Tumor necrosis factor alters synaptic transmission in rat hippocampal slices

Tancredi, Virginia; D’Arcangelo, Giovanna; Grassi, Francesca; Tarroni, Paola; Palmieri, Gabriella; Santoni, Angela; Eusebi, Fabrizio

doi:10.1016/0304-3940(92)90071-e

Cited by 283 publications

(164 citation statements)

References 11 publications

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“…IL-1a is believed to be one of the key factors in triggering brain immune responses by inducing the expressions of IL-6 , Frei et al, 1989 and TNFa (Bethea et al, 1992;Chung and Benveniste, 1990). In neuron, TNFa can modulate calcium channels (Soliven and Albert, 1992), decrease catecholamine secretion (Soliven and Albert, 1992), alter synaptic transmission (Tancredi et al, 1992) and protect CNS neurons against metabolic-excitotoxic insults and promote calcium homeostasis (Cheng et al, 1994). IL-6 can induce astrocyte to secrete nerve growth factor (Frei et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Lau

2000

Neurochemistry International

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Section: Discussionmentioning

confidence: 99%

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Lau

2000

Neurochemistry International

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“…In particular, TNFα and IL-6 inhibit the induction of LTP in the CA1 region of the hippocampus [24,25].…”

Section: Behavioural Brain Research 332 (2017) 59-63mentioning

confidence: 99%

Modulation of synaptic plasticity by short-term aerobic exercise in adult mice

D’Arcangelo

Triossi

Buglione

et al. 2017

Behavioural Brain Research

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“…This finding suggests that the early degeneration of LC neurons and their terminals, which will result first in a local but later in an overall NE deficiency, may facilitate the inflammatory reaction in response to Aβ deposition in the AD brain. Given the fact that several inflammatory molecules have been found to impair neuronal functions that contribute to memory formation and consolidation, such as long-term potentiation (20)(21)(22), NE deficits may directly contribute to early neuronal dysfunction by subsequent elevation of inflammatory molecules. Next, it has been shown that proinflammatory cytokines, such as TNFα and IL-1β, can alone or in concert up-regulate the secretion of Aβ by increasing key players of the APP processing (23).…”

Section: Ne Depletion Decreases Microglial Phagocytosis and Recruitmementioning

confidence: 99%

Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine

Heneka

Nadrigny

Regen

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

434

420

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Locus ceruleus (LC)-supplied norepinephrine (NE) suppresses neuroinflammation in the brain. To elucidate the effect of LC degeneration and subsequent NE deficiency on Alzheimer's disease pathology, we evaluated NE effects on microglial key functions. NE stimulation of mouse microglia suppressed Aβ-induced cytokine and chemokine production and increased microglial migration and phagocytosis of Aβ. Induced degeneration of the locus ceruleus increased expression of inflammatory mediators in APP-transgenic mice and resulted in elevated Aβ deposition. In vivo laser microscopy confirmed a reduced recruitment of microglia to Aβ plaque sites and impaired microglial Aβ phagocytosis in NE-depleted APP-transgenic mice. Supplying the mice the norepinephrine precursor L-threo-DOPS restored microglial functions in NE-depleted mice. This indicates that decrease of NE in locus ceruleus projection areas facilitates the inflammatory reaction of microglial cells in AD and impairs microglial migration and phagocytosis, thereby contributing to reduced Aβ clearance. Consequently, therapies targeting microglial phagocytosis should be tested under NE depletion.neuroinflammation | amyloid beta | neurodegeneration | phagocytosis A lzheimer's disease (AD) is characterized by neocortical and hippocampal atrophy due to neuronal loss, the deposition of Aβ peptides, and the formation of neurofibrillar tangles. In addition, there is a progressive degeneration of cholinergic nuclei in the basal forebrain and of noradrenergic nuclei in the brainstem, most importantly the locus ceruleus (LC). This nucleus is the major source of norepinephrine (NE) supply in the mammalian brain. The LC provides the neurotransmitter via an extensive network of neuronal projections to all major brain regions. These regions include the neocortex and hippocampus, the seat of cognitive functions, learning, and memory.Research dating back to the 1960s implicated LC degeneration in the pathogenesis of AD (1-3). Of particular relevance, several studies show that AD patients present with a prominent loss of LC cells, reaching 70% within the rostral nucleus and causing reduction of cortical and limbic NE levels (4). The drop in NE concentration tightly correlates with the progression and extent of memory dysfunction and cognitive impairment. Degeneration of LC neurons has been observed in patients exhibiting "mild cognitive impairment" (MCI) (5), an early form of AD, with 80% of MCI patients eventually succumbing to full AD (6).Degeneration of LC neurons results in progressive loss of two different types of axons, those with either conventional synaptic contacts or varicosities. Varicosities are believed to release transmitter extrasynaptically into the microenvironment, where it may act on surrounding neurons, glial cells, and blood vessels (7). Locally diffusing NE is thought to execute additional functions apart from its role as a classical neurotransmitter. Indeed, NE negatively regulates transcription of inflammatory genes in astrocytes and microglia (8), both expressi...

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Tumor necrosis factor alters synaptic transmission in rat hippocampal slices

Cited by 283 publications

References 11 publications

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Modulation of synaptic plasticity by short-term aerobic exercise in adult mice

Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine

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