Antidepressant- and anticompulsive-like effects of purinergic receptor blockade: Involvement of nitric oxide

Pereira, Vitor Silva; Casarotto, Plínio; Hiroaki-Sato, Vinícius A.; Sartim, Ariandra Guerini; Guimarães, Francisco Silveira; Joca, Sâmia Regiane Lourenço

doi:10.1016/j.euroneuro.2013.01.008

Cited by 59 publications

(55 citation statements)

References 73 publications

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“…To our knowledge, this is the first work that reports the beneficial actions of NGEN against iron-mediated anxiolytic-like behavior and memory impairment in rats. Another important aspect to be discussed here is the effect of iron on the cholinergic, nitrergic and purinergic signaling involved in the neurobiology of stress-related anxiety [58,59]. The purinergic system employs extracellular nucleotides as signaling molecules.…”

Section: Discussionmentioning

confidence: 99%

Naringenin Mitigates Iron-Induced Anxiety-Like Behavioral Impairment, Mitochondrial Dysfunctions, Ectonucleotidases and Acetylcholinesterase Alteration Activities in Rat Hippocampus

et al. 2015

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Studies demonstrated that the iron chelating antioxidant restores brain dysfunction induced by iron toxicity in animals. Earlier, we found that iron overload-induced cerebral cortex apoptosis correlated with oxidative stress could be protected by naringenin (NGEN). In this respect, the present study is focused on the mechanisms associated with the protective efficacy of NGEN, natural flavonoid compound abundant in the peels of citrus fruit, on iron induced impairment of the anxiogenic-like behaviour, purinergic and cholinergic dysfunctions with oxidative stress related disorders on mitochondrial function in the rat hippocampus. Results showed that administration of NGEN (50 mg/kg/day) by gavage significantly ameliorated anxiogenic-like behaviour impairment induced by the exposure to 50 mg of Fe-dextran/kg/day intraperitoneally for 28 days in rats, decreased iron-induced reactive oxygen species formation and restored the iron-induced decrease of the acetylcholinesterase expression level, mitochondrial membrane potential and mitochondrial complexes activities in the hippocampus of rats. Moreover, NGEN was able to restore the alteration on the activity and expression of ectonucleotidases such as adenosine triphosphate diphosphohydrolase and 5'-nucleotidase, enzymes which hydrolyze and therefore control extracellular ATP and adenosine concentrations in the synaptic cleft. These results may contribute to a better understanding of the neuroprotective role of NGEN, emphasizing the influence of including this flavonoid in the diet for human health, possibly preventing brain injury associated with iron overload.

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Section: Discussionmentioning

confidence: 99%

Naringenin Mitigates Iron-Induced Anxiety-Like Behavioral Impairment, Mitochondrial Dysfunctions, Ectonucleotidases and Acetylcholinesterase Alteration Activities in Rat Hippocampus

et al. 2015

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“…In addition to P2Y 12 receptor expression on microglia, oligodendrocytic expression may be an important marker of demyelinating lesions in the neuroinflammatory disease, ALS (Amadio et al, 2014). P2Y 13 receptors expressed by cerebellar astrocytes and neurons confer neuroprotection through the activation of the GSK3 ERK1/2 pathway (Perez-Sen et al, 2015). Finally P2Y 14 receptors are also expressed by microglia, however these receptors are exclusively sensitive to UDP-glucose and other conjugates of UDP but not adenine or uracil nucleotides (Bianco et al, 2005).…”

Section: The Role Of P2y Receptors In Neuroinflammationmentioning

confidence: 99%

“…In rodent studies mimicking depressive-like behaviors, both genetic deletion and pharmacological inhibition of P2X7 receptors lead to an antidepressant phenotype, which is manifested in the widely used forced swim (FST) and tail suspension tests (TST) (Basso et al, 2009;Boucher et al, 2011;Csolle et al, 2013a,b;Pereira et al, 2013;Wilkinson et al, 2014), but can also be measured using more complex paradigms such as learned helplessness (Iwata et al, 2013). Acute stress induced depressiveelike behaviors, following LPS challenge are also alleviated by P2X7 receptor antagonism, (Csolle et al, 2013b;Ma et al, 2014).…”

Section: Purinergic Regulation Of Neuroinflammation In Cns Disordersmentioning

confidence: 99%

“…Rather, P2X7-regulated intrinsic neuronal mechanisms such as the modulation of glutamatergic neurotransmission (Csolle et al, 2013b) or nitric oxide signaling (Pereira et al, 2013) may represent the underlying mechanisms of the antidepressant phenotype. On the other hand, amphetamine induced induction of IL-1b and oxidative stress (Gubert et al, 2014) in the striatum were reversed by a P2X7 receptor antagonist coincidently with the alleviation of amphetamine induced behavior and amphetamine induced striatal dopamine release is attenuated by the P2X7 receptor deficient genotype (Csolle et al, 2013a).…”

Section: Purinergic Regulation Of Neuroinflammation In Cns Disordersmentioning

confidence: 99%

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Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

et al. 2016

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a b s t r a c tThe principle functions of neuroinflammation are to limit tissue damage and promote tissue repair in response to pathogens or injury. While neuroinflammation has utility, pathophysiological inflammatory responses, to some extent, underlie almost all neuropathology. Understanding the mechanisms that control the three stages of inflammation (initiation, propagation and resolution) is therefore of critical importance for developing treatments for diseases of the central nervous system. The purinergic signaling system, involving adenosine, ATP and other purines, plus a host of P1 and P2 receptor subtypes, controls inflammatory responses in complex ways. Activation of the inflammasome, leading to release of pro-inflammatory cytokines, activation and migration of microglia and altered astroglial function are key regulators of the neuroinflammatory response. Here, we review the role of P1 and P2 receptors in mediating these processes and examine their contribution to disorders of the nervous system. Firstly, we give an overview of the concept of neuroinflammation. We then discuss the contribution of P2X, P2Y and P1 receptors to the underlying processes, including a discussion of cross-talk between these different pathways. Finally, we give an overview of the current understanding of purinergic contributions to neuroinflammation in the context of specific disorders of the central nervous system, with special emphasis on neuropsychiatric disorders, characterized by chronic low grade inflammation or maternal inflammation. An understanding of the important purinergic contribution to neuroinflammation underlying neuropathology is likely to be a necessary step towards the development of effective interventions.

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“…Glutamato-NO-sGC do mPFC na modulação de comportamentos relacionados à depressão, causados por estresse incontrolável (Pereira et al, 2013;Pereira et al, 2015). Pereira e cols.…”

Section: Trabalhos Do Nosso Grupo De Pesquisa Mostram a Relação Da VIunclassified

Substratos neurais envolvidos com o desenvolvimento do comportamento de desamparo em ratos: possível envolvimento do NO

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Antidepressant- and anticompulsive-like effects of purinergic receptor blockade: Involvement of nitric oxide

Cited by 59 publications

References 73 publications

Naringenin Mitigates Iron-Induced Anxiety-Like Behavioral Impairment, Mitochondrial Dysfunctions, Ectonucleotidases and Acetylcholinesterase Alteration Activities in Rat Hippocampus

Naringenin Mitigates Iron-Induced Anxiety-Like Behavioral Impairment, Mitochondrial Dysfunctions, Ectonucleotidases and Acetylcholinesterase Alteration Activities in Rat Hippocampus

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

Substratos neurais envolvidos com o desenvolvimento do comportamento de desamparo em ratos: possível envolvimento do NO

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