Emerging Trends in Retrograde Signaling

Suvarna, Yashasvi; Maity, Nivedita; Shivamurthy, M.

doi:10.1007/s12035-015-9280-5

Cited by 12 publications

(10 citation statements)

References 49 publications

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“…PAF mediates a wide variety of cellular functions and cell–cell interactions. Therefore, PAF is involved in several physiological processes including apoptosis, physiological inflammation, wound healing, reproduction, angiogenesis, long-term potentiation, and potentially retrograde signalling [4,5,6,7]. However, PAF is also a potent pro-inflammatory mediator that is implicated in a variety of conditions and chronic diseases such as cancer, renal diseases, cerebrovascular and central nervous system disorders, allergies, asthma, infections, and cardiovascular diseases (CVD) [5,8,9,10,11,12,13].…”

Section: Platelet-activating Factormentioning

confidence: 99%

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

2019

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In the late 1960s, Barbaro and Zvaifler described a substance that caused antigen induced histamine release from rabbit platelets producing antibodies in passive cutaneous anaphylaxis. Henson described a ‘soluble factor’ released from leukocytes that induced vasoactive amine release in platelets. Later observations by Siraganuan and Osler observed the existence of a diluted substance that had the capacity to cause platelet activation. In 1972, the term platelet-activating factor (PAF) was coined by Benveniste, Henson, and Cochrane. The structure of PAF was later elucidated by Demopoulos, Pinckard, and Hanahan in 1979. These studies introduced the research world to PAF, which is now recognised as a potent phospholipid mediator. Since its introduction to the literature, research on PAF has grown due to interest in its vital cell signalling functions and more sinisterly its role as a pro-inflammatory molecule in several chronic diseases including cardiovascular disease and cancer. As it is forty years since the structural elucidation of PAF, the aim of this review is to provide a historical account of the discovery of PAF and to provide a general overview of current and future perspectives on PAF research in physiology and pathophysiology.

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Section: Platelet-activating Factormentioning

confidence: 99%

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

2019

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“…If so, could there be a retrograde mechanism involved in the effect? [36]. Because the effect was rapid, we thought that it could be produced by nitric oxide (NO), a retrograde messenger, known to be involved in presynaptic neurotransmitter release [37][38][39] and produced by nitric oxide synthase (NOS).…”

Section: Increased No-production In Iaβo-treated In Recorded (Rn) Andmentioning

confidence: 99%

Functional spreading of hyperexcitability induced by human and synthetic intracellular Aβ oligomers

Fernández-Pérez

Muñoz

Bascuñán

et al. 2020

Preprint

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Background: Intracellular amyloid-beta oligomers (iAβo) accumulation and neuronal hyperexcitability are two crucial events at early stages of Alzheimer’s disease (AD). However, to date, no mechanism linking them has been reported. Methods: Here, the effects of human AD brain-derived (h-iAβo) and synthetic (iAβo) peptides on synaptic currents and action potential (AP) firing were investigated in hippocampal neurons in vitro , ex vivo and in vivo. Results: Starting from 500 pM, iAβo rapidly increased the frequency of synaptic currents and higher concentrations potentiated the AMPA receptor-mediated current. Both effects were PKC-dependent. Parallel recordings of synaptic currents and nitric oxide (NO)-related fluorescence changes indicated that the increased frequency, related to pre-synaptic release, was dependent on a NO-mediated retrograde signaling. Moreover, increased synchronization in NO production was also observed in neurons neighboring those dialyzed with iAβo, indicating that iAβo can increase network excitability at a distance. Current-clamp recordings suggested that iAβo increased neuronal excitability via AMPA-driven synaptic activity without altering membrane intrinsic properties. Conclusion: These results strongly indicate that iAβo causes functional spreading of hyperexcitability through a synaptic-driven mechanism and offer an important neuropathological significance to intracellular species in the initial stages of AD, which include brain hyperexcitability and seizures.

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Section: Increased No-production In Iaβo-treated In Recorded (Rn) Andmentioning

confidence: 99%

Functional spreading of hyperexcitability induced by human and synthetic intracellular Aβ oligomers

Fernández-Pérez

Muñoz

Bascuñán

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Intracellular amyloid-beta oligomers (iAβo) accumulation and neuronal hyperexcitability are two crucial events at early stages of Alzheimer's disease (AD). However, to date, no mechanism linking them has been reported. Methods: Here, the effects of human AD brain-derived (h-iAβo) and synthetic (iAβo) peptides on synaptic currents and action potential (AP) firing were investigated in hippocampal neurons in vitro, ex vivo and in vivo. Results: Starting from 500 pM, iAβo rapidly increased the frequency of synaptic currents and higher concentrations potentiated the AMPA receptor-mediated current. Both effects were PKC-dependent. Parallel recordings of synaptic currents and nitric oxide (NO)-related fluorescence changes indicated that the increased frequency, related to pre-synaptic release, was dependent on a NO-mediated retrograde signaling. Moreover, increased synchronization in NO production was also observed in neurons neighboring those dialyzed with iAβo, indicating that iAβo can increase network excitability at a distance. Current-clamp recordings suggested that iAβo increased neuronal excitability via AMPA-driven synaptic activity without altering membrane intrinsic properties. Conclusion: These results strongly indicate that iAβo causes functional spreading of hyperexcitability through a synaptic-driven mechanism and offer an important neuropathological significance to intracellular species in the initial stages of AD, which include brain hyperexcitability and seizures.

show abstract

Emerging Trends in Retrograde Signaling

Cited by 12 publications

References 49 publications

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

Functional spreading of hyperexcitability induced by human and synthetic intracellular Aβ oligomers

Functional spreading of hyperexcitability induced by human and synthetic intracellular Aβ oligomers

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