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1

Regulation of extracellular signal-regulated kinases activity by morphine in mouse brain

100%
Wawrzczak-Bargiela A., Bilecki W., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2007
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tom 67
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nr 3
2

Morphine regulates the level of kinesin light chain 1, a molecule involved in neuronal trafficking

100%
Bilecki W., Wawrzczak-Bargiela A., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2007
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tom 67
|
nr 3
3

Modulation of the expression of opioid inducible genes using RNA interference

88%
Ligeza A., Wawrzczak-Bargiela A., Kaminska D., Korostynski M., Przewlocki M.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 3
4

Molecular biomarkers of addiction in a model of long-term morphine self-administration in mice

76%
Skupio U., Sikora M., Korostynski M., Wawrzczak-Bargiela A., Piechota M., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
INTRODUCTION: Chronic exposure to opioids induces various adaptations in brain physiology that lead to formation of dependence and addiction. Commonly used approaches for modeling morphine dependence, such as conditioned place preference and morphine self-administration typically last less than two weeks, which is presumably too short to observe long-lasting alterations in the brain that accompany drug addiction. AIM(S): In the present study, we aimed to establish a novel model of long-term morphine self-administration in C57BL/6J mice. Our second goal was to identify molecular biomarkers, specific transcriptional patterns and signs of genetic predispositions to opiate addiction. METHOD(S): We used automated IntelliCage system to observe the animals in groups. The animals in two separate cages were allowed access to morphine or saccharin solutions for 3 months. We tested animals for symptoms of addiction using paradigms like progressive ratio schedule and intermittent access. Gene expression profiles were evaluated in the striatum using whole-genome microarrays and qPCR. RESULTS: The animals drinking morphine showed addiction-related behavioral pattern when compared with control animals. The analysis of molecular changes revealed long-lasting alterations in gene expression profiles between the analyzed groups of animals. Interestingly, correlation analyses between individual gene expression levels and motivation allowed to identify genes (Epha5, Ncam) that possibly indicate predisposition to addiction-like behaviors. CONCLUSIONS: Our model represents a novel approach for investigating both behavioral and molecular mechanisms of addiction. Mice drinking morphine exhibit many of the addiction-like symptoms compared to control animals. Prolonged morphine intake resulted in adaptive processes in the brain that manifested as altered transcriptional sensitivity to opioids. FINANCIAL SUPPORT: Supported by Polish National Science Centre Grant no. 2013/08/A/NZ3/00848.
5

Hanges of genes expression in the nucleus accumbens during neuropathic pain in mouse brain

76%
Wawrzczak-Bargiela A., Ziołkowska B., Bilecki W., Rojewska E., Mika J., Przewlocka B., Przewlocki R.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
6

The involvement of giycogen synthase and cyclin dependent kinases in morphine analgesia in rats

76%
Obara I., Wawrzczak-Bargiela A., Rodriguez Parkitna J. M., Makuch W., Przewlocki R., Przewlocka B.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 3
7

The role of astrocytic glucocorticoid receptor in behavioral effects of opioids

76%
Kudla L., Skupio U., Marut L., Tertil M., Wawrzczak-Bargiela A., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Glucocorticoid receptor (GR)-dependent mechanisms are considered to affect behavioral effects of multiple drugs of abuse, including opioids. Recent evidence points to the important role of astrocytes in mediating GR-dependent effects in the brain. However, the exact mechanisms of astrocytic GR contribution to behavioral response to opioids remain unknown. AIM(S): Here, we aimed to evaluate effects of opioid receptors ligands in astrocytic GR knockout mice. We assessed the animals in nociception and addiction assays. METHOD(S): We used transgenic mice in which GR is selectively ablated in astrocytes expressing connexin 30 (C×30×GR flox/flox) and non‑transgenic littermates. To investigate nociceptive sensitivity and morphine-induced analgesia, animals were assessed in tail flick test. To evaluate addiction-like behavior, morphine tolerance and naloxone-precipitated morphine withdrawal symptoms were measured. Moreover, sensitivity to opioid reward was tested in conditioned place preference (CPP) paradigm and response to aversive properties of naloxone was measured using conditioned place aversion (CPA) test. RESULTS: Mutant and control mice presented similar nociceptive sensitivity, did not differ in morphine analgesia, developed similar opioid tolerance and morphine-induced CPP. However, when subjected to naloxone-precipitated morphine withdrawal, mutants showed decreased number of jumps, indicating attenuated physical signs of opioid withdrawal. What is more, astrocytic GR knockout mice did not acquire naloxone-induced CPA, suggesting alternations in behavioral response to naloxone-evoked aversion. CONCLUSIONS: Our data indicate that astrocytic GR may be involved in regulation of naloxone-induced aversion and morphine withdrawal. However, knockout of GR in astrocytes does not influence pain sensitivity, morphine analgesia, tolerance and reward-associated memory. In conclusion, our results shed a light on the causal role of GR-dependent signaling in astrocytes in mediating behavioral effects of opioids. FINANCIAL SUPPORT: Funding for this study was provided by Polish National Science Centre Grant: 2013/08/A/ NZ3/00848.
8

Changes of genes expression in the nucleus accumbens during neuropathic pain in mouse brain

76%
Wawrzczak-Bargiela A., Ziołkowska B., Bilecki W., Rojewska E., Mika J., Przewlocka B., Przewlocki R.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: The nucleus accumbens (NAc), which is known to be an important component of the mesolimbic dopaminergic reward system also plays a role in pain, however the molecular mechanisms of this involvement are not known. In the present study we explored molecular pathways involved in the neuropathic pain. Understanding of this process would allow us brain mapping and find biomarkers for pain transmission. AIM(S): The aim of this study was to investigate the alterations in genes expression after CCI in the NAc. METHOD(S): Neuropathic pain was induced by applying a Chronic Constriction Injury (CCI) model in C57BL/6J mice. Two behavioral tests for neuropathic pain were used: the von Frey’s test and the cold plate test. In our biochemical researches we used qRT-PCR. RESULTS: We found that nerve injury produced a significant increase in the expression of opioid genes (PDYN, PENK), opioid kappa and delta receptors genes (KOR, DOR) and calcium/calmodulin - dependent protein kinase kinase 1 (CAMKK1) in the nucleus accumbens. Furthermore, we observed that neuropathic pain augmented the expression of stress – and inflammatory response genes coding for the glucocorticoid receptor (GR), FK506 binding protein5 (FKBP5), and interleukins IL1 beta and IL6 in the nucleus accumbens. Moreover, elevated levels of GFAP (astrocyte marker) but not C1q (microglia marker) mRNAs were detected. CONCLUSIONS: Our results demonstrate that CCI produces lasting biochemical changes in the NAc.Taking into account the well-known roles of opioid systems in pain transmission and emotional processes, the observed changes in the expression of the opioid propeptides and receptors genes may contribute to changes in pain sensitivity and in affective response to nociceptive stimulation. Furhermore, increased expression of GFAP, GR, FKBP5, Il6 and Il1beta genes suggests that cellular stress and inflammatory processes are involved in this type of pain not only on the level of the spinal cord but also in the brain. FINANCIAL SUPPORT: Research supported by HEALTH-F2-2013-602891 NEUROPAIN.
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