Chronic caffeine prevents changes in inhibitory avoidance memory and hippocampal BDNF immunocontent in middle-aged rats

Sallaberry, Cássia; Nunes, Fernanda Costa; Costa, Marcelo Silveira da; Fioreze, Gabriela T.; Ardais, Ana Paula; Botton, Paulo Henrique S.; Klaudat, Bruno; Forte, Thomás; Souza, Diogo O.; Elisabetsky, Elaine; Porciúncula, Lisiane O.

doi:10.1016/j.neuropharm.2012.07.010

Cited by 50 publications

(22 citation statements)

References 78 publications

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“…In particular, the neuronal activity‐dependent secretion of BDNF plays a fundamental role in the classical LTP induced by electrical stimulation protocols (Gärtner & Staiger 2002; Rex et al 2007). Interestingly, caffeine increases BDNF levels (Costa et al 2008; Sallaberry et al 2013) and BDNF can induce NMDAR‐independent LTP (Kang & Schuman 1995). Our present results provide the first experimental demonstration that caffeine, at moderate to high concentration, evokes an increase of calcium and neuronal activity‐dependent BDNF secretion during CAF LTP in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

“…Several lines of evidence indicate that caffeine modulates the brain‐derived neurotrophic factor (BDNF) system (Costa et al 2008; Sallaberry et al 2013). On other hand, BDNF is associated with learning and memory (Greenberg et al 2009) and modulates neuronal plasticity by inducing changes in synaptic efficacy and morphology (McAllister et al 1999; Thoenen 2000; Poo 2001).…”

Section: Introductionmentioning

confidence: 99%

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Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling

et al. 2016

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Caffeine has cognitive‐enhancing properties with effects on learning and memory, concentration, arousal and mood. These effects imply changes at circuital and synaptic level, but the mechanism by which caffeine modifies synaptic plasticity remains elusive. Here we report that caffeine, at concentrations representing moderate to high levels of consumption in humans, induces an NMDA receptor‐independent form of LTP (CAFLTP) in the CA1 region of the hippocampus by promoting calcium‐dependent secretion of BDNF, which subsequently activates TrkB‐mediated signaling required for the expression of CAFLTP. Our data include the novel observation that insulin receptor substrate 2 (IRS2) is phosphorylated during induction of CAFLTP, a process that requires cytosolic free Ca2+. Consistent with the involvement of IRS2 signals in caffeine‐mediated synaptic plasticity, phosphorylation of Akt (Ser473) in response to LTP induction is defective in Irs2−/− mice, demonstrating that these plasticity changes are associated with downstream targets of the phosphoinositide 3‐kinase (PI3K) pathway. These findings indicate that TrkB‐IRS2 signals are essential for activation of PI3K during the induction of LTP by caffeine.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling

et al. 2016

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“…Costa et al, 2008 reported that caffeine improved behavioral performance of the adult rodents via the increased level of BDNF and TrkB. Sallaberry et al, 2013 investigated that chronic caffeine improved hippocamal dependent cognitive functions in the middle-aged rats. In the rats caffeine attenuates metabolic M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT 5 disorder and ameliorates memory deficits in the chronic psychosocial stress and/or high fat-high carbohydrate diet (Panchal et., 2012;Alzoubi et al, 2013;Moy et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Caffeine prevents d-galactose-induced cognitive deficits, oxidative stress, neuroinflammation and neurodegeneration in the adult rat brain

Ullah

Ali

Ullah

et al. 2015

Neurochemistry International

167

103

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“…The beneficial effects exerted by caffeine on cognitive functions have been documented [18], and it was reported that caffeine consumption prevents memory disturbances associated with ageing [19,20,21]. Also, increasing attention has been given to caffeine since its intake has been associated with a reduced neurological damage in several neurodegenerative diseases [22].…”

Section: Caffeine: Potential Beneficial Effectsmentioning

confidence: 99%

Therapeutic Opportunities for Caffeine and A<sub>2A</sub> Receptor Antagonists in Retinal Diseases

Boia

Ambrósio²,

Santiago³

2016

Ophthalmic Res

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Caffeine, the major component of coffee, is the most consumed psychostimulant in the world. Caffeine is an adenosine analog and acts as a nonselective adenosine receptor antagonist. The majority of the effects of caffeine are mainly mediated by the blockade of adenosine receptors, and the proved neuroprotective effects of caffeine in brain disorders have been mimicked by the blockade of adenosine A_2A receptor (A_2AR). A growing body of evidence demonstrates that microglia-mediated neuroinflammation plays a key role in the pathophysiology of brain and retinal diseases. Moreover, the control of microglia reactivity by blocking A_2AR has been proposed to be the mechanism underlying the observed protective effects of caffeine. Hence, it is conceivable that caffeine and A_2AR antagonists offer therapeutic value for the treatment of retinal diseases, mainly those involving microglia-mediated neuroinflammation.

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Chronic caffeine prevents changes in inhibitory avoidance memory and hippocampal BDNF immunocontent in middle-aged rats

Cited by 50 publications

References 78 publications

Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling

Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling

Caffeine prevents d-galactose-induced cognitive deficits, oxidative stress, neuroinflammation and neurodegeneration in the adult rat brain

Therapeutic Opportunities for Caffeine and A<sub>2A</sub> Receptor Antagonists in Retinal Diseases

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