Astrocyte–neuron interplay in maladaptive plasticity

Papa, Michèle; Luca, Ciro De; Petta, Filomena; Alberghina, Lilia; Cirillo, Giovanni

doi:10.1016/j.neubiorev.2014.01.010

Cited by 90 publications

(63 citation statements)

References 213 publications

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“…As the primary mechanism for glutamate elimination in the synapse, astrocyte action is integral to maintaining glutamatergic tone. 40 Dopaminergic signaling is intimately linked to glutamatergic signaling in the striatum, notably in the context of ethanol exposure. 41 It follows, then, that dopaminergic signaling could be indirectly affected by alterations in glutamatergic signaling resulting from reactive astrocytosis.…”

Section: Discussionmentioning

confidence: 99%

Experimental Traumatic Brain Injury Alters Ethanol Consumption and Sensitivity

Lowing

Susick

Caruso

et al. 2014

Journal of Neurotrauma

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Altered alcohol consumption patterns after traumatic brain injury (TBI) can lead to significant impairments in TBI recovery. Few preclinical models have been used to examine alcohol use across distinct phases of the post-injury period, leaving mechanistic questions unanswered. To address this, the aim of this study was to describe the histological and behavioral outcomes of a noncontusive closed-head TBI in the mouse, after which sensitivity to and consumption of alcohol were quantified, in addition to dopaminergic signaling markers. We hypothesized that TBI would alter alcohol consumption patterns and related signal transduction pathways that were congruent to clinical observations. After midline impact to the skull, latency to right after injury, motor deficits, traumatic axonal injury, and reactive astrogliosis were evaluated in C57BL/6J mice. Amyloid precursor protein (APP) accumulation was observed in white matter tracts at 6, 24, and 72 h post-TBI. Increased intensity of glial fibrillary acidic protein (GFAP) immunoreactivity was observed by 24 h, primarily under the impact site and in the nucleus accumbens, a striatal subregion, as early as 72 h, persisting to 7 days, after TBI. At 14 days post-TBI, when mice were tested for ethanol sensitivity after acute high-dose ethanol (4 g/kg, intraperitoneally), brain-injured mice exhibited increased sedation time compared with uninjured mice, which was accompanied by deficits in striatal dopamine-and cAMP-regulated neuronal phosphoprotein, 32 kDa (DARPP-32) phosphorylation. At 17 days post-TBI, ethanol intake was assessed using the Drinking-in-the-Dark paradigm. Intake across 7 days of consumption was significantly reduced in TBI mice compared with sham controls, paralleling the reduction in alcohol consumption observed clinically in the initial post-injury period. These data demonstrate that TBI increases sensitivity to ethanol-induced sedation and affects downstream signaling mediators of striatal dopaminergic neurotransmission while altering ethanol consumption. Examining TBI effects on ethanol responsitivity will improve our understanding of alcohol use post-TBI in humans.

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Section: Discussionmentioning

confidence: 99%

Experimental Traumatic Brain Injury Alters Ethanol Consumption and Sensitivity

Lowing

Susick

Caruso

et al. 2014

Journal of Neurotrauma

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“…The central nervous system’s own immune cells, microglia and astrocytes are required for normal synaptic functions including synaptic pruning, synapse formation and synaptic transmission (Benarroch, 2013; Papa, De Luca, Petta, Alberghina, & Cirillo, 2014; Stephan, Barres, & Stevens, 2012). A wealth of literature in animal models of inflammation supports the causal role of inflammatory signaling in memory and cognitive deficits.…”

Section: Introductionmentioning

confidence: 99%

Modulation of learning and memory by cytokines: Signaling mechanisms and long term consequences

Donzis

Tronson

2014

Neurobiology of Learning and Memory

218

154

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This review describes the role of cytokines and their downstream signaling cascades on the modulation of learning and memory. Immune proteins are required for many key neural processes and dysregulation of these functions by systemic inflammation can result in impairments of memory that persist long after the resolution of inflammation. Recent research has demonstrated that manipulations of individual cytokines can modulate learning, memory, and synaptic plasticity. The many conflicting findings, however, have prevented a clear understanding of the precise role of cytokines in memory. Given the complexity of inflammatory signaling, understanding its modulatory role requires a shift in focus from single cytokines to a network of cytokine interactions and elucidation of the cytokine-dependent intracellular signaling cascades. Finally, we propose that whereas signal transduction and transcription may mediate short-term modulation of memory, long-lasting cellular and molecular mechanisms such as epigenetic modifications and altered neurogenesis may be required for the long lasting impact of inflammation on memory and cognition.

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“…In this context, it has been proposed that synaptic plasticity may not only be impaired under disease conditions, but dysregulated synaptic plasticity could initiate and even sustain the remodeling of neuronal networks and promote behavioral and cognitive deficits (Nava and Roder, 2011;Ferguson et al, 2012;Leuner and Shors, 2013;Moxon et al, 2014;Papa et al, 2014). This concept of 'maladaptive synaptic plasticity' has been suggested to contribute to the pathogenesis of various neurological diseases such as epilepsy (Swann and Rho, 2014;Winkelmann et al, 2014;Zenonos and Richardson, 2014), ischemic stroke (Calabresi et al, 2003;Di Filippo et al, 2008;Takeuchi and Izumi, 2012) and spinal cord injury (Cirillo et al, 2011;Gwak and Hulsebosch, 2011;Ferguson et al, 2012).…”

Section: Introductionmentioning

confidence: 99%