(Putative) sex differences in neuroimmune modulation of memory

Tronson, Natalie C.; Collette, Katie M.

doi:10.1002/jnr.23921

Cited by 28 publications

(19 citation statements)

References 213 publications

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“…Thus, regulation of TLR3-associated inflammation is of both physiological and potentially therapeutic significance. Sex-related differences in inflammation, neural functioning, and behavior are increasingly being recognized (Nelson & Lenz, 2017;Rosen, Ham, & Mogil, 2017;Tronson & Collette, 2017) and have highlighted that data obtained in one sex are not always applicable to both (see special issue [Cahill, 2017]). Sex differences have been reported in the manifestation of, and susceptibility to, bacterial and viral infection (Klein & Flanagan, 2016;Marriott & Huet-Hudson, 2006); however, sex-related differences in TLR-induced inflammatory responses have not been widely studied.…”

mentioning

confidence: 99%

FAAH, but not MAGL, inhibition modulates acute TLR3‐induced neuroimmune signaling in the rat, independent of sex

Flannery

Henry

Kerr

et al. 2017

J of Neuroscience Research

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Toll-like receptor (TLR)3 is a key component of the innate immune response to viral infection. The present study firstly examined whether sex differences exist in TLR3-induced inflammatory, endocrine, and sickness responses. The data revealed that TLR3-induced expression of interferon- or NFkB-inducible genes (IFN-α/β, IP-10, or TNF-α), either peripherally (spleen) or centrally (hypothalamus), did not differ between male and female rats, with the exception of TLR3-induced IFN-α expression in the spleen of female, but not male, rats 8 hr post TLR3 activation. Furthermore, TLR3 activation increased plasma corticosterone levels, induced fever, and reduced locomotor activity and body weight - effects independent of sex. Thus, the acute-phase inflammatory, endocrine, and sickness responses to TLR3 activation exhibit minimal sex-related differences. A further aim of this study was to examine whether enhancing endocannabinoid tone - namely, 2-arachidonylglycerol (2-AG) or N-arachidonoylethanolamine (AEA), exhibited similar effects on TLR3-induced inflammatory responses in male versus female rats. Systemic administration of the monoacylglycerol lipase (MAGL) inhibitor MJN110 and subsequent increases in 2-AG levels did not alter the TLR3-induced increase in IP-10, IRF7, or TNF-α expression in the spleen or the hypothalamus of male or female rats. In contrast, the fatty acid amide hydrolase (FAAH) inhibitor URB597 increased levels of AEA and related N-acylethanolamines, an effect associated with the attenuation of TLR3-induced inflammatory responses in the hypothalamus, but not the spleen, of male and female rats. These data support a role for FAAH, but not MAGL, substrates in the modulation of TLR3-induced neuroinflammatory responses, effects independent of sex.

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mentioning

confidence: 99%

FAAH, but not MAGL, inhibition modulates acute TLR3‐induced neuroimmune signaling in the rat, independent of sex

Flannery

Henry

Kerr

et al. 2017

J of Neuroscience Research

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“…This is a particularly important avenue for research into individual differences and sex differences in susceptibility to immune-related disorders of cognition, memory and emotion (Perry et al, 2016; Snyder et al, 2016; Tronson and Collette, 2017; Choleris et al, 2018; Fisher et al, 2018; Speirs and Tronson, 2018). …”

Section: Discussionmentioning

confidence: 99%

Neuroimmune Activation Drives Multiple Brain States

Tchessalova

Posillico

Tronson

2018

Front. Syst. Neurosci.

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Neuroimmune signaling is increasingly identified as a critical component of neuronal processes underlying memory, emotion and cognition. The interactions of microglia and astrocytes with neurons and synapses, and the individual cytokines and immune signaling molecules that mediate these interactions are a current focus of much research. Here, we discuss neuroimmune activation as a mechanism triggering different states that modulate cognitive and affective processes to allow for appropriate behavior during and after illness or injury. We propose that these states lie on a continuum from a naïve homeostatic baseline state in the absence of stimulation, to acute neuroimmune activity and chronic activation. Importantly, consequences of illness or injury including cognitive deficits and mood impairments can persist long after resolution of immune signaling. This suggests that neuroimmune activation also results in an enduring shift in the homeostatic baseline state with long lasting consequences for neural function and behavior. Such different states can be identified in a multidimensional way, using patterns of cytokine and glial activation, behavioral and cognitive changes, and epigenetic signatures. Identifying distinct neuroimmune states and their consequences for neural function will provide a framework for predicting vulnerability to disorders of memory, cognition and emotion both during and long after recovery from illness.

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“…The hippocampus cognitive performance is directly connected to ER-α,o t h e rE R ss u c ha sE R -β and GPR30 [8]. The ERs have similar distribution in female and male brains, but may differ in relative expression [77]. ER-α and ER-β expression patterns generally overlap, where ER-α is associated with reproductive behavior, whereas ER-β is associated with non-reproductive behaviors such as learning and memory [78] and anxiety-related behaviors.…”

Section: Estrogen Receptors (Ers) Genetic Polymorphism and Epigenetimentioning

confidence: 99%

New Insights for Hormone Therapy in Perimenopausal Women Neuroprotection

Russu¹,

Antonescu²

2018

Sex Hormones in Neurodegenerative Processes and Diseases

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Perimenopause is a mandatory period in women's life, when the medical staff may initiate hormone therapy with sex steroids for the delay of brain aging and neurodegenerative diseases, during the so-called "window of opportunity." Animals' models are helpful to sustain the still controversial results of human clinical observational and/or randomized controlled studies. Estrogens, progesterone, and androgens, with their nuclear and membrane receptors, genes, and epigenetics, with their connections to cholinergic, GABAergic, serotoninergic, and glutamatergic systems are involved in women'sn o r m a lb r a i no ri n brain's pathology. The sex steroids are active through direct and/or indirect mechanisms to modulate and/or to protect brain plasticity, and vessels network, fuel metabolism-glucose, ketones, ATP, to reduce insulin resistance, and inflammation of the aging brain through blood-brain barrier disruption, microglial aberrant activation, and neural cell survival/loss.

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(Putative) sex differences in neuroimmune modulation of memory

Cited by 28 publications

References 213 publications

FAAH, but not MAGL, inhibition modulates acute TLR3‐induced neuroimmune signaling in the rat, independent of sex

FAAH, but not MAGL, inhibition modulates acute TLR3‐induced neuroimmune signaling in the rat, independent of sex

Neuroimmune Activation Drives Multiple Brain States

New Insights for Hormone Therapy in Perimenopausal Women Neuroprotection

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