Dear All,

 We cordially invite you to the Ph.D. Seminar, which will be held on May 26, 2023 at 10.30 in the Konorski room (2^nd floor). The program includes 4 presentations:

1   MSc Anna Głowacka

2    MSc Anna Kozak

3    MSc Ilke Guntan

4    MSc Martyna Pękała

Information regarding speakers together with abstracts can be found below.

The seminar will be held in a hybrid mode.

Link to the meeting

https://zoom.us/j/96292522633?pwd=VlRPOWUxaDlVMlhiOFpvcnlQdzhOZz09

With best regards,

Anna Filipek & Anna Nowicka

ABSTRACTS

1. MSc Anna Głowacka

Group of Restorative Neurobiology
Supervisor: Prof. Małgorzata Skup, PhD, DSc

Title: Effects of Intraspinal AAV-BDNF Treatment on Motoneurons and Peripheral Synapses in Rats with Complete Spinal Cord Transection

Abstract:

Spinal cord transection (SCT) causes loss of motor ability by disrupting supraspinal tracts and affecting the preserved spinal network. Our studies on the rat model of SCT revealed reduced innervation of lumbar motoneurons (MNs) by glutamatergic and cholinergic inputs, along with changes in perineuronal net density. Functionally important, the vulnerability of hindlimb extensor and flexor circuits to spinal injury differed by distinct time-course of loss of inputs on ankle extensor and flexor MNs. Maintenance of the structure and function of spinal interneurons and MNs is supported by brain-derived neurotrophic factor (BDNF), signaling via TrkB receptor. We and others showed previously that AAV-BDNF administration to SCT rats resulted in improved locomotor movements with body weight support and foot placement on a treadmill. These positive effects were evident from the second week post-SCT, lasting at least 7 weeks. My aim was to investigate whether intraspinal AAV-BDNF treatment can alleviate post-lesion changes in MNs and peripheral synapses. Overexpressed BDNF, detected in multiple fibers penetrating upper lumbar segments, counteracted a decrease of TrkB and BDNF expression in lower lumbar MNs, partially protected extensor (Soleus) NMJs from disintegration, and upregulated VAChT and AChE transcripts in the Soleus, but not the flexor (Tibialis Anterior) MNs.

2. MSc Anna Kozak

Laboratory of Brain Imaging

Supervisor: Dr. Kalina Burnat, PhD, DSc

 Title: Animal model of central photoreceptor degeneration (AMD) - Behavioral and MRIstudy.

 Abstract

The central photoreceptor degeneration is a main factor of vision loss in adults. Firstly, to measure central and peripheral vision simultaneously we developed an acuity test based on motion. Next, I used this test to investigate the animal model of AMD, the laser induction of retinal lesions in cat. I examined controls and two groups of retina-lesioned cats: naive (RLN) and trained (RLT). Behavioral analysis showed a superior performance in RLT animals compared to controls. To identify differences occurring within the structure of white matter in the presence of training and/or lesion, I performed the whole brain Fixel Based Analysis (FBA, Raffelt et al, 2017). In RLN the decrease in FBA metrics 40-15% as compared to CT in: V5, dLGN, hippocampus, caudate nucleus, and optical tract. In RLT, the similar pattern was observed. To follow the post lesion temporal dynