Intranet Areál web

Neuroinflammation and pain

PhD Project: Neuroinflammation and pain

The main research interest of our department is to study mechanisms of pain and to explore new possibilities of pain treatment, especially in chronic states. Our experimental work is concentrated on the modulation of nociceptive information at the spinal cord level that is the first relay center between the periphery and higher brain areas. Our goal is to study these modulatory mechanisms in order to improve therapy for pain conditions such as neuropathic and cancer related pain. This project will be focused on the role of neuroinflammation in modulation of synaptic transmission and chronic pain development. Lately we are interested in the role of TRPV1 receptors, cannabinoids, endogenous lipids, opioids and inflammatory cytokines in this process. In our research we use mainly electrophysiological, optogenetic, OMICS analysis,  functional imaging, immunohistochemical, molecular and behavioral methods. In collaboration with clinics we aim to study human pathology in pain patients.

Candidate Requirements: 

The candidate should have a Masters' degree in biological, medical or chemical sciences, or be due to complete their studies in this academic year. Experience in physiology, neurophysiology, cell biology, molecular biology or electrophysiology techniques would be an advantage. Candidates should be fluent in Czech or English.  

Supervisor:  Jiri Palecek, M.D., Ph.D.,

Selected relevant publications:

Li Y, Adamek P, Zhang H, Tatsui CE, Rhines LD, Mrozkova P, Li Q, Kosturakis AK, Cassidy, Harrison,.Cata,P. Sapire,K. Zhang,H. Kennamer, R. M. Jawad, A.B.  Ghetti, Yan, J., Paleček, J. Dougherty, P. M. The Cancer Chemotherapeutic Paclitaxel Increases Human and Rodent Sensory Neuron Responses to TRPV1 by Activation of TLR4. J Neurosci. 2015;35(39):13487-13500. IF=6.3

Nerandzic V, Mrozkova P, Adamek P, Spicarova D, Nagy I, Palecek J. Peripheral inflammation affects modulation of nociceptive synaptic transmission in the spinal cord induced by N-arachidonoylphosphatidylethanolamine. British Journal of Pharmacology 2018, 175, 2322-2356. IF = 6.8

Adamek P, Heles M, Palecek J, Mechanical allodynia and enhanced responses to capsaicin are mediated by PI3K in paclitaxel model of peripheral neuropathy. Neuropharmacology. 2019,146:163-174. IF=4.3

Heleš M, Mrózková P, Šulcová D, Adámek P, Špicarová D, Paleček J. Chemokine CCL2 prevents opioid-induced inhibition of nociceptive synaptic transmission in spinal cord dorsal horn. Journal of Neuroinflammation. 2021; 18(1)); 279 . IF = 9.6

Uchytilová; E, Špicarová D, Paleček J. Hypersensitivity Induced by Intrathecal Bradykinin Administration Is Enhanced by N-oleoyldopamine (OLDA) and Prevented by TRPV1 Antagonist. Int. J. Mol. Sci. 2021; 22(7)); 3712. IF = 6.2

P. Adamek, M. Heles, A. Bhattacharyya, M. Pontearso, J. Slepicka, J. Palecek. Dual PI3K-δ/γ Inhibitor Duvelisib Prevents Development of Neuropathic Pain in Model of Paclitaxel-Induced Peripheral Neuropathy. Journal of Neuroscience. 2022 Mar 2; 42(9):1864-1881. IF=6.7

Spicarova D, Nerandzic V, Muzik D, Pontearso M, Bhattacharyya A, Nagy I and Palecek J. Inhibition of synaptic transmission by anandamide precursor 20:4-NAPE is mediated by TRPV1 receptors under inflammatory conditions. Frontiers in Mol. Neuroscience 2023, 16:1188503,1-11, 2023,  IF = 6.2.