Could BDNF be involved in compensatory mechanisms to maintain cognitive performance despite acute sleep deprivation? An exploratory study

Giacobbo, Bruno Lima; Corrêa, Márcio Silveira; Vedovelli, Kelem; Souza, C.E.B. de; Spitza, Letícia Martins; Gonçalves, Lucas Immich; Paludo, Nathália; Molina, Rachel Dias; Rosa, Eduarda Dias da; Argimon, Irani Iracema de Lima; Bromberg, Elke

doi:10.1016/j.ijpsycho.2015.11.008

Cited by 28 publications

(16 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, the levels of BDNF in the cerebral cortex rise with extended wakefulness (Cirelli & Tononi, 2000). The increase of BDNF after sleep deprivation in this research (Figure 3c) were consistent with human studies and rat studies following sleep deprivation protocols (Giacobbo et al, 2016; Wallingford, Deurveilher, Currie, Fawcett, & Semba, 2014). Increase in BDNF protein level could be caused by enhanced expression and secretion, or reduced degradation of BDNF (Lessmann & Brigadski, 2009).…”

Section: Discussionsupporting

confidence: 90%

“…Of interest, brain‐derived neurotrophic factor (BDNF) emerges as a crucial protein in the regulation of both sleep and memory (Alzoubi, Khabour, Salah, & Abu Rashid, 2013; Bachmann et al, 2012; Datta, Siwek, & Huang, 2009; Giacobbo et al, 2016; Mascetti et al, 2013). It can bind to and activate tropomyosin receptor kinase B (TrkB) receptors, thereby regulating the activity of phospholipase C‐γ1 (PLCγ1) pathway (Hyungju & Mu‐Ming, 2013; Zhao & Levine, 2014).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Zhang²,

et al. 2020

Brain and Behavior

View full text Add to dashboard Cite

Introduction:The mechanisms underlying sleep deprivation-induced memory impairments and relevant compensatory signaling pathways remain elusive. We tested the hypothesis that increased brain-derived neurotrophic factor (BDNF) expression in the basal forebrain following acute sleep deprivation was a compensatory mechanism to maintain fear memory performance. Methods: Adult male Wistar rats were deprived of 6-hr total sleep from the beginning of the light cycle. The effects of sleep deprivation on BDNF protein expression and activation of downstream tropomyosin receptor kinase B (TrkB)/phospholipase C-γ1 (PLCγ1) signaling in the basal forebrain and fear memory consolidation were examined. BDNF or selective downstream TrkB receptor antagonist ANA-12 was further injected into the basal forebrain bilaterally to observe the changes in fear memory consolidation in response to modulation of the BDNF/TrkB signaling. Results: Six hours of sleep deprivation-induced both short-and long-term fear memory impairments. Increased BDNF protein expression and TrkB and PLCγ1 phosphorylation in the basal forebrain were observed after sleep deprivation. Microinjection of BDNF into the basal forebrain partly reversed fear memory deficits caused by sleep deprivation, which were accompanied by increased BDNF protein levels and TrkB/PLCγ1 activation. After ANA-12 microinjection, sleep deprivation-induced activation of the BDNF/TrkB pathway was inhibited and impairments of fear memory consolidation were further aggravated. Conclusions: Acute sleep deprivation induces compensatory increase of BDNF expression in the basal forebrain. Microinjection of BDNF into the basal forebrain mitigates the fear memory impairments caused by sleep deprivation by activating TrkB/ PLCγ1 signaling.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Zhang²,

et al. 2020

Brain and Behavior

View full text Add to dashboard Cite

show abstract

“…It has been hypothesized based on neuroimaging studies in humans that repeated sleep deprivation may induce compensatory mechanisms including the recruitment of additional neuronal groups to counteract the adverse effects on cognitive performance (Drummond and Brown, 2001; Drummond et al, 2005). Recently, researchers found increased serum BDNF levels in individuals with 24 h total wakefulness raising the possibility that molecular mechanisms modulating neural circuit activity may also adapt to sleep deprivation to maintain cognitive performance (Giacobbo et al, 2016). Thus, it is possible in our studies that LTM was more resistant than STM to the effects of sleep deprivation as a result of the greater potential for adaptation during long-term memory formation.…”

Section: Discussionmentioning

confidence: 99%

Chronic sleep deprivation differentially affects short and long-term operant memory in Aplysia

