Combined actions of blueberry extract and lithium on neurochemical changes observed in an experimental model of mania: exploiting possible synergistic effects

Spohr, Luíza; Soares, Mayara Sandrielly Pereira; Oliveira, Pathise Souto; Mattos, Bruna da Silveira de; Bona, Natália Pontes; Pedra, Nathália Stark; Teixeira, Fernanda Cardoso; Couto, Carlus Augustu Tavares do; Chaves, Vítor Clasen; Reginatto, Flávio Henrique; Lisboa, Meibel Teixeira; Ribeiro, Anderson Schwingel; Lencina, Claiton Leoneti; Stefanello, Francieli Moro; Spanevello, Rosélia Maria

doi:10.1007/s11011-018-0353-9

Cited by 22 publications

(14 citation statements)

References 77 publications

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“…Lithium was effective in reducing hyperlocomotion, brain oxidative stress, and AChE activity. These results corroborate with others studies from research group (Debom et al., 2016; Spohr et al., 2019). The antioxidant effect of lithium has also been demonstrated in other experimental models of mania as well as in patients with BD (Bengesser et al., 2016; Jornada et al., 2011).…”

Section: Discussionsupporting

confidence: 93%

“…Our research group demonstrated that antioxidant compounds prevent hyperlocomotion and protect the brain against oxidative stress in the model of mania (Chaves et al., 2020; Spohr et al., 2019). Gallic acid has received much attention due to its potent free radical scavenging activity and its role as a neuroprotective agent (Can et al., 2017; Mirshekar et al., 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Locomotor behavior was evaluated using the open field test (Spohr et al., 2019). The apparatus consisted of a wooden box measuring 72 × 72 × 33 cm (width × length × height), with the floor divided into 16 equal squares (18 × 18 cm).…”

Section: Methodsmentioning

confidence: 99%

“…AChE inhibitors have been used to increase synaptic levels of ACh in neurodegenerative diseases (Galimberti & Scarpini, 2016). However, there is conflicting evidence regarding the efficacy of AChE inhibitors in BD patients (Veronese et al., 2016), and the role of this enzyme in experimental models of mania (Spohr et al., 2019).…”

Section: Introductionmentioning

confidence: 99%

“…Ketamine is a dissociative anesthetic that acts as a noncompetitive antagonist of the NMDA glutamate receptor. Thus, at non‐anesthetic doses, ketamine administration induces manic‐like behavior in rats, as demonstrated by hyperlocomotion (Chaves et al., 2020; Debom et al., 2016; Ghedim et al., 2012; Spohr et al., 2019).…”

Section: Introductionmentioning

confidence: 99%

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Gallic acid protects cerebral cortex, hippocampus, and striatum against oxidative damage and cholinergic dysfunction in an experimental model of manic‐like behavior: Comparison with lithium effects

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Spohr

Soares

et al. 2021

Intl J of Devlp Neuroscience

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Bipolar disorder is characterized by episodes of depression and mania, and oxidative stress has been associated with the observed neurochemical changes in this disease. We evaluated the effects of gallic acid on hyperlocomotion, acetylcholinesterase activity, and oxidative stress in an animal model of ketamine‐induced mania. Rats were pretreated orally with vehicle, gallic acid (50 or 100 mg/kg), or lithium (45 mg/kg twice a day) for 14 days. Between days 8 and 14, the animals also received ketamine (25 mg/kg) or saline daily. On the 15th day, hyperlocomotion was assessed, following which the animals were euthanized, and brains were collected. Results showed that ketamine‐induced hyperlocomotion and caused oxidative damage by increasing reactive oxygen species levels, lipid peroxidation, and nitrite levels, and decreasing the total thiol content and the activities of catalase, superoxide dismutase, and glutathione peroxidase in the brain. Pretreatment with gallic acid and lithium prevented hyperlocomotion and brain oxidative damage. Further, ketamine increased the acetylcholinesterase activity in the hippocampus and striatum, whereas gallic acid and lithium ameliorated this alteration. Thus, gallic acid may provide effective protection against manic‐like behavior by reducing oxidative stress and preventing cholinergic signaling dysfunction in the brain regions involved in emotion regulation.

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