Noradrenaline acting at central β-adrenoceptors induces interleukin-10 and suppressor of cytokine signaling-3 expression in rat brain: Implications for neurodegeneration

McNamee, Eóin N.; Ryan, Karen M.; Griffin, Éadaoin W.; González-Reyes, Rodrigo E.; Ryan, Katie J.; Harkin, Andrew; Connor, Thomas J.

doi:10.1016/j.bbi.2010.02.005

Cited by 58 publications

(39 citation statements)

References 77 publications

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“…Formoterol (Tocris) was administered IP at a dose of 2 mg/kg 4 hours before behavioral tests in order to achieve maximum effects of formoterol in the brain (22)(23)(24)(25). The half-life of formoterol is approximately 10 hours (26).…”

Section: Pharmacological Treatmentsmentioning

confidence: 99%

“…It can cross the blood brain barrier (BBB) in mammals and remains stable in the brain for over 24 hours (24). Interestingly, intraperitoneal (IP) injections of formoterol in rodents have led to increased gene expression for interleukin-10, within 4 hours of administration (25). Importantly, this effect can be blocked by pretreating with propranolol (β-AR antagonist with ability to cross the BBB) but not with nadolol (a β-AR antagonist with no ability to cross the BBB).…”

mentioning

confidence: 99%

“…Importantly, this effect can be blocked by pretreating with propranolol (β-AR antagonist with ability to cross the BBB) but not with nadolol (a β-AR antagonist with no ability to cross the BBB). Therefore, it has been concluded that increased gene expression by formoterol was due to its central effects (25). In light of this, we conducted our behavioral studies 4 hours after the administration of formoterol.…”

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confidence: 99%

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Formoterol, a Long-Acting β2 Adrenergic Agonist, Improves Cognitive Function and Promotes Dendritic Complexity in a Mouse Model of Down Syndrome

Medina

Das

et al. 2014

Biological Psychiatry

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Section: Pharmacological Treatmentsmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Formoterol, a Long-Acting β2 Adrenergic Agonist, Improves Cognitive Function and Promotes Dendritic Complexity in a Mouse Model of Down Syndrome

Medina

Das

et al. 2014

Biological Psychiatry

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“…Immunomodulatory effects on inflammatory and cellular immune processes, as well as neuroplastic processes, are outside the scope of this review and are summarised in Table 2. In brief, ADs appear to reduce neuroinflammation (Janssen et al 2010), attenuate microglial and astrocytic pro-inflammatory cytokine production activity (O'Sullivan et al 2009;McNamee et al 2010). The effect of ADs on CNS-specific autoreactive CD4?…”

Section: Antidepressantsmentioning

confidence: 96%

Neuroimmunomodulation in unipolar depression: a focus on chronobiology and chronotherapeutics

Eyre

Baune

2012

J Neural Transm

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The rising burden of unipolar depression along with its often related sleep disturbances, as well as increasing rates of sleep restriction in modern society, make the search for an extended understanding of the aetiology and pathophysiology of depression necessary. Accumulating evidence suggests an important role for the immune system in mediating disrupted neurobiological and chronobiological processes in depression. This review aims to provide an overview of the neuroimmunomodulatory processes involved with depression and antidepressant treatments with a special focus on chronobiology, chronotherapeutics and the emerging field of immune-circadian bi-directional crosstalk. Increasing evidence suggests that chronobiological disruption can mediate immune changes in depression, and likewise, immune processes can mediate chronobiological disruption. This may suggest a bi-directional relationship in immune-circadian crosstalk. Furthermore, given the immunomodulatory effects of antidepressants and chronotherapeutics, as well as their associated beneficial effects on circadian disturbance, we--and others--suggest that these therapeutic agents may exert their chronobiotic effects partially via the neuroimmune system. Further research is required to better elucidate the mechanisms of immune involvement in the chronobiology of depression.

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“…This neuronal protection encompassed amyloid-induced toxicity (Madrigal et al 2007), excitotoxicity (Madrigal et al 2009), metabolic stress (Madrigal et al 2009), and oxidative stress (including mitochondrial depolarization), and caspase activation (Troadec et al 2001;Traver et al 2005;Counts and Mufson 2010;Daulatzai 2016b). Further, increasing NE induces antiinflammatory cytokine IL-10 production protected against neurodegeneration (McNamee et al 2010). Consequently, in being neuroprotective (mediated by b-adrenergic receptors through the canonical badrenoceptor cAMP second messenger pathway-Counts and Mufson 2010), NE signaling maintains selective attention, memory storage and retrieval, arousal, vigilance, and mood (Foote et al 1983;Levine et al 1990;Ressler and Nemeroff 1999;Berridge and Waterhouse 2003;Weinshenker 2008;Sara 2009).…”

Section: Locus Coeruleus Dysfunction Upregulates Inflammationmentioning

confidence: 97%

Dysfunctional Sensory Modalities, Locus Coeruleus, and Basal Forebrain: Early Determinants that Promote Neuropathogenesis of Cognitive and Memory Decline and Alzheimer’s Disease

Daulatzai

2016

Neurotox Res

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Sporadic Alzheimer's disease (AD) is a devastating neurodegenerative disorder. It is essential to unravel its etiology and pathogenesis. This should enable us to study the presymptomatic stages of the disease and to analyze and reverse the antemortem behavioral, memory, and cognitive dysfunction. Prima facie, an ongoing chronic vulnerability involving neural insult may lead normal elderly to mild cognitive impairment (MCI) and then to AD. Development of effective preventive and therapeutic strategies to thwart the disease pathology obviously requires a thorough delineation of underlying disruptive neuropathological processes. Our sensory capacity for touch, smell, taste, hearing, and vision declines with advancing age. Declines in different sensory attributes are considered here to be the primary "first-tier pathologies." Olfactory loss is among the first clinical signs of neurodegenerative diseases including AD and Parkinson's disease (PD). Sensory dysfunction in the aged promotes pathological disturbances in the locus coeruleus, basal forebrain, entorhinal cortex, hippocampus, and several key areas of neocortex and brainstem. Hence, sensory dysfunction is the pivotal factor that may upregulate cognitive and memory dysfunction. The age-related constellation of comorbid pathological factors may include apolipoprotein E (APOE) genotype, obesity, diabetes, hypertension, alcohol abuse, head trauma, and obstructive sleep apnea. The concepts and trajectories delineated here are the dynamic pillars of the current hypothesis presented-it postulates that the sensory decline, in conjunction with the above pathologies, is crucial in triggering neurodegeneration and promoting cognitive/memory dysfunction in aging and AD. The application of this thesis can be important in formulating new multifactorial preventive and treatment strategies (suggested here) in order to attenuate cognitive and memory decline and ameliorate pathological dysfunction in aging, MCI, and AD.

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Noradrenaline acting at central β-adrenoceptors induces interleukin-10 and suppressor of cytokine signaling-3 expression in rat brain: Implications for neurodegeneration

Cited by 58 publications

References 77 publications

Formoterol, a Long-Acting β2 Adrenergic Agonist, Improves Cognitive Function and Promotes Dendritic Complexity in a Mouse Model of Down Syndrome

Formoterol, a Long-Acting β2 Adrenergic Agonist, Improves Cognitive Function and Promotes Dendritic Complexity in a Mouse Model of Down Syndrome

Neuroimmunomodulation in unipolar depression: a focus on chronobiology and chronotherapeutics

Dysfunctional Sensory Modalities, Locus Coeruleus, and Basal Forebrain: Early Determinants that Promote Neuropathogenesis of Cognitive and Memory Decline and Alzheimer’s Disease

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