Tyrosine Hydroxylase

Dickson, Phillip W.; Briggs, Gabrielle D.

doi:10.1016/b978-0-12-411512-5.00002-6

Cited by 45 publications

(21 citation statements)

References 20 publications

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“…In contrast, another study found enhanced expression of tyrosine hydroxylase (TH), which is capable of catalyzing the conversion of the amino acid L-tyrosine to L-3,4-dihydroxy-phenylalanine (L-DOPA), a precursor for DP (171; Fan et al, unpublished data). TH is present in the adrenal medulla, the peripheral sympathetic neurons, and the CNS (171). Substantial studies have indicated that an alteration of TH activity is related to disorders such as Parkinson's disease and schizophrenia (172).…”

Section: Schizophreniamentioning

confidence: 99%

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

et al. 2015

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SUMMARY Toxocara canis and T. cati are highly prevalent nematode infections of the intestines of dogs and cats. In paratenic hosts, larvae do not mature in the intestine but instead migrate through the somatic tissues and organs of the body. The presence of these migrating larvae can contribute to pathology. Toxocara larvae can invade the brains of humans, and while case descriptions of cerebral toxocariasis are historically rare, improved diagnosis and greater awareness have contributed to increased detection. Despite this, cerebral or neurological toxocariasis (NT) remains a poorly understood phenomenon. Furthermore, our understanding of cognitive deficits due to toxocariasis in human populations remains particularly deficient. Recent data describe an enhanced expression of biomarkers associated with brain injury, such as GFAP, AβPP, transforming growth factor β1 (TGF-β1), NF-L, S100B, tTG, and p-tau, in mice receiving even low doses of Toxocara ova. Finally, this review outlines a hypothesis to explore the relationship between the presence of T. canis larvae in the brain and the progression of Alzheimer's disease (AD) due to enhanced AD-associated neurodegenerative biomarker expression.

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Section: Schizophreniamentioning

confidence: 99%

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

et al. 2015

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“…TH is the rate‐limiting enzyme of NE production with its activity regulated by phosphorylation at Ser 31 (but not Ser 40 ; Zigmond et al , 1989; Dickson & Briggs, 2013; Tekin et al , 2014). Particularly, CNTF, like physical stressors (Ong et al , 2014), stimulates TH activity through Ser 31 phosphorylation (Shi et al , 2012b).…”

Section: Resultsmentioning

confidence: 99%

Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress

et al. 2018

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Stress‐induced cortical alertness is maintained by a heightened excitability of noradrenergic neurons innervating, notably, the prefrontal cortex. However, neither the signaling axis linking hypothalamic activation to delayed and lasting noradrenergic excitability nor the molecular cascade gating noradrenaline synthesis is defined. Here, we show that hypothalamic corticotropin‐releasing hormone‐releasing neurons innervate ependymal cells of the 3rd ventricle to induce ciliary neurotrophic factor (CNTF) release for transport through the brain's aqueductal system. CNTF binding to its cognate receptors on norepinephrinergic neurons in the locus coeruleus then initiates sequential phosphorylation of extracellular signal‐regulated kinase 1 and tyrosine hydroxylase with the Ca2+‐sensor secretagogin ensuring activity dependence in both rodent and human brains. Both CNTF and secretagogin ablation occlude stress‐induced cortical norepinephrine synthesis, ensuing neuronal excitation and behavioral stereotypes. Cumulatively, we identify a multimodal pathway that is rate‐limited by CNTF volume transmission and poised to directly convert hypothalamic activation into long‐lasting cortical excitability following acute stress.

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“…TH activity is regulated by the activation of protein kinases that increase TH phosphorylation at serine residues 19, 31, and 40 (Ser19, Ser31, and Ser40), but it is the phosphorylation of Ser40 that is most directly associated with activation of the enzyme [41]. Evidence of ANS activation was examined using Western blotting and probing for total TH (tTH) protein levels and phosphorylation at serine residue 40 (phospho-TH Ser 40; pSer40) in the neonate and adult adrenals.…”

Section: Methodsmentioning

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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Tyrosine Hydroxylase

Cited by 45 publications

References 20 publications

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress

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

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