Pawan BistaInstitute of Physiology I Robert-Koch-Str. 27a D-48149 Münster Phone: +49 (0) 251/83 55566 Fax.: +49 (0) 251/83 55551 E-mail: dr_pawanbista@yahoo.com |
![]() |
Joined OCC in 2011
Pawan BistaInstitute of Physiology I Robert-Koch-Str. 27a D-48149 Münster Phone: +49 (0) 251/83 55566 Fax.: +49 (0) 251/83 55551 E-mail: dr_pawanbista@yahoo.com |
![]() |
Joined OCC in 2011
Role of TASK channels in thalamocortical relay neurons
The principal thalamic neuron, the thalamocortical relay neuron can operate with two different firing modes according to the arousal state of the brain. 1) The relay mode under the condition of the active vigilance, during which the thalamus relays afferent sensory information to the cortex and is characterized by single spike or tonic firing corresponding to a desynchronized EEG state and 2) the oscillatory mode, which is intimately involved in cortical synchronization through the generation of rhythmic discharges and is associated with rhythmic bursts of high frequency action potentials during sleep, drowsiness and epileptic seizures. The switch between these activity modes is mediated by neurons of the ascending brainstem system including brainstem cholinergic neurons that release acetylcholine (ACh). These neurotransmitters act by depolarizing the membrane potential of the thalamocortical relay neurons, leading to cessation of rhythmic bursts and occurrence of tonic activity. One crucial step of membrane depolarization is the decrease in a leak K+ conductance, which is mainly carried by members of the two pore domain K+ ( K2P) channels, namely TASK-1 and TASK-3. In 2003, Meuth and Budde et al., have shown that TASK1 and TASK3 contribute to the muscarine-sensitive conductance in thalamocortical relay neurons, thereby contributing to the change in the activity mode of thalamocortical networks observed during the sleep-wake cycle. But the exact muscarinic mechanism of TASK channel modulation is still unknown. So our specific interest in this project is to understand the (muscarinic) modulation of TASK channels in the thalamocortical relay neuron and analyze the role of PIP2 (Phosphatidylinositol 4,5-bisphospahte) in this modulation
Prof. Dr. T. Budde
Prof. Dr. W.-M. Weber
Prof. Dr. E. Liebau
Köhler C, Bista P, Götz J, Schröder H. Analysis of the cholinergic pathology in the P301L tau transgenic pR5 model of tauopathy. Brain Res. 2010 Aug 6;1347:111-24. Epub 2010 May 31.
Pawan Bista, Sven G. Meuth1, Tatyana Kanyshkova, Manuela Cerina, Matthias Pawlowski, Petra Ehling, Peter Landgraf, Hans-Christian Pape, Thomas Baukrowitz, and Thomas Budde*. Mechanisms of muscarinic inhibition of TASK channels in rat thalamocortical relay neurons. Under review
Tatyana Kanyshkova, Patrick Meuth, Pawan Bista, Zhiqiang Liu, Petra Ehling, Luigi Caputi, Dane M. Chetkovich, Hans-Christian Pape and Thomas Budde*. Differential regulation of HCN channel isoform expression in thalamic neurons of epileptic and non-epileptic rat strains. Under review.
Phosphatidylinositol 4, 5- bisphosphate (PIP2)-dependent modulation of TASK channels in the thalamocortical relay neurons.
Poster presented at the 9th Göttingen meeting of the German neuroscience society, March 2011.
Web
Birthdate | 19. October 1981 |
Birth place | Kathmandu, Nepal |
Nationality | Nepali |
1988-1998 | SLC, Bagh bhairab boarding school, Kirtipur, Kathmandu, Nepal |
1998-2000 | Higher secondary education, National School of Sciences, Kathmandu, Nepal |
2000-2005 | Dental medicine, Tribhuvan University, Kathmandu, Nepal |
2007-2009 | Master of Biomedical engineering, Martin Luther University, Halle, Germany |
2009- | Westfälische Wilhelms University Münster, Münster, Germany; PhD student (PhD supervisor: Prof. Dr. Thomas Budde) |
07.2005-07.2006 | Dental Internee, People’s Dental college & Hospital, Kathmandu, Nepal. |
01.2006-08.2006 | Dental surgeon, Kathmandu Dental Clinic, Kathmandu, Nepal |
10.2008-03.2009 | Master thesis student at Neuroanatomy Lab of Prof. Dr. med. Hannsjörg Schröder, Uniclinic Köln, Germany Thesis: Analysis of the cholinergic pathology in the P301L tautransgenic pR5 model of tauopathy |
Since 10. 2009 | PhD student at Institute of Physiology I, Uni Münster, Germany |
2000-2005 | Ministry of Education and Sports, Nepal, Scholarship to study Dental medicine. |