Schizophrenic Birth Seasonality in Relation to the Incidence of Infectious Diseases and Temperature Extremes

Watson, Charles G.; Kucala, Teresa; Tilleskjor, Curt; Jacobs, Lloyd A.

doi:10.1001/archpsyc.1984.01790120089011

Cited by 196 publications

(78 citation statements)

References 30 publications

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“…Obstetric complications, low birth weight, intrauterine malnutrition, smaller head circumference, congenital malformations, and maternal influenza during the second trimester are all positively correlated with the development of schizophrenia Kunugi et al, 1996;McNeil et al, 1994;O'Callaghan et al, 1991;Wahlbeck et al, 2001;Watson et al, 1984;Willinger et al, 2001;Wright et al, 1995). Moreover, during childhood and early adolescence, neuro-motor dysfunction, psychological abnormalities, social mal-adjustment, and cognitive problems are observed long before schizophrenia is diagnosed (Done et al, 1994;Jones et al, 1994;Rosso et al, 2000;Walker et al, 1993Walker et al, , 1994.…”

Section: Schizophrenia As a Neurodevelopmental Disorder: Role Of Glutmentioning

confidence: 99%

Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment

Konradi

Heckers

2003

Pharmacology & Therapeutics

296

165

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The glutamate system is involved in many aspects of neuronal synaptic strength and function during development and throughout life. Synapse formation in early brain development, synapse maintenance, and synaptic plasticity are all influenced by the glutamate system. The number of neurons and the number of their connections are determined by the activity of the glutamate system and its receptors. Malfunctions of the glutamate system affect neuroplasticity and can cause neuronal toxicity. In schizophrenia, many glutamate-regulated processes seem to be perturbed. Abnormal neuronal development, abnormal synaptic plasticity, and neurodegeneration have been proposed to be causal or contributing factors in schizophrenia. Interestingly, it seems that the glutamate system is dysregulated and that N-methyl-D-aspartate receptors operate at reduced activity. Here we discuss how the molecular aspects of glutamate malfunction can explain some of the neuropathology observed in schizophrenia, and how the available treatment intervenes through the glutamate system.

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Section: Schizophrenia As a Neurodevelopmental Disorder: Role Of Glutmentioning

confidence: 99%

Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment

Konradi

Heckers

2003

Pharmacology & Therapeutics

296

165

View full text Add to dashboard Cite

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“…The potential role of cytokines is underscored by findings that prenatal exposure to a variety of infections has been associated with an increased incidence of schizophrenia (O'Callaghan et al, 1994;Torrey et al, 1982Torrey et al, , 1988Watson et al, 1984;Yolken et al, 2000), indicating that such an association may be mediated by a host response that is common to all infections Marx et al, 2001;Nawa et al, 2000;Pearce, 2001). …”

Section: Introductionmentioning

confidence: 99%

Immune Activation During Pregnancy in Rats Leads to a PostPubertal Emergence of Disrupted Latent Inhibition, Dopaminergic Hyperfunction, and Altered Limbic Morphology in the Offspring: A Novel Neurodevelopmental Model of Schizophrenia