Krishnan

Noakes

Lyons

2016

Neurobiology of Learning and Memory

View full text Add to dashboard Cite

The induction, formation and maintenance of memory represent dynamic processes modulated by multiple factors including the circadian clock and sleep. Chronic sleep restriction has become common in modern society due to occupational and social demands. Given the impact of cognitive impairments associated with sleep deprivation, there is a vital need for a simple animal model in which to study the interactions between chronic sleep deprivation and memory. We used the marine mollusk Aplysia californica, with its simple nervous system, nocturnal sleep pattern and well-characterized learning paradigms, to assess the effects of two chronic sleep restriction paradigms on short-term (STM) and long-term (LTM) associative memory. The effects of sleep deprivation on memory were evaluated using the operant learning paradigm, learning that food is inedible, in which the animal associates a specific netted seaweed with failed swallowing attempts. We found that two nights of 6 h sleep deprivation occurring during the first or last half of the night inhibited both STM and LTM. Moreover, the impairment in STM persisted for more than 24 hours. A milder, prolonged sleep deprivation paradigm consisting of 3 consecutive nights of 4 h sleep deprivation also blocked STM, but had no effect on LTM. These experiments highlight differences in the sensitivity of STM and LTM to chronic sleep deprivation. Moreover, these results establish Aplysia as a valid model for studying the interactions between chronic sleep deprivation and associative memory paving the way for future studies delineating the mechanisms through which sleep restriction affects memory formation.

show abstract

“…During exposure to the STROOP‐CWT, the presentation of a word stimulus and a colour stimulus simultaneously causes interference when the processing of one stimulus interferes with the simultaneous processing of the second stimulus . Giacobbo et al (2016) suggested that higher levels of BDNF were optimal for response inhibition capacity assessed by the STROOP‐CWT …”

Section: Introductionmentioning

confidence: 99%

“…8,9 Giacobbo et al (2016) suggested that higher levels of BDNF were optimal for response inhibition capacity assessed by the STROOP-CWT. 10 Increasing evidence has shown that BDNF may have a protective effect in the cardiovascular system. 11 Indeed, Smith et al (2015) have shown that BDNF decreases atherosclerotic plaque formation in the carotid artery of Black South African men.…”

Section: Introductionmentioning

confidence: 99%

BDNF increases associated with constant troponin T levels and may protect against poor cognitive interference control: The SABPA prospective study

Vuren

Malan

Känel

et al. 2019

Eur J Clin Investigation

View full text Add to dashboard Cite

Background Brain‐derived neurotrophic factor (BDNF) modulates brain health and cognition, which can interfere with executive cognitive function. BDNF was implicated with microcirculatory ischaemia and may reflect cardiomyocyte injury. We aimed to determine whether prospective changes (%Δ) in BDNF and cardiac troponin T (cTnT) will be associated with executive cognitive function in a bi‐ethnic cohort. Design A prospective investigation was conducted over a three‐year period in a bi‐ethnic sex cohort (N = 338; aged 20‐65 years) from South Africa. Fasting serum samples for BDNF and cTnT were obtained. The STROOP‐color‐word conflict test (CWT) was applied to assess executive cognitive function at baseline. Results In Blacks, BDNF (P < 0.001) increased over the three‐year period while cTnT did not change. In contrast, in Whites, BDNF and cTnT decreased over three years. In Black men, no change in cTnT was associated with increased ΔBDNF (β = 0.25; 95% CI 0.05‐0.45; P = 0.02). In the Black men, constant cTnT levels were inversely associated with executive cognitive function (β = −0.33; 95% CI −0.53 to −0.12; P = 0.003). Three‐year increases in BDNF increased the likelihood for chronic lower cTnT levels at a pre‐established cut‐point of <4.2 ng/L [OR = 2.35 (1.12‐4.94), P = 0.02]. The above associations were not found in the White sex groups. Conclusions Central neural control mechanisms may have upregulated BDNF in Black men as a way to protect against myocardial stress progression and to possibly improve processes related to cognitive interference control. High‐sensitive cTnT levels may act as an early predictor of disturbed neural control mechanisms.

show abstract

Could BDNF be involved in compensatory mechanisms to maintain cognitive performance despite acute sleep deprivation? An exploratory study

Cited by 28 publications

References 61 publications

Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Chronic sleep deprivation differentially affects short and long-term operant memory in Aplysia

BDNF increases associated with constant troponin T levels and may protect against poor cognitive interference control: The SABPA prospective study

Contact Info

Product

Resources

About