NeuroScienceLab Essen
Biosketch
 
PD Dr. med. Tim Hagenacker

Group leader "Diseases of the peripheral nervous system"
Office: MZ, 1st floor, room 1.104
Email: tim.hagenacker@uk-essen.de
Phone: +49 201 723 6513
Fax: +49 201 723 6161
Bio

Tim Hagenacker received his medical degree in 2007 at the University of Duisburg-Essen, Germany. His doctoral thesis focused on modulation of voltage gated calcium channels and interactions with thermoreceptors in sensory neurons. In 2009 he earned his Dr. med. with the "summa cum laude" degree. Since 2009 he works as post-doctoral scientist and clinician in the NeuroScienceLab / Department of Neurology initially in the group of Prof. Maria Schäfers, since 2011 as group leader of the research group "Diseases of the peripheral nervous system".
Research interests

Tim Hagenacker is interested in pathomechanisms of neuropathic pain, neurotoxicity and neuroprotective strategies in the peripheral nervous system. Current projects focus on interactions of voltage gated channels with cold sensing receptors and strategies for neuroprotection after chemotherapy. The group combines electrophysiological methods with imaging platforms, behavioral pain assessments and molecular biology techniques.
Key publications

Hagenacker T, Splettstoesser F, Greffrath W, Treede RD, Büsselberg D. Capsaicin differentially modulates voltage-activated calcium channel currents in dorsal root ganglion neurones of rats. Brain Res. 2005; 1062(1-2):74-85.

Hagenacker T, Hillebrand I, Wissmann A, Büsselberg D, Schäfers M. Anti-allodynic effect of the flavonoid myricetin in a rat model of neuropathic pain: Involvement of p38 and protein kinase C mediated modulation of Ca2+-channels. Eur J Pain. 2010; 14(10):992-8.

Hagenacker T, Hillebrand I, Büsselberg D, Schäfers M. Myricetin reduces voltage activated potassium channel currents in DRG neurons by a p38 dependent mechanism. Brain Res Bull. 2010; 83(5):292-6.

Hagenacker T, Ledwig D, Büsselberg D. Additive inhibitory effects of calcitonin and capsaicin on voltage-activated calcium channel currents in nociceptive neurones of rat. Brain Res Bull. 2011; 85(1-2):75-80.

Hagenacker T, Schäfer N, Büsselberg D, Schäfers M. Analgesic inffectiveness of lacosamide after spinal nerve ligation and its sodium channel activity in injured neurons. Eur J Pain. 2012; 17(6):881-92.

Hagenacker T, Lampe M, Schäfers M. Icilin reduces voltage gated calcium channel currents in naïve and injured DRG neurons in the rat spinal nerve ligation model. Brain Res. 2014; 1557:171-9.

Leo M, Argalski S, Schäfers M, Hagenacker T. Modulation of voltage-gated sodium channels by activation of tumor necrosis factor receptor-1 and receptor-2 in small DRG neurons of rats. Mediators Inflamm. 2015; 2015:124942.

Totzeck A, Stettner M, Hagenacker T. Early platelet and leukocyte decline in patients with neuroinflammatory disorders after intravenous immunoglobulins. Eur J Neurol. 2017; 24(4):638-44.

Leo M, Schmitt LI, Erkel M, Melnikova M, Thomale J, Hagenacker T. Cisplatin-induced neuropathic pain is mediated by N-type VGCC in DRG neurons. Exp Neurol. 2017; 288:62-74.
NeuroScienceLab Sekretariat
+49-201-723-2180
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