The effect of caffeine in animal models of learning and memory

Angelucci, Miriam Elizabeth Mendes; Vital, Maria A.B.F.; Cesário, Clérson; Zadusky, Carla R; Rosalen, Pedro Luiz; Cunha, Cláudio Da

doi:10.1016/s0014-2999(99)00225-3

Cited by 101 publications

(78 citation statements)

References 22 publications

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“…Several studies indicate that caffeine may act as a cognitive enhancer (Lieberman et al 1987; Durlach 1998; Angelucci et al 1999) and recent reports confirm that this substance improves consolidation of long‐term memory in humans (Borota et al 2014). However, the indirect action of caffeine on arousal, mood and concentration contributes significantly to its cognitive benefits (Nehlig 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Caffeine, a central nervous system (CNS) stimulant (Nehlig 2010) that enhances cognitive function in both humans and experimental animals (Lieberman et al 1987; Durlach 1998; Angelucci et al 1999; Borota et al 2014), is the most widely consumed behaviorally active substance in the world. Caffeine modulates CNS activities through several mechanisms of action including antagonism of adenosine and GABA A receptors (Daly 2007), phosphodiesterase inhibition (Smellie et al 1979) and sensitization of calcium‐induced calcium release through ryanodine‐sensitive channels (McPherson et al 1991; Martín & Buño 2003).…”

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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“…This disruption of acquisition or retrieval induced by caffeine (a non-selective A 1 and A 2A adenosine receptor antagonist) might be due to the concomitant participation of both A 1 and A 2A receptors with various effects of different brain regions that control the different phases of memory processing. Inactivation of both A 1 and A 2A receptors has been found to counteract the age related cognitive decline [50,51]. Because of these cognition enhancement properties from combined blockade of A 1 and A 2A receptors, caffeine has been proposed as a potential therapeutic agent to reverse age-related cognitive decline [50].…”

Section: Discussionmentioning

confidence: 99%

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized clinically by cognitive decline and memory loss. Caffeine and nicotine are the most commonly co-used psycho stimulants. Caffeine is one of the major contributors to the dietary antioxidants which prevent oxidative damage and may reduce the risk of chronic neurodegenerative diseases. Nicotine has the ability to decrease level of reactive oxygen species (ROS) in the hippocampus and suggested to attenuate the impairment of memory associated with AD. The study aimed to evaluate the influence of caffeine and nicotine co-administration against aluminium-induced neurotoxicity that mimics AD in rats. Five groups of rats were used and received daily for five weeks: Saline for control, aluminium chloride (AlCl 3 ) (70 mg/kg, IP) for AD mimic group, while treated groups received together with AlCl 3 , either Caffeine (5mg/kg, IP), Nicotine (1 mg/kg, SC) or their combination. Three behavioral experiments were performed: Forced Swimming Test (FST), Morris Water Maze (MWM) task and Conditioned-Avoidance and Learning (CAL) test. Histo pathological changes in the brain and biochemical changes in Acetyl cholinesterase (AchE) as well as oxidative parameters; malon dialdehyde (MDA), superoxide dismutase (SOD), total anti oxidane capacity (TAC) were also evaluated for all groups. Results of the behavioral tests showed that caffeine and nicotine co-administration had more pronounced protecting effect from learning and memory impairment induced by AlCl 3 than each one alone. Caffeine and nicotine co-administration also prevent neuronal degeneration in the hippocampus and the eosinophilic plagues in the striatum induced by AlCl 3 while nicotine alone still showed mild gliosis in striatum. The marked protection of caffeine and nicotine co-administration confirmed also by the significant increase in TAC and SOD and decrease in MDA and AchE in brain tissue. In conclusion, co-administration of caffeine and nicotine can reduce the risk of neuronal degeneration in the hippocampus and attenuate the impairment of learning and memory associated with AD.

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“…Molinengo et al (12) reported re-duction in memory decay in rats receiving chronic administration of caffeine after interruption of training in the staircase task. There are also some reports of caffeine improving memory consolidation when administered after training for a habituation task in rats (10), inhibitory avoidance in mice (13) and in rats (10), a multi-chamber maze in mice (14), and active avoidance in rats (15,16).…”

Section: Discussionmentioning

confidence: 99%

Effects of caffeine on learning and memory in rats tested in the Morris water maze

Angelucci

Cesário

Hiroi

et al. 2002

Braz J Med Biol Res

116

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We studied some of the characteristics of the improving effect of the non-specific adenosine receptor antagonist, caffeine, using an animal model of learning and memory. Groups of 12 adult male Wistar rats receiving caffeine (0.3-30 mg/kg, ip, in 0.1 ml/100 g body weight) administered 30 min before training, immediately after training, or 30 min before the test session were tested in the spatial version of the Morris water maze task. Post-training administration of caffeine improved memory retention at the doses of 0.3-10 mg/kg (the rats swam up to 600 cm less to find the platform in the test session, P£0.05) but not at the dose of 30 mg/kg. Pre-test caffeine administration also caused a small increase in memory retrieval (the escape path of the rats was up to 500 cm shorter, P£0.05). In contrast, pre-training caffeine administration did not alter the performance of the animals either in the training or in the test session. These data provide evidence that caffeine improves memory retention but not memory acquisition, explaining some discrepancies among reports in the literature. Correspondence

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The effect of caffeine in animal models of learning and memory

Cited by 101 publications

References 22 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

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Effects of caffeine on learning and memory in rats tested in the Morris water maze

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