Early life peripheral lipopolysaccharide challenge reprograms catecholaminergic neurons

Ong, Lin Kooi; Fuller, E.A.; Sominsky, Luba; Hodgson, Deborah M.; Dunkley, Peter R.; Dickson, Phillip W.

doi:10.1038/srep40475

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…These data are consistent with the early immunohistochemical studies where Ser40 phosphorylation is difficult to observe in the absence of PKA activators (Xu et al 1998). An increase in TH phosphorylation in the VTA at only Ser40 by 1.4-fold increases TH activity by twofold (Ong et al 2017a).…”

Section: Ser40mentioning

confidence: 94%

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Tyrosine hydroxylase phosphorylation in vivo

Dunkley

Dickson

2019

Journal of Neurochemistry

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Tyrosine hydroxylase (TH) is the rate‐limiting enzyme in the synthesis of the catecholamines dopamine, noradrenaline and adrenaline. One of the major mechanisms for controlling the activity of TH is protein phosphorylation. TH is phosphorylated at serine residues 8, 19, 31 and 40. There have been a number of previous reviews focused on TH phosphorylation in vitro and in situ. This review on TH phosphorylation in vivo has three main sections focusing on: (1) the methods used to investigate TH phosphorylation in vivo, including the animals used, the sacrifice procedures, the tissue preparation, the measurement of TH protein levels and TH phosphorylation and the measurement of TH activation. (2) The regulation of TH phosphorylation and its consequences in vivo, including the kinases and phosphatases acting on TH, the stoichiometry of TH phosphorylation, the proteins that bind TH and TH subcellular location. (3) The acute and prolonged TH phosphorylation changes in specific catecholaminergic tissues, including the adrenal medulla, the nigrostriatal pathway and the mesolimbic pathway.

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Section: Ser40mentioning

confidence: 94%

“…An increase in TH phosphorylation in the VTA at only Ser40 by 1.4‐fold increases TH activity by twofold (Ong et al . ).…”

Section: Ser40mentioning

confidence: 97%

Tyrosine hydroxylase phosphorylation in vivo

Dunkley

Dickson

2019

Journal of Neurochemistry

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“…In addition, neonatal exposure to LPS induces enhanced prostaglandin-mediated HPA axis reactivity to LPS in adulthood [ 51 ]. In addition to affecting the HPA axis, neonatal exposure to LPS is able to reprogram catecholaminergic neurons [ 52 ]. Thus, LPS-challenged neonates show marked increases in tyrosine hydroxylase activity and protein expression in adulthood, in particular in the locus coeruleus [ 52 ].…”

Section: Gut Microbiota As the Source Of Microbial Constituents That mentioning

confidence: 99%

Gut Microbiota and the Neuroendocrine System

2018

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The microbial ecosystem that inhabits the gastrointestinal tract of all mammals—the gut microbiota—has been in a symbiotic relationship with its hosts over many millennia. Thanks to modern technology, the myriad of functions that are controlled or modulated by the gut microbiota are beginning to unfold. One of the systems that is emerging to closely interact with the gut microbiota is the body’s major neuroendocrine system that controls various body processes in response to stress, the hypothalamic–pituitary–adrenal (HPA) axis. This interaction is of pivotal importance; as various disorders of the microbiota–gut–brain axis are associated with dysregulation of the HPA axis. The present contribution describes the bidirectional communication between the gut microbiota and the HPA axis and delineates the potential underlying mechanisms. In this regard, it is important to note that the communication between the gut microbiota and the HPA axis is closely interrelated with other systems, such as the immune system, the intestinal barrier and blood–brain barrier, microbial metabolites, and gut hormones, as well as the sensory and autonomic nervous systems. These communication pathways will be exemplified through preclinical models of early life stress, beneficial roles of probiotics and prebiotics, evidence from germ-free mice, and antibiotic-induced modulation of the gut microbiota.Electronic supplementary materialThe online version of this article (10.1007/s13311-017-0600-5) contains supplementary material, which is available to authorized users.

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“…Alterations in immune responses may be modulated by the ANS, which is part of the GBA and one of the primary systems for the maintenance or reinstatement of homeostasis during stress. Following exposure to a stressor, such as infection, the ANS affords the most immediate response, inducing a rapid increase in the formation of noradrenaline from tyrosine hydroxylase (TH) in the sympathetic nerve terminals and in the adrenal medulla [21-23], leading to prompt alterations in physiological states through neural innervation of end organs [24]. During inflammation the ANS is activated to restore homeostasis, in part by regulating the inflammatory and subsequent immune response [25] through the release of inflammatory mediators [16].…”

Section: Introductionmentioning

confidence: 99%

A Rodent Model of Anxiety: The Effect of Perinatal Immune Challenges on Gastrointestinal Inflammation and Integrity

Hollins

Brock

Barreto

et al. 2018

Neuroimmunomodulation

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Objectives: Gastrointestinal (GI) inflammation and GI integrity deficits are common comorbidities of neuropsychiatric disorders. Ongoing research suggests that these aberrations may be contributing to heightened immune signals that have the potential to disrupt neuronal homeostasis and exacerbate behavioural deficits. The current study aimed to determine whether the well-characterized animal model of neuropsychopathology, the maternal immune activation (MIA) model, produced GI inflammation and integrity disruptions in association with anxiety-like behaviour. Methods: Pregnant Wistar rats were exposed to the viral mimetic polyriboinosinic:polyribocytidilic acid (polyI:C) on gestational days (GD) 10 and 19. Evidence of ANS activation, GI inflammation, and GI barrier integrity was assessed in both neonatal (postnatal day, P7) and adult (P84) offspring. Anxiety-like behaviour was assessed at P100. Results: Neonatal MIA offspring exhibited an altered intestinal inflammatory profile and evidence of an increase in lymphoid aggregates. MIA neonates also displayed disruptions to GI barrier tight junction protein mRNA. In addition, adult MIA offspring exhibited an increase in anxiety-like behaviours. Conclusion: These results indicate that the MIA rat model, which is well documented to produce behavioural, neurochemical, and neuroanatomical abnormalities, also produces GI inflammation and integrity disruptions. We suggest that this model may be a useful tool to elucidate biological pathways associated with neuropsychiatric disorders.

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Early life peripheral lipopolysaccharide challenge reprograms catecholaminergic neurons

Cited by 8 publications

References 33 publications

Tyrosine hydroxylase phosphorylation in vivo

Tyrosine hydroxylase phosphorylation in vivo

Gut Microbiota and the Neuroendocrine System

A Rodent Model of Anxiety: The Effect of Perinatal Immune Challenges on Gastrointestinal Inflammation and Integrity

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