Zuckerman

Rehavi

Nachman

et al. 2003

Neuropsychopharmacol

445

355

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Prenatal exposure to infection is associated with increased liability to schizophrenia, and it is believed that such an association is mediated by the maternal immune response, in particular, the proinflammatory cytokines released by the maternal immune system, which may disrupt fetal brain development. Impaired capacity to ignore irrelevant stimuli is one of the central deficits in schizophrenia, and is manifested, among others, in loss of latent inhibition (LI), a phenomenon whereby repeated inconsequential pre-exposure to a stimulus impairs its subsequent capacity to signal significant consequences. We tested the effects of prenatal immune activation induced by peripheral administration of the synthetic cytokine releaser polyriboinosinic-polyribocytidilic acid (poly I : C) to pregnant dams, on LI in juvenile and adult offspring. Consistent with the characteristic maturational delay of schizophrenia, prenatal immune activation did not affect LI in the juvenile offspring, but led to LI disruption in adulthood. Both haloperidol (0.1 mg/kg) and clozapine (5 mg/kg) reinstated LI in the adult offspring. In addition, prenatal immune activation led to a postpubertal emergence of increased sensitivity to the locomotorstimulating effects of amphetamine and increased in vitro striatal dopamine release, as well as to morphological alterations in the hippocampus and the entorhinal cortex in the adult offspring, consistent with the well-documented mesolimbic dopaminergic and temporolimbic pathology in schizophrenia. These results suggest that prenatal poly I : C administration may provide a neurodevelopmental model of schizophrenia that reproduces a putative inducing factor; mimics the temporal course as well as some central abnormalities of the disorder; and predicts responsiveness to antipsychotic drugs.

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“…Epidemiological studies have demonstrated that prenatal exposure of pregnant women to environmental challenges, such as obstetric complications, 3 psychosocial stressors 4 and maternal infection, 5 all increase the risk of the offspring developing schizophrenia at adulthood. Maternal infection with viruses including influenza, 6 measles, 7 polio 8 and herpes simplex type 2, 9 and bacteria such as diphtheria and pneumonia, 5,10 have been shown to be risk factors associated with the development of schizophrenia. In experimental studies using rodents at different stages during pregnancy, infection with human influenza virus, 11 the viral mimic polyinosinic: polycytidylic acid (poly I: C), [11][12][13][14] or bacterial endotoxin (lipopolysaccharide (LPS)), 15,16 resulted in behavioral changes relevant to schizophrenia in the adult offspring, such as decreased latent inhibition, 11,13,14 increased amphetamine-induced locomotion 12,16 and disrupted prepulse inhibition (PPI) of acoustic startle.…”

Section: Introductionmentioning

confidence: 99%

The role of cytokines in mediating effects of prenatal infection on the fetus: implications for schizophrenia

et al. 2005

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Maternal infections with bacterial or viral agents during pregnancy are associated with an increased incidence of schizophrenia in the offspring at adulthood although little is known about the mechanism by which maternal infection might affect fetal neurodevelopment. Exposure of pregnant rodents to the bacterial endotoxin, lipopolysaccharide (LPS), results in behavioral deficits in the adult offspring that are relevant to schizophrenia. It is however unknown whether these effects are due to the direct action of the inflammatory stimulus on the developing fetus, or due to secondary immune mediators (cytokines) activated at maternal/ fetal sites. In this study we sought to elucidate the site of action of LPS, following a single intraperitoneal (i.p.) injection, in pregnant rats at gestation day 18. Animals received 5 lCi of iodinated LPS ( 125 I-LPS) and its distribution was assessed in maternal/fetal tissues (1-8 h). In addition, induction of the inflammatory cytokines, TNF-a, IL-1b and IL-6, was measured in maternal/fetal tissues following maternal LPS challenge (0.05 mg/kg, i.p.) (2-8 h). 125I-LPS was detected in maternal tissues and placenta, but not the fetus. This distribution was accompanied by significant increases in TNF-a, IL-1b and IL-6 in maternal plasma and placenta, but not in fetal liver or brain. A significant increase in IL-1b was however detected in fetal plasma, possibly due to transfer from the maternal circulation or placenta. Collectively, these data suggest that effects of maternal LPS exposure on the developing fetal brain are not mediated by the direct action of LPS, but via indirect actions at the level of the maternal circulation or placenta.

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Schizophrenic Birth Seasonality in Relation to the Incidence of Infectious Diseases and Temperature Extremes

Cited by 196 publications

References 30 publications

Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment

Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment

Immune Activation During Pregnancy in Rats Leads to a PostPubertal Emergence of Disrupted Latent Inhibition, Dopaminergic Hyperfunction, and Altered Limbic Morphology in the Offspring: A Novel Neurodevelopmental Model of Schizophrenia

The role of cytokines in mediating effects of prenatal infection on the fetus: implications for schizophrenia

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