α-Synuclein expression in the brain and blood during abstinence from chronic alcohol drinking in mice

Ziółkowska, Barbara; Gieryk, Agnieszka; Wawrzczak-Bargieła, Agnieszka; Krowka, Tomasz; Kaminska, Dorota; Korkosz, Agnieszka; Bieńkowski, Przemysław; Przewłocki, Ryszard

doi:10.1016/j.neuropharm.2008.04.001

Cited by 16 publications

(22 citation statements)

References 53 publications

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“…There have however been reports of increased α-synuclein gene and protein expression in the amygdala upon abstinence from alcohol [24]. Downregulation of α-synuclein mRNA level together with increased α-synuclein protein level was reported upon morphine-withdrawal [25] in mice.…”

Section: Discussionmentioning

confidence: 99%

Response of α-Synuclein Expression to Amyloid β40 and Amyloid β42 administration into Rat Brain

Mishra¹,

Kumar²,

Singh³

et al. 2017

J Alzheimers Dis Parkinsonism

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Section: Discussionmentioning

confidence: 99%

Response of α-Synuclein Expression to Amyloid β40 and Amyloid β42 administration into Rat Brain

Mishra¹,

Kumar²,

Singh³

et al. 2017

J Alzheimers Dis Parkinsonism

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“…The high expression of α -synuclein in the brain inhibits the activity of enzymes involved in dopamine synthesis [9], thus affecting the function of dopamine transporter [10] and inhibiting the release of dopamine [11], thus preventing the neurosecretion [12]. The alteration in dopaminergic system in the brain stimulated by α -synuclein contributes to an exhibition of dependence and abuse of drug and alcohol [12, 31]. Elevated expression of α -synuclein was suggested to downregulate the activity of dopaminergic.…”

Section: Discussionmentioning

confidence: 99%

Morphine Antidependence of Erythroxylum cuneatum (Miq.) Kurz in Neurotransmission Processes In Vitro

Suliman

Moklas

Taib

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Opiate abuse has been studied to cause adaptive changes observed in the presynaptic release and the mediated-synaptic plasticity proteins. The involvement of neuronal SNARE proteins reveals the role of the neurotransmitter release in expressing the opioid actions. The present study was designed to determine the effect of the alkaloid extract of Erythroxylum cuneatum (E. cuneatum) against chronic morphine and the influences of E. cuneatum on neurotransmission processes observed in vitro. The human neuroblastoma cell line, SK-N-SH, was treated with the morphine, methadone, or E. cuneatum. The cell lysates were collected and tested for α-synuclein, calmodulin, vesicle-associated membrane protein 2 (VAMP 2), and synaptotagmin 1. The extract of E. cuneatum was observed to upregulate the decreased expression of dependence proteins, namely, α-synuclein and calmodulin. The effects were comparable to methadone and control. The expressions of VAMP 2 and synaptotagmin 1 were normalised by the plant and methadone. The extract of E. cuneatum was postulated to treat dependence symptoms after chronic morphine and improve the soluble N-ethylmaleimide-sensitive factor activating protein receptor (SNARE) protein involved in synaptic vesicle after.

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“…, 2007) or rodent (Liang et al. , 2003; Liang & Carr, 2006; Walker & Grant, 2006; Ziolkowska et al. , 2008) subjects using genetic (Liang et al.…”

Section: Discussionmentioning

confidence: 99%

“…, 2007) or tissue‐based outcomes (Bonsch et al. , 2004, 2005a; Liang & Carr, 2006; Walker & Grant, 2006; Ziolkowska et al. , 2008).…”

Section: Discussionmentioning

confidence: 99%

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Biochemical and morphological consequences of human α-synuclein expression in a mouse α-synuclein null background

Prasad

Tarasewicz

Ohman‐Strickland

et al. 2011

European Journal of Neuroscience

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A consensus about the functions of human wild-type or mutated α-synuclein (αSYN) is lacking. Both forms of αSYN are implicated in Parkinson’s disease, whereas the wild-type form is implicated in substance abuse. Interactions with other cellular proteins and organelles may meditate its functions. We developed a series of congenic mouse lines containing various allele doses or combinations of the human wild type αSYN (hwαSYN) or a doubly mutated (A30P*A53T) αSYN (hm2αSYN) in a C57Bl/6J line spontaneously deleted in mouse αSYN (C57BL/6JOla). Both transgenes had a functional role in the nigrostriatal system, demonstrated by significant elevations in striatal catecholamines, metabolites, and the enzyme tyrosine hydroxylase compared to null-mice without a transgene. Consequences occurred when the transgenes were expressed at a fraction of the endogenous level. Hemizygous congenic mice did not exhibit any change in the number or size of dopaminergic neurons in the ventral midbrain at nine months of age. Human αSYN was predominantly located in neuronal cell bodies, neurites, synapses, and in intraneuronal/intraneuritic aggregates. The hm2αSYN transgene resulted in more aggregates and dystrophic neurites than did the hw5 transgene. The hwαSYN transgene resulted in higher expression of two striatal proteins, synaptogamin 7 and UCHL1, compared to the levels of the hm2αSYN transgene. These observations suggest that mutations in αSYN may impair specific functional domains, leaving others intact. These lines may also be useful for exploring interactions between hαSYN and environmental or genetic risk factors in dopamine-related disorders using a mouse model.

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α-Synuclein expression in the brain and blood during abstinence from chronic alcohol drinking in mice

Cited by 16 publications

References 53 publications

Response of α-Synuclein Expression to Amyloid β40 and Amyloid β42 administration into Rat Brain

Response of α-Synuclein Expression to Amyloid β40 and Amyloid β42 administration into Rat Brain

Morphine Antidependence of Erythroxylum cuneatum (Miq.) Kurz in Neurotransmission Processes In Vitro

Biochemical and morphological consequences of human α-synuclein expression in a mouse α-synuclein null background

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