Evidence for activation of microglia in patients with psychiatric illnesses

Bayer, Thomas A.; Buslei, Rolf; Havas, László; Falkai, Peter

doi:10.1016/s0304-3940(99)00545-5

Cited by 296 publications

(184 citation statements)

References 18 publications

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“…Furthermore, infiltrated leukocytes and activated astrocytes and microglia are important sources of cytokines in the CNS (Becher et al 2000). In schizophrenia, mild astrocyte hypertrophy (but not hyperplasia), microglial activation and expression of MHC class II molecules have been described (Arnold et al 1996;Bayer et al 1999;Radewicz et al 2000).…”

Section: Discussionmentioning

confidence: 99%

Prenatal Immune Challenge Disrupts Sensorimotor Gating in Adult Rats Implications for the Etiopathogenesis of Schizophrenia

Borrell

Vela²,

Arévalo-Martı́n³

et al. 2002

Neuropsychopharmacology

280

191

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Increasing evidence associates schizophrenia with prenatal exposure to infection. Impaired ability to "gate out" sensory and cognitive information is considered to be a central feature of schizophrenia and is manifested, among others, in disrupted prepulse inhibition (PPI) of the acoustic startle reflex. We analyzed the effect of a prenatal immune challenge-peripheral administration of bacterial endotoxin lipopolysaccharide (LPS) to pregnant female rats-upon PPI and immune function in adult offspring. Prenatal LPS treatment disrupted PPI which was reversed by antipsychotics. Serum levels of interleukin-2 and interleukin-6 were increased. In addition, histopathological features in brain areas related with PPI circuitry were observed. These results illustrate the critical influence of prenatal immune events upon adult CNS functioning in association with the putative role of the immune system in (Braff et al. 1978;Kumari et al. 1999). A well-established sensorimotor gating paradigm is the prepulse inhibition (PPI) of the startle response. PPI refers to the reduction in startle reactivity toward an intense pulse stimulus when it is shortly preceded by a weak prepulse stimulus (Hoffman and Ison 1980). It is thought that the prepulse response activates an inhibitory process that attenuates or "gates" the startle response. Because identical stimulus parameters can be used for animal and human studies, it is considered that animal models of PPI disruption represent a promising way to study the neural mechanisms underlying sensorimotor gating dysfunction (Swerdlow et al. 1994(Swerdlow et al. , 1999Swerdlow and Geyer 1998) and as a screening test for potential antipsychotics (Swerdlow et al. 1994;Depoortere et al. 1997). In fact, antipsychotics remove PPI deficits in schizophrenic patients (Kumari et al. 1999;Weike et al. 2000). Nevertheless, it must be taken into consideration that deficiency of PPI has been reported in other selected neuropsychiatric disorders where inability to inhibit movements is involved (Huntington's disease (Swerdlow et al. 1995 Tourette's syndrome (Castellanos et al. 1996)), where inability to control attentional and cognitive processes is involved (obsessive-compulsive disorder (Swerdlow et al. 1993)), or where anxiety and exaggerated startle occur (posttraumatic stress disorder (Grillon et al. 1996)). The focus of schizophrenia research has been turning from studies of structural and functional brain abnormalities to an increasing emphasis on possible etiologic factors. Neurodevelopmental theories of schizophrenia postulate that the psychopathology of schizophrenia may derive from alterations of brain organization secondary to defective ontogenesis (Weinberger 1996;Raedler et al. 1998). A causal relationship pertaining to disturbed brain ontogenesis and schizophrenia comes from epidemiological studies that have identified several risk factors that, acting during pregnancy, increase the incidence of the disease in offspring. Maternal infection with influenza virus in the second trimester of preg...

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Section: Discussionmentioning

confidence: 99%

Prenatal Immune Challenge Disrupts Sensorimotor Gating in Adult Rats Implications for the Etiopathogenesis of Schizophrenia

Borrell

Vela²,

Arévalo-Martı́n³

et al. 2002

Neuropsychopharmacology

280

191

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“…8) Even in psychiatric illnesses, it is reported that mononuclear phagocytes accumulate in the cerebrospinal fluid of schizophrenic patients during acute psychotic episodes, 9) and microglial activation is often observed in the postmortem pathohistologic examination of patients with schizophrenia. 10) In addition to the CNS, potential participation of microglial activation is also reported in glaucomatous optic nerve degeneration 11) and diabetic retinopathy. 12) 3.…”

Section: Microglial Activation In Various Neuro-logical Diseasesmentioning

confidence: 99%

Regulating Factors for Microglial Activation.

Nakamura

2002

Biological & Pharmaceutical Bulletin

223

114

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“…In particular, several postmortem brain studies indicate that activated microglia are involved in both schizophrenia (Steiner et al., 2006) and major depression (Bayer, Busleia, Havasb, & Falkaia, 1999; Steiner et al., 2011). In accordance with, microglial activation may be a common finding in the pathogenesis of both the psychiatric diseases.…”

Section: Introductionmentioning

confidence: 99%

Gunn rats with glial activation in the hippocampus show prolonged immobility time in the forced swimming test and tail suspension test

et al. 2018

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IntroductionRecent studies imply that glial activation plays a role in the pathogenesis of psychiatric disorders, such as schizophrenia and major depression. We previously demonstrated that Gunn rats with hyperbilirubinemia show congenital gliosis and schizophrenia‐like behavior.MethodsAs it has been suggested that major depression involves glial activation associated with neuroinflammation, we examined whether Gunn rats show depression‐like behavior using the forced swimming test (FST) and the tail suspension test (TST). In addition, we quantitatively evaluated both microgliosis and astrogliosis in the hippocampus of Gunn rats using immunohistochemistry analysis of the microglial marker ionized calcium‐binding adaptor molecule (Iba) 1 and the astrocytic marker S100B.ResultsBoth the FST and TST showed that immobility time of Gunn rats was significantly longer than that of normal control Wistar rats, indicating that Gunn rats are somewhat helpless, a sign of depression‐like behavior. In the quantification of immunohistochemical analysis, Iba1immunoreactivity in the dentate gyrus (DG), cornu ammonis (CA) 1, and CA3 and the number of Iba1‐positive cells in the CA1 and CA3 were significantly increased in Gunn rats compared to Wistar rats. S100B immunoreactivity in the DG, CA1, and CA3 and the number of S100B‐positive cells in the DG and CA3 were significantly increased in Gunn rats compared to Wistar rats.ConclusionOur findings suggest that both microglia and astrocyte are activated in Gunn rats and their learned helplessness could be related to glial activation.

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Evidence for activation of microglia in patients with psychiatric illnesses

Cited by 296 publications

References 18 publications

Prenatal Immune Challenge Disrupts Sensorimotor Gating in Adult Rats Implications for the Etiopathogenesis of Schizophrenia

Prenatal Immune Challenge Disrupts Sensorimotor Gating in Adult Rats Implications for the Etiopathogenesis of Schizophrenia

Regulating Factors for Microglial Activation.

Gunn rats with glial activation in the hippocampus show prolonged immobility time in the forced swimming test and tail suspension test

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