Alcohol administration during adulthood induces alterations of parvalbumin and glial fibrillary acidic protein immunoreactivity in rat hippocampus and cingulate cortex

Vongvatcharanon, Uraporn; Mukem, Sirirak; Udomuksorn, Wandee; Kumarsit, Ekkasit; Vongvatcharanon, Surapong

doi:10.1016/j.acthis.2009.04.001

Cited by 19 publications

(12 citation statements)

References 35 publications

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“…GFAP levels increase in response to acute stressors like ischaemia and neurotoxins. Acute and chronic ethanol exposure in rats dose-dependently increases GFAP expression in several brain regions (Vongvatcharanon et al 2010; Udomuksorn et al 2011). However, with chronic ethanol exposure, GFAP downregulation and astrocyte cell death have been observed (Khokhrina et al 1991).…”

Section: Methodsmentioning

confidence: 99%

Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?

Niciu

Henter

Sanacora

2013

The World Journal of Biological Psychiatry

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Objectives Preclinical and clinical research in neuropsychiatric disorders, particularly mood and substance use disorders, have historically focused on neurons; however, glial cells – astrocytes, microglia, and oligodendrocytes – also play key roles in these disorders. Methods Peer-reviewed PubMed/Medline articles published through December 2012 were identified using the following keyword combinations: glia, astrocytes, oligodendrocytes/glia, microglia, substance use, substance abuse, substance dependence, alcohol, opiate, opioid, cocaine, psychostimulants, stimulants, and glutamate. Results Depressive and substance use disorders are highly comorbid, suggesting a common or overlapping aetiology and pathophysiology. Reduced astrocyte cell number occurs in both disorders. Altered glutamate neurotransmission and metabolism – specifically changes in the levels/activity of transporters, receptors, and synaptic proteins potentially related to synaptic physiology – appear to be salient features of both disorders. Glial cell pathology may also underlie the pathophysiology of both disorders via impaired astrocytic production of neurotrophic factors. Microglial/neuroinflammatory pathology is also evident in both depressive and substance use disorders. Finally, oligodendrocyte impairment decreases myelination and impairs expression of myelin-related genes in both substance use and depressive disorders. Conclusions Glial-mediated glutamatergic dysfunction is a common neuropathological pathway in both substance use and depression. Therefore, glutamatergic neuromodulation is a rational drug target in this comorbidity.

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Section: Methodsmentioning

confidence: 99%

Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?

Niciu

Henter

Sanacora

2013

The World Journal of Biological Psychiatry

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“…These neuroimmune factors include the proinflammatory cytokines IL-6, IL-1β and TNF-α and the chemokine CCL2 (Alfonso-Loeches et al, 2010; Blanco et al, 2005; He and Crews, 2008; Kane et al, 2013; Kane et al, 2014; Lippai et al, 2013; Qin and Crews, 2012; Tiwari et al, 2009; Valles et al, 2004; Vongvatcharanon et al, 2010; Ward et al, 2009; Zhang et al, 2014; Zhao et al, 2013). Ethanol-induced CNS expression of these neuroimmune factors appears to depend on brain region, cell type, and/or dose, duration and method of ethanol exposure.…”

Section: Introductionmentioning

confidence: 99%

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

et al. 2016

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A growing body of evidence has revealed that resident cells of the central nervous system (CNS), and particularly the glial cells, comprise a neuroimmune system that serves a number of functions in the normal CNS and during adverse conditions. Cells of the neuroimmune system regulate CNS functions through the production of signaling factors, referred to as neuroimmune factors. Recent studies show that ethanol can activate cells of the neuroimmune system, resulting in the elevated production of neuroimmune factors, including the cytokine interleukin-6 (IL-6). Here we analyzed the consequences of this CNS action of ethanol using transgenic mice that express elevated levels of IL-6 through increased astrocyte expression (IL-6-tg) to model the increased IL-6 expression that occurs with ethanol use. Results show that increased IL-6 expression induces neuroadaptive changes that alter the effects of ethanol. In hippocampal slices from non-transgenic (non-tg) littermate control mice, synaptically evoked dendritic field excitatory postsynaptic potential (fEPSP) and somatic population spike (PS) at the Schaffer collateral to CA1 pyramidal neuron synapse were reduced by acute ethanol (20 or 60 mM). In contrast, acute ethanol enhanced the fEPSP and PS in hippocampal slices from IL-6 tg mice. Long-term synaptic plasticity of the fEPSP (i.e., LTP) showed the expected dose-dependent reduction by acute ethanol in non-tg hippocampal slices, whereas LTP in the IL-6 tg hippocampal slices was resistant to this depressive effect of acute ethanol. Consistent with altered effects of acute ethanol on synaptic function in the IL-6 tg mice, EEG recordings showed a higher level of CNS activity in the IL-6 tg mice than in the non-tg mice during the period of withdrawal from an acute high dose of ethanol. These results suggest a potential role for neuroadaptive effects of ethanol-induced astrocyte production of IL-6 as a mediator or modulator of the actions of ethanol on the CNS, including persistent changes in CNS function that contribute to cognitive dysfunction and the development of alcohol dependence.

