149. Poly I:C-induced activation of the innate immune response is accompanied by symptoms of depression and anxiety

Gibney, Sinead M.; McGuinness, B. W.; Prendergast, Catriona T.; Harkin, Andrew; Connor, Thomas J.

doi:10.1016/j.bbi.2011.07.152

Cited by 3 publications

(5 citation statements)

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“…Previous studies in rats have suggested that poly I:C treatment acutely reduced BDNF signalling (Gibney et al, 2013) but that BDNF and TrkB gene expression were upregulated in the frontal cortex and striatum, respectively, in poly I:C offspring in adulthood (Hemmerle et al, 2015). Our finding of significantly increased levels of BDNF protein in the frontal cortex of MIA offspring compared to controls is in line with the reported increase of BDNF gene expression in this region.…”

Section: Discussionsupporting

confidence: 92%

“…For example, both BDNF levels (Toyooka et al, 2002;Angelucci et al, 2005;Ikeda et al, 2008;Chen et al, 2009) and the expression of TrkB receptors (Takahashi et al, 2000) have been found to be significantly reduced in the serum or brains of first-episode and chronic patients with schizophrenia. Acute administration of poly I:C in adult rats resulted in lowered expression of BDNF and TrkB in the hippocampus and frontal cortex (Gibney et al, 2013), while reduced BDNF levels were also found in the placenta and foetal liver and spleen of pregnant dams exposed to poly I:C (Gilmore et al, 2005). However, in adult rat MIA offspring, BDNF gene expression was significantly increased in the prefrontal cortex (PFC) while TrkB gene expression was increased in the striatum (Hemmerle et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

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TrkB agonist 7,8-dihydroxyflavone reverses an induced prepulse inhibition deficit selectively in maternal immune activation offspring: implications for schizophrenia

Jaehne

Chong

Sbisa

et al. 2021

Behavioural Pharmacology

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Reduced brain-derived neurotrophic factor (BDNF) signalling has been implicated in schizophrenia endophenotypes, including deficits in prepulse inhibition (PPI). Maternal immune activation (MIA) is a widely used neurodevelopmental animal model for schizophrenia but it is unclear if BDNF and its receptor, tropomyosin receptor kinase B (TrkB), are involved in PPI regulation in this model. Pregnant Long Evans rats were treated with the viral mimetic, polyinosinic–polycytidylic acid (poly I:C; 4 mg/kg i.v.), and nine male offspring from these dams were compared in adulthood to 11 male Long Evans controls. Offspring underwent PPI testing following injection with the TrkB agonist, 7,8-dihydroxyflavone (7,8-DHF) (10 mg/kg i.p.), with or without the dopamine receptor agonist, apomorphine (APO; 1 mg/kg s.c.), or the dopamine releasing drug, methamphetamine (METH; 2 mg/kg s.c.). Acute administration of APO and METH caused the expected significant reduction of PPI. Acute administration of 7,8-DHF did not alter PPI on its own; however, it significantly reversed the effect of APO on PPI in poly I:C rats, but not in controls. A similar trend was observed in combination with METH. Western blot analysis of frontal cortex revealed significantly increased levels of BDNF protein, but not TrkB or phosphorylated TrkB/TrkB levels, in poly I:C rats. These findings suggest that, selectively in MIA offspring, 7,8-DHF has the ability to reverse PPI deficits caused by dopaminergic stimulation. This effect could be associated with increased BDNF expression in the frontal cortex. These data suggest that targeting BDNF signalling may have therapeutic potential for the treatment of certain symptoms of schizophrenia.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

TrkB agonist 7,8-dihydroxyflavone reverses an induced prepulse inhibition deficit selectively in maternal immune activation offspring: implications for schizophrenia

Jaehne

Chong

Sbisa

et al. 2021

Behavioural Pharmacology

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“…Indeed, neuroinflammation can impact several BDNF-related signaling pathways, as proinflammatory signaling cascades lead to neuronal malfunction (Lima Giacobbo et al, 2019). Studies have also shown that increased proinflammatory signaling reduces the BDNF mRNA and protein expression (Guan and Fang, 2006;Gibney et al, 2013). Specifically, activated microglia can regulate BDNF function by lessening BDNF expression and/or its high-affinity receptor TrkB (Frühauf-Perez et al, 2018;Jin et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

A single intranasal dose of human mesenchymal stem cell-derived extracellular vesicles after traumatic brain injury eases neurogenesis decline, synapse loss, and BDNF-ERK-CREB signaling

Kodali

Madhu

Reger

et al. 2023

Front. Mol. Neurosci.

