We cordially invite you to the first Ph.D. seminar, which will be held on November 19 at 10.30 in the CN Conference Room (1st floor). The program includes 2 presentations:
1) Anna Kaźmierowska,
2) Aleksandra Oksiejuk.
Detailed information regarding presentations together with Abstracts can be found below.
The seminar will be held in a hybrid mode (people in the CN Room are asked to follow the safety rules).
Link to the meeting: https://zoom.us/j/92187526214?pwd=OFN3NXJkVEdOV2lnZlR2Z0h3RFhKZz09
Laboratory of Brain Imaging, Pracownia Obrazowania Mózgu, Laboratory of Emotions Neurobiology
Supervisor I: dr hab. Ewelina Knapska, prof. IBD
Supervisor II: dr hab. Jarosław Michałowski, prof. SWPS
Title: "Rats get affected by the humans’ fear: neural and behavioural results of the inter-species study on fear contagion"
Fear contagion is a process that involves automatic tuning into the emotional state of another scared animal. It has been well described in both humans and rats but no reports have so far investigated whether the social transfer of threat is possible between these two species.
We investigated whether human fear can be transmitted to rats through social interaction. Fear-conditioned humans were asked to interact with previously handled rats. In the control condition, human handlers underwent an emotionally neutral task prior to the interaction with rats.
The c-Fos mapping performed in the rats’ amygdalae indicated increased activation of this brain region following the interaction with a fear-conditioned human as compared to the control condition. The response to the experimental manipulation was particularly robust in the basal and the centro-lateral nuclei. We also observed less human-exploration behaviors in rats from the experimental group compared to the ones from the control condition during the first minute of interaction.
These findings show that fear contagion between humans and rats is possible. The basal and centro-lateral nuclei are typically described as related to the fear response in rat studies, which provokes a reflection about the universality of the fear processing among humans and rats.
Data collection and analysis were sponsored by National Science Centre grant 2015/19/B/HS6/02209. Ewelina Knapska was supported by European Research Council Starting Grant (H 415148).
Laboratory of Cellular Metabolism
Supervisor: prof. dr hab. Krzysztof Zabłocki
Title: Mutation in the dystrophin-encoding gene affects myoblast motility in the mdx mouse model of Duchenne muscular dystrophy
Duchenne Muscular Dystrophy (DMD) is the X-linked, inherited, neuromuscular disorder caused by mutations in the DMD gene. The major cause of a severity of this disease is neuromuscular complications due to lack of 427 kDa dystrophin. However, many DMD related consequences are also observed in cells which do not synthesize this protein regardless of DMD mutation. Myoblasts belong to this category because of too early step of their differentiation. Previously we described mdx-related changes in myoblasts’ calcium homeostasis. In the present study effects of mdx mutation on myoblast motility and adhesion are in focus. Using random motility assay we found that immortalized as well as primary dystrophic myoblasts move faster than wild type cells and are slowed down upon treatment with a spectrum of nucleotide receptor agonists. Wild type myoblasts seem to be insensitive in this matter. We also found different effects of nucleotides on adhesive properties of mdx and w/t myoblasts. The former are more sensitive to such a treatment. To identify biochemical base of these differences we performed transcriptomic analysis of immortalized mdx and w/t myoblasts and confirmed some of observations using western blot technique. We also used specific inhibitors to point out particular elements of signalling pathways which are affected in mdx cells. Finally we postulate different contribution of the RhoA-associated kinase (RhoA/ROCK) and the Ca2+/calmodulin-dependent myosin light chain kinase (MLCK) to cell motility in dystrophic myoblast than in their wild type counterparts. These results will be discussed in the context of muscle regeneration and DMD pathophysiology. This work was supported by the National Science Centre, Poland, accordingly to the decision number DEC-2013/11/B/NZ3/01573.
Anna Filipek & Anna Nowicka