Caffeine-induced synaptic potentiation in hippocampal CA2 neurons

Simons, Stephen B.; Caruana, Douglas A.; Zhao, Mei; Dudek, Serena M.

doi:10.1038/nn.2962

Cited by 73 publications

(73 citation statements)

References 15 publications

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“…Consistent with the enrichment of A 1 Rs in CA2, a brief 5-min application of a physiologically relevant concentration of caffeine or other selective A 1 R antagonist induced a lasting potentiation of synaptic transmission in CA2 (Fig. 3A), but not in areas CA1 or CA3 (Simons et al 2011;CA1, Fig. 3D; CA3, Fig.…”

supporting

confidence: 66%

“…The finding that LTP is not normally expressed in SC inputs to CA2 suggests, however, that either the SC to CA2 pathway is a stable component of the hippocampal trisynaptic circuit not required for memory formation or that memories requiring the SC to CA2 pathway can be formed only under very specific conditions. Consistent with the latter possibility and as noted above, several stimuli, including vasopressin and caffeine, are capable of potentiating SC synapses in CA2 (Zhao and Dudek 2010;Simons et al 2011;Zhao et al 2011). Given that both caffeine and vasopressin influence social behavior (Wersinger et al 2002;Prediger and Takahashi 2005;DeVito et al 2009), we support the proposal of DeVito et al (2009) that regulation of plasticity at CA2 synapses may play a role in some forms of social memory, such as social recognition.…”

Section: Role For Ca2 In Learning and Memorysupporting

confidence: 55%

“…Consistent with the finding that calcium levels are severely restricted in CA2 pyramidal cells, there is no evidence that calcium-dependent pathways are required for the A 1 R-mediated potentiation observed in CA2 (Simons et al 2011). Instead, the potentiation is sensitive to inhibitors of adenylyl cyclase or protein kinase A, which is suggested by the enrichment of the calcium-independent adenylyl cyclases 5 and 6 present in CA2 (Visel et al 2006;Lein et al 2007).…”

supporting

confidence: 55%

“…Preliminary evidence has been presented showing that pharmacological activation in vitro of receptors for the social neuropeptides oxytocin and vasopressin (specifically Avpr1b) readily induces a long-lasting potentiation of synaptic transmission in area CA2 Dudek 2010: Zhao et al 2011). Additionally, a recent report presents evidence that the high expression of A 1 Rs in area CA2 (Ochiishi et al 1999) is associated with persistent changes in synaptic efficacy in SC inputs to CA2 in response to A 1 R antagonists, including caffeine (Simons et al 2011).…”

mentioning

confidence: 99%

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New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

2012

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The search for molecules that restrict synaptic plasticity in the brain has focused primarily on sensory systems during early postnatal development, as critical periods for inducing plasticity in sensory regions are easily defined. The recent discovery that Schaffer collateral inputs to hippocampal area CA2 do not readily support canonical activity-dependent long-term potentiation (LTP) serves as a reminder that the capacity for synaptic modification is also regulated anatomically across different brain regions. Hippocampal CA2 shares features with other similarly "LTP-resistant" brain areas in that many of the genes linked to synaptic function and the associated proteins known to restrict synaptic plasticity are expressed there. Add to this a rich complement of receptors and signaling molecules permissive for induction of atypical forms of synaptic potentiation, and area CA2 becomes an ideal model system for studying specific modulators of brain plasticity. Additionally, recent evidence suggests that hippocampal CA2 is instrumental for certain forms of learning, memory, and social behavior, but the links between CA2-enriched molecules and putative CA2-dependent behaviors are only just beginning to be made. In this review, we offer a detailed look at what is currently known about the synaptic plasticity in this important, yet largely overlooked component of the hippocampus and consider how the study of CA2 may provide clues to understanding the molecular signals critical to the modulation of synaptic function in different brain regions and across different stages of development.

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supporting

confidence: 66%

Section: Role For Ca2 In Learning and Memorysupporting

confidence: 55%

supporting

confidence: 55%

mentioning

confidence: 99%

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New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

2012

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“…Adenosine A 1 receptors are highly expressed in the CA2 region, 26) and caffeine is more likely to induce synaptic plasticity in the CA2 region, compared to CA1 or CA3 regions. 27) Because bidirectional projections exist between the CA2 and CA3 regions, 28) it is possible that caffeine acts on adenosine A 1 receptors in the CA2 region and thereby increases hippocampal SWs. To address this possibility, we surgically removed the CA2 and CA1 regions from hippocampal slices using a scalpel and prepared dentate-CA3 mini-slices (Fig.…”

Section: Resultsmentioning

confidence: 99%

Caffeine Increases Hippocampal Sharp Waves <i>in Vitro</i>

Watanabe

Ikegaya

2017

Biological & Pharmaceutical Bulletin

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Caffeine promotes memory consolidation. Memory consolidation is thought to depend at least in part on hippocampal sharp waves (SWs). In the present study, we investigated the effect of bath-application of caffeine in spontaneously occurring SWs in mouse acute hippocampal slices. Caffeine induced an about 100% increase in the event frequency of SWs at concentrations of 60 and 200 µM. The effect of caffeine was reversible after washout of caffeine and was mimicked by an adenosine A 1 receptor antagonist, but not by an A 2A receptor antagonist. Caffeine increased SWs even in dentate-CA3 mini-slices without the CA2 regions, in which adenosine A 1 receptors are abundantly expressed in the hippocampus. Thus, caffeine facilitates SWs by inhibiting adenosine A 1 receptors in the hippocampal CA3 region or the dentate gyrus.

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Association of caffeine consumption with cerebrospinal fluid biomarkers in mild cognitive impairment and Alzheimer's disease: A BALTAZAR cohort study

Blum,

Cailliau,

Béhal

et al. 2024

Alzheimer's & Dementia

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INTRODUCTIONWe investigated the link between habitual caffeine intake with memory impairments and cerebrospinal fluid (CSF) biomarkers in mild cognitive impairment (MCI) and Alzheimer's disease (AD) patients.METHODSMCI (N = 147) and AD (N = 116) patients of the Biomarker of AmyLoid pepTide and AlZheimer's diseAse Risk (BALTAZAR) cohort reported their caffeine intake at inclusion using a dedicated survey. Associations of caffeine consumption with memory impairments and CSF biomarkers (tau, p‐tau181, amyloid beta 1‐42 [Aβ1‐42], Aβ1‐40) were analyzed using logistic and analysis of covariance models.RESULTSAdjusted on Apolipoprotein E (APOE ε4), age, sex, education level, and tobacco, lower caffeine consumption was associated with higher risk to be amnestic (OR: 2.49 [95% CI: 1.13 to 5.46]; p = 0.023) and lower CSF Aβ1‐42 (p = 0.047), Aβ1‐42/Aβ1‐40 (p = 0.040), and Aβ1‐42/p‐tau181 (p = 0.020) in the whole cohort.DISCUSSIONData support the beneficial effect of caffeine consumption to memory impairments and CSF amyloid markers in MCI and AD patients.Highlights We studied the impact of caffeine consumption in the BALTAZAR cohort. Low caffeine intake is associated with higher risk of being amnestic in MCI/AD patients. Caffeine intake is associated with CSF biomarkers in AD patients.

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Caffeine-induced synaptic potentiation in hippocampal CA2 neurons

Cited by 73 publications

References 15 publications

New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

Caffeine Increases Hippocampal Sharp Waves <i>in Vitro</i>

Association of caffeine consumption with cerebrospinal fluid biomarkers in mild cognitive impairment and Alzheimer's disease: A BALTAZAR cohort study

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