Modulation of neuroimmunity by adenosine and its receptors: Metabolism to mental illness

Chiu, Gabriel Sean-Hang; Freund, Gregory G.

doi:10.1016/j.metabol.2014.09.003

Cited by 32 publications

(18 citation statements)

References 112 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Since overnutrition is associated with endoplasmic reticulum (ER) stress (Mollica et al, 2011 ), it is theorized that the overnutrition-associated oxidative stress causes dysregulated purine metabolism (Al-Rubaye and Morad, 2013 ). Subsequent cellular release of ATP and its precursors rapidly increases the interstitial concentration of adenosine (Chiu and Freund, 2014 ) which through the A2A adenosine receptor triggers neuronal hyperpolarization in a K ATP channel dependent manner (Popoli et al, 2002 ). Hence the relevance of adenosine to neurodegeneration and sleep (Portas et al, 1997 ; Stone, 2005 ) and the interest in caffeine and its derivatives as neuroprotectants and CNS stimulants (Schwarzschild et al, 2002 ; Barranco Quintana et al, 2007 ).…”

Section: Discussionmentioning

confidence: 99%

Short-Term High-Fat Diet (HFD) Induced Anxiety-Like Behaviors and Cognitive Impairment Are Improved with Treatment by Glyburide

Gainey

Kwakwa

Bray

et al. 2016

Front. Behav. Neurosci.

Self Cite

View full text Add to dashboard Cite

Obesity-associated comorbidities such as cognitive impairment and anxiety are increasing public health burdens that have gained prevalence in children. To better understand the impact of childhood obesity on brain function, mice were fed with a high-fat diet (HFD) from weaning for 1, 3 or 6 weeks. When compared to low-fat diet (LFD)-fed mice (LFD-mice), HFD-fed mice (HFD-mice) had impaired novel object recognition (NOR) after 1 week. After 3 weeks, HFD-mice had impaired NOR and object location recognition (OLR). Additionally, these mice displayed anxiety-like behavior by measure of both the open-field and elevated zero maze (EZM) testing. At 6 weeks, HFD-mice were comparable to LFD-mice in NOR, open-field and EZM performance but they remained impaired during OLR testing. Glyburide, a second-generation sulfonylurea for the treatment of type 2 diabetes, was chosen as a countermeasure based on previous data exhibiting its potential as an anxiolytic. Interestingly, a single dose of glyburide corrected deficiencies in NOR and mitigated anxiety-like behaviors in mice fed with HFD-diet for 3-weeks. Taken together these results indicate that a HFD negatively impacts a subset of hippocampal-independent behaviors relatively rapidly, but such behaviors normalize with age. In contrast, impairment of hippocampal-sensitive memory takes longer to develop but persists. Since single-dose glyburide restores brain function in 3-week-old HFD-mice, drugs that block ATP-sensitive K+ (KATP) channels may be of clinical relevance in the treatment of obesity-associated childhood cognitive issues and psychopathologies.

show abstract

Section: Discussionmentioning

confidence: 99%

Short-Term High-Fat Diet (HFD) Induced Anxiety-Like Behaviors and Cognitive Impairment Are Improved with Treatment by Glyburide

Gainey

Kwakwa

Bray

et al. 2016

Front. Behav. Neurosci.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Furthermore, cognitive disorders such as Alzheimer's (Angulo et al, 2003 ) and Parkinson's (Schwarzschild et al, 2006 ) disease are associated with elevated circulating adenosine levels. However, inhibition of adenosine signaling has been associated with cognitive deficits in models of hypoxia (Chiu et al, 2012 ) and Alzheimer's disease (Dall'igna et al, 2007 ), as well as with depressive- (Sarges et al, 1990 ) and anxiety-like behaviors in rodents (Florio et al, 1998 ; Chiu and Freund, 2014 ; Chiu et al, 2014 ).…”

Section: Alternative Mechanisms For Chemotherapy-induced Behavioral Tmentioning

confidence: 99%

Mechanisms of chemotherapy-induced behavioral toxicities

et al. 2015

Self Cite

View full text Add to dashboard Cite

While chemotherapeutic agents have yielded relative success in the treatment of cancer, patients are often plagued with unwanted and even debilitating side-effects from the treatment which can lead to dose reduction or even cessation of treatment. Common side effects (symptoms) of chemotherapy include (i) cognitive deficiencies such as problems with attention, memory and executive functioning; (ii) fatigue and motivational deficit; and (iii) neuropathy. These symptoms often develop during treatment but can remain even after cessation of chemotherapy, severely impacting long-term quality of life. Little is known about the underlying mechanisms responsible for the development of these behavioral toxicities, however, neuroinflammation is widely considered to be one of the major mechanisms responsible for chemotherapy-induced symptoms. Here, we critically assess what is known in regards to the role of neuroinflammation in chemotherapy-induced symptoms. We also argue that, based on the available evidence, neuroinflammation is unlikely the only mechanism involved in the pathogenesis of chemotherapy-induced behavioral toxicities. We evaluate two other putative candidate mechanisms. To this end we discuss the mediating role of damage-associated molecular patterns (DAMPs) activated in response to chemotherapy-induced cellular damage. We also review the literature with respect to possible alternative mechanisms such as a chemotherapy-induced change in the bioenergetic status of the tissue involving changes in mitochondrial function in relation to chemotherapy-induced behavioral toxicities. Understanding the mechanisms that underlie the emergence of fatigue, neuropathy, and cognitive difficulties is vital to better treatment and long-term survival of cancer patients.

show abstract

“…Reviews have been published previously about purinergic signalling and neurological disorders [7][8][9][10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Purinergic Signalling and Neurological Diseases: An Update

Burnstock

2017

CNSNDDT

105

View full text Add to dashboard Cite

Purinergic signalling, i.e. ATP as an extracellular signalling molecule and cotransmitter in both peripheral and central neurons, is involved in the physiology of neurotransmission and neuromodulation. Receptors for purines have been cloned and characterised, including 4 subtypes of the P1(adenosine) receptor family, 7 subtypes of the P2X ion channel nucleotide receptor family and 8 subtypes of the P2Y G protein-coupled nucleotide receptor family. The roles of purinergic signalling in diseases of the central nervous system and the potential use of purinergic compounds for their treatment are attracting increasing attention. In this review, the focus is on the findings reported in recent papers and reviews to update knowledge in this field about the involvement of purinergic signalling in Alzheimer's, Parkinson's and Huntington's diseases, multiple sclerosis, amyotrophic lateral sclerosis, degeneration and regeneration after brain injury, stroke, ischaemia, inflammation, migraine, epilepsy, psychiatric disorders, schizophrenia, bipolar disorder, autism, addiction, sleep disorders and brain tumours. The use in particular of P2X7 receptor antagonists for the treatment of neurodegenerative diseases, cancer, depression, stroke and ischaemia, A2A receptor antagonists for Parkinson's disease and agonists for brain injury and depression and P2X3 receptor antagonists for migraine and seizures has been recommended. P2Y receptors have also been claimed to be involved in some central nervous disorders.

show abstract

Modulation of neuroimmunity by adenosine and its receptors: Metabolism to mental illness

Cited by 32 publications

References 112 publications

Short-Term High-Fat Diet (HFD) Induced Anxiety-Like Behaviors and Cognitive Impairment Are Improved with Treatment by Glyburide

Short-Term High-Fat Diet (HFD) Induced Anxiety-Like Behaviors and Cognitive Impairment Are Improved with Treatment by Glyburide

Mechanisms of chemotherapy-induced behavioral toxicities

Purinergic Signalling and Neurological Diseases: An Update

Contact Info

Product

Resources

About