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1

Spinal peptidergic mechanisms of neuropathy after nerve injury

100%
Przewlocka B.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 3
2

Endogenous opioid systems in the control of chronic pain

100%
Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1992
|
tom 52
|
nr 3
3

Is there a common mechanism of drugs of abuse?

100%
Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
4

Modulation of glia activation in neuropathic pain

100%
Przewlocka B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
There is a growing body of evidence indicating that glial cells have causal role in the pathogenesis of pain hypersensitivity following nerve injury. We aimed to examine how chronic constriction injury (CCI) to the sciatic nerve infl uences glia activity markers, cytokine levels and expression of mGlu receptors in the spinal cord and dorsal root ganglia (DRG) as well as features of the neuropathic pain, such as allodynia and hyperalgesia in rats and mice. Our study showed that glial markers (C1q, GFAP), interleukins (IL-1β, IL-6) and mGlu receptor (mGlu5, mGlu3) mRNAs were strongly elevated ipsilaterally in the spinal cord after CCI. Microglial cells were more activated in the spinal cord in contrast to DRG where astrocytic activation prevailed. In the ipsilateral DRG, IL-1α, IL-6, and IL-10 mRNA levels were increased. Western blot analysis showed the presence of IL-1α protein in the DRG and down-regulation of these proteins after CCI. Minocycline and/or pentoxifylline administration reversed the injury-induced changes in glia markers and mGlu receptor mRNAs and protein levels, and signifi cantly attenuated CCI-induced allodynia and hyperalgesia. The implication of glial activation paralleled with upregulation of mGlu receptors in neurodegenerative processes suggests that pharmacological targeting of spinal microglia in chronic pain may provide an effective therapy for controlling clinical pain syndromes. Support: statutory funds of the Institute of Pharmacology, PAS.
5

Effects of drugs of abuse on the prodynorphin system activity in the rat brain

100%
Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
6

Uklady hamujace przewodzenie bodzcow bolowych

88%
Przewlocka B.
Wszechświat
|
2003
|
tom 104
|
nr 04-06
75-77
7

Role of opioids in neuropathic pain

75%
Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
8

Materiały Szkoły Zimowej n.t. Neuropeptydów

63%
Vetulani J., Przewlocka B.
Postępy Biochemii
|
1985
|
tom 31
|
nr 3-4
9

Changes in the opioid systemsand CRF in the amygdala in various models of drug dependence

51%
Turchan J., Maj M., Przewlocki R., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
10

Influence of preemptive administration of pentoxifiline on nociception. Experimental and clinical studies

51%
Wordliczek J., Przewlocka B., Szczepanik A., Dobrogowski J.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
11

Interactions between melanocortins and opioids. In vivo and in vitro studies

51%
Starowicz K., Przewlocka B., Przewlocki R.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
12

Opposite dopaminergic regulation of neuropeptide Y and corticotropin releasing factor in the rat amygdala

51%
Smialowska M., Bajkowska M., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
13

Effect of reserpine or 6-OHDA on NPY and CRF expression and synthesis in rat amygdala

51%
Smialowska M., Bajkowska M., Mika J., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
14
Content available remote

Efficacy of tramadol in combination with doxepin or venlafaxine in inhibition of nociceptive process in the rat model of neuropathic pain: an isobolographic analysis

51%
Wrzosek A., Obara I., Wordliczek J., Przewlocka B.
Journal of Physiology and Pharmacology
|
2009
|
tom 60
|
nr 4
71-78
Neuropathic pain constitutes a serious therapeutic problem. In most cases polytherapy is necessary. Tramadol and antidepressants have common mechanisms of action and are frequently used together in clinical practice, thus interaction between them is very important. In the present study isobolographic analysis for equivalent doses of drugs was applied to examine the nature of interaction between tramadol and doxepin or venlafaxine in a neuropathic pain model in rats. Allodynia and hyperalgesia were assessed after intraperitoneal administration of each drug alone or in combination. Dose response curves were obtained and ED50 doses were calculated. All drugs were effective in reducing thermal hyperalgesia and mechanical allodynia, however doxepin was more effective than venlafaxine. Combined administration of tramadol and doxepin demonstrated synergistic action in reducing thermal hyperalgesia and additive action in reducing mechanical allodynia. Combined administration of tramadol and venlafaxine showed additive action in reducing hyperalgesia and allodynia. Moreover, combined administration of tramadol and doxepin was more effective than combined administration of tramadol and venlafaxine. The experiments demonstrated that the nature of interaction between tramadol and doxepin is synergistic, which is not the case for tramadol and venlafaxine, what provides a valuable information referring to clinical practice, rationalizing administration of such drug combination.
15