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An optimal intranasal (IN) dose of human mesenchymal stem cell-derived extracellular vesicles (hMSC-EVs), 90 min post-traumatic brain injury (TBI), has been reported to prevent the evolution of acute neuroinflammation into chronic neuroinflammation resulting in the alleviation of long-term cognitive and mood impairments. Since hippocampal neurogenesis decline and synapse loss contribute to TBI-induced long-term cognitive and mood dysfunction, this study investigated whether hMSC-EV treatment after TBI can prevent hippocampal neurogenesis decline and synapse loss in the chronic phase of TBI. C57BL6 mice undergoing unilateral controlled cortical impact injury (CCI) received a single IN administration of different doses of EVs or the vehicle at 90 min post-TBI. Quantifying neurogenesis in the subgranular zone-granule cell layer (SGZ-GCL) through 5′-bromodeoxyuridine and neuron-specific nuclear antigen double labeling at ~2 months post-TBI revealed decreased neurogenesis in TBI mice receiving vehicle. However, in TBI mice receiving EVs (12.8 and 25.6 × 109 EVs), the extent of neurogenesis was matched to naive control levels. A similar trend of decreased neurogenesis was seen when doublecortin-positive newly generated neurons were quantified in the SGZ-GCL at ~3 months post-TBI. The above doses of EVs treatment after TBI also reduced the loss of pre-and post-synaptic marker proteins in the hippocampus and the somatosensory cortex. Moreover, at 48 h post-treatment, brain-derived neurotrophic factor (BDNF), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and phosphorylated cyclic AMP response-element binding protein (p-CREB) levels were downregulated in TBI mice receiving the vehicle but were closer to naïve control levels in TBI mice receiving above doses of hMSC-EVs. Notably, improved BDNF concentration observed in TBI mice receiving hMSC-EVs in the acute phase was sustained in the chronic phase of TBI. Thus, a single IN dose of hMSC-EVs at 90 min post-TBI can ease TBI-induced declines in the BDNF-ERK-CREB signaling, hippocampal neurogenesis, and synapses.

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“…Neuroinflammation may alter normal brain development, resulting in adverse neuropsychiatric outcomes during childhood and adulthood, such as developmental delay/intellectual disability (DD/ID), autism spectrum disorder (ASD), cerebral palsy (CP), attention-deficit/hyperactivity disorder (ADHD), schizophrenia, depression, anxiety, and bipolar disorder. activation may sustain neuroinflammation and impair neurodevelopment by secreting inflammatory products (i.e., TNF-α) and reducing the production of neurotrophins, such as brain-derived neurotrophic factor (BDNF) (Harry et al, 2006;Gibney et al, 2013). Neurotrophins, especially BDNF, are critical mediators of neuronal survival, and their altered levels have been linked to several neurodevelopmental disorders .…”

Section: Maternal Immune Activation and Brain Developmentmentioning

confidence: 99%

“…Several animal models and epidemiological studies have investigated the association between MIA and neuropsychiatric disorders, including schizophrenia, bipolar disorder, ADHD, cerebral palsy, developmental delay, cognitive dysfunction, anxiety/depression, and ASD (Garbett et al, 2012;Gibney et al, 2013;Canetta et al, 2014;Knuesel et al, 2014;Jiang et al, 2016;Han et al, 2021). It has been hypothesized that inflammatory responses to insults, such as respiratory infections and autoimmunity, might cause alterations in neural activity and brain connectivity (Kwon et al, 2022).…”

Section: Maternal Immune Activation and Brain Developmentmentioning

confidence: 99%

Impact of respiratory viral infections during pregnancy on the neurological outcomes of the newborn: current knowledge

Manti,

Spoto,

Nicotera

et al. 2024

Front. Neurosci.

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Brain development is a complex process that begins during pregnancy, and the events occurring during this sensitive period can affect the offspring’s neurodevelopmental outcomes. Respiratory viral infections are frequently reported in pregnant women, and, in the last few decades, they have been related to numerous neuropsychiatric sequelae. Respiratory viruses can disrupt brain development by directly invading the fetal circulation through vertical transmission or inducing neuroinflammation through the maternal immune activation and production of inflammatory cytokines. Influenza virus gestational infection has been consistently associated with psychotic disorders, such as schizophrenia and autism spectrum disorder, while the recent pandemic raised some concerns regarding the effects of severe acute respiratory syndrome coronavirus 2 on neurodevelopmental outcomes of children born to affected mothers. In addition, emerging evidence supports the possible role of respiratory syncytial virus infection as a risk factor for adverse neuropsychiatric consequences. Understanding the mechanisms underlying developmental dysfunction allows for improving preventive strategies, early diagnosis, and prompt interventions.

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149. Poly I:C-induced activation of the innate immune response is accompanied by symptoms of depression and anxiety

Cited by 3 publications

References 0 publications

TrkB agonist 7,8-dihydroxyflavone reverses an induced prepulse inhibition deficit selectively in maternal immune activation offspring: implications for schizophrenia

TrkB agonist 7,8-dihydroxyflavone reverses an induced prepulse inhibition deficit selectively in maternal immune activation offspring: implications for schizophrenia

A single intranasal dose of human mesenchymal stem cell-derived extracellular vesicles after traumatic brain injury eases neurogenesis decline, synapse loss, and BDNF-ERK-CREB signaling

Impact of respiratory viral infections during pregnancy on the neurological outcomes of the newborn: current knowledge

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