and peripheral secretion of prototypical inflammatory factors.
Q9. What is the effect of stress on the development of anxiety-like behavior in the peripuber?
Stress exposure increased anxiety-like behavior in the elevated plus maze test independently of the prenatal immunological manipulation (Fig. 1A), which suggests that peripubertal offspring with a prenatal infectious history do not differ from prenatal controls in the development of stress-induced anxiety-like abnormalities.
Q10. What is the mean IL-1b content in the HPC?
(E) Contents of IL-1b, TNF-a, and PGE2 in the HPC measured by using particle-based flow cytometry; **P < 0.01 and ***P < 0.001, post hoc comparisons.
Q11. What is the role of the prenatal immune challenge in the development of neuropsychiatric?
the authors show in a translational mouse model that combined exposure to prenatal immune challenge and peripubertal stress induces synergistic pathological effects on adult behavioral functions and neurochemistry.
Q12. What is the mean PPI of the acoustic startle reflex?
(Left) % PPI as a function of increasing prepulse intensities (dB above background of 65 dB); (right) the mean % PPI across all prepulse levels.
Q13. What is the effect of stress on the development of a conditioned associative learning paradigm?
The authors further revealed independent effects of immune challenge and stress in the disruption of selective associative learning as measured by the paradigm of latent inhibition (LI): Nonstressed control offspring displayed a robust LI effect in the conditioned active avoidance paradigm (Fig. 1B).