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“…Voluntary intake of alcohol, as well as forced exposure, increases both GFAP and GFAP mRNA expression [90][91][92][93], while withdrawal reduces the number of GFAP positive cells [94,95]. Alcohol also affects astrocyte morphology and induces rearrangements of actin filaments, which may further impair Ca 2+ signaling [64,96].…”

Section: Astrocytic Protein Expression and Morphological Transformationsmentioning

confidence: 99%

Astrocyte Function in Alcohol Reward and Addiction

Adermark¹

2015

J Alcohol Drug Depend

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Glial cells, particularly astrocytes, play essential roles in the regulation of neurotransmission, metabolism, and supply of energy substrates for synaptic transmission. One astrocyte can receive inputs from several hundreds of synapses, and synchronized neuronal activity correlates with astrocyte calcium signaling. Astrocyte pathology is a common feature of ethanol exposure in both humans and animal models, and brief alcohol intake is sufficient to cause long-lasting changes in astrocyte gene expression, activity and proliferation. Recent research also suggests that astrocytes shape the rewarding sensation of ethanol, and might be involved in modulating alcohol consumption. Considering the role of astrocytes in regulating glutamate homeostasis, a crucial component of alcohol abuse disorders, the astrocyte might be an important target for the development of new pharmacological treatments of alcoholism.Keywords: Alcohol; Astrocytes; Astroglia; Glia; GFAP; Dopamine; Ethanol AstrocytesThe astroglial cell, or astrocyte, is the most numerous cell type of the glial cell family. Astrocytes give structural and metabolic support to surrounding neurons and are pivotal for neuronal functioning and signal processing in the CNS [1,2] (Figure 1). The end feet of astrocytic processes encapsulate blood vessels and participate in building up the blood brain barrier [3,4]. The contact with blood vessels also enables the astrocytes to provide neurons with lactate under anaerobic conditions [1,5] (Figure 1). The astrocyte was first acknowledged as the primary cell type responsible for potassium buffering [6], and combined with the clearance of amino acids from the extracellular space, astrocytes warrants a high signal to noise ratio, and reduced receptor desensitization [7,8]. One single astrocyte can enwrap several neuronal somata and receive inputs from thousands of synapses, enabling them to sense and integrate synaptic activity [9,10]. Activation of astrocytes also appears to be a crucial component for the induction of synaptic plasticity mechanisms, and both long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus may be regulated by astrocytes [11,12].Astrocytes enwrap both presynaptic and postsynaptic terminals, forming the tripartite synapse. Astrocytic end feet encapsulate blood vessels, enabling the astrocyte to give metabolic support to surrounding neurons. Astrocytic clearance of neuroactive substances is crucial for synaptic transmission. The excitatory amino acid glutamate (Glu) is rapidly metabolized to its non-excitable precursor glutamine (Gln), released back to the extracellular space, and taken up by neurons for synthesis of glutamate or GABA. See text for further details. Astrocytic transportersOne of the most prominent functions of the astrocyte is the clearance of glutamate, and astrocytic glutamate transporters EAAT2 (GLT-1) and EAAT1 (GLAST) are the most abundant transporters for removal of glutamate in the brain [13]. Impaired astrocytic glutamate clearance appears to contribut...

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Alcohol administration during adulthood induces alterations of parvalbumin and glial fibrillary acidic protein immunoreactivity in rat hippocampus and cingulate cortex

Cited by 19 publications

References 35 publications

Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?

Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

Astrocyte Function in Alcohol Reward and Addiction

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