The involvement of NOS inhibitors in effects of morphine and endomorphine-1 in neuropathic pain

51%
Makuch W., Sieja A., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
16

Novel pharmacotherapy of osteoarthritis: TRPV1 and CB1 receptors as targets for pharmacological intervention

45%
Starowicz K., Malek N., Makuch W., Kolosowska N., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Osteoarthritis (OA) is the most common degenerative joint disease, which leads to pain during joint loading and to chronic physical disability. The management of OA is often frustrating for both patients and physicians as adequate pain relief is difficult to achieve and no treatment modality seems to reverse the disease progression. Clearly, OA is a large, unmet medical need, there is a strong need to develop new treatments for OA. Considerable evidence has uncovered new mechanisms underlying the generation and transduction of pain, many of which represent new targets for pharmacological intervention. The endogenous agonist of cannabinoid receptor 1 (CB1), anandamide (AEA), also stimulates transient receptor potential vanilloid channel-1 (TRPV1) channels, which instead plays a key role in the induction of inflammation and the development of pain associated with OA. AEA degradation by fatty acid amides hydrolase (FAAH) limits its activity. Inhibiting FAAH, and TRPV1 with the same molecule might produce more efficacious anti-hyperalgesic actions than the targeting of FAAH or TRPV1 alone. An update of the relationship CB1 and TRPV1 channels and their possible implications for OA pain will also be provided. Bases for the possible future development of new therapeutic approaches that might be used for the treatment of pain will be suggested.
17

Effects of the pentylenetetrazole-lnduced kindling on the NMDA receptor gene expression ik the rat hippocampus

45%
Turchan J., Labuz D., Przewlocka B., Przewlocki R., Lason W.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
18

Involvement of endogenous opiold systems in neuropathic pain

45%
Mika J., Schafer M. K.-H., Przewlocki R., Weihe E., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
19

Regulation of proenkephalin gene expression by transcription factors Fos and CREB: an antisense oligonucleotide approach

45%
Ziolkowska B., Przewlocka B., Bilecki W., Machelska H., Przewlocki R.
Biotechnologia
|
1996
|
nr 4
20

The role of microglia cells activation in the effects of opioids

39%
Popiolek-Barczyk K., Rojewska E., Zychowska M., Makuch V., Przewlocka B., Mika J.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Development of neuropathic pain is accompanied by many changes in immune and glial cells. These changes correspond to activation of immune and glial cells that have been shown to influence the opioid effectiveness and can be modulated by minocycline (a potent inhibitor of microglial activation). In earlier study we have demonstrated that function of opioidergic neurons may be modulated by the immune system. These changes have been shown to be responsible for the efficacy of opioids. The aim of our study was to examine the effect of the minocycline-triggered inhibition of microglia activation on the injury-induced changes and the efficacy of mu and delta opioid receptor ligands in a rat model of neuropathic pain (chronic constriction injury to the sciatic nerve). In cell culture studies, we examined the influence of opioids (morphine, DAMGO, DPDPE, deltorphin II) on activated primary cultured rat microglia by using MTT and/or NO assays. All experiments were performed according to the IASP recommendations and were approved by a local Bioethics Committee. On the spinal cord level the injury to the sciatic nerve induced an up-regulation of IL-1beta, IL-6 expression, CX3CR1 and C1q (marker of microglia, macrophage and leukocyte activation). Chronic administration of minocycline not only diminished neuropathic pain-related behavior and C1q-positive cell activation, but also attenuate the changes in proinflammatory factors like IL1beta, IL-6 and CX3CR1 in the spinal cord and DRG. In in vivo experiments, the analgesic effects of mu-opioid (morphine and DAMGO), but not delta-opioid (DPDPE, deltorphin II) receptor ligands were lower in the rats under neuropathic pain. Moreover, the analgesic effects of morphine and DAMGO, but not DPDPE and deltorphin II were significantly potentiated by minocycline chronic administration. Our in vitro findings that non-stimulated microglia cells respond differently to opioids in comparisons with stimulated cells as measured by MTT and/or NO assays, corresponded well with the results of in vivo studies. Our study underlined that inhibition of microglial activation could differently influence analgesic effects of mu- but not delta-opioid ligands in injury-induced pathologies, which may influence the effect of various opioid drugs used in chronic pain therapy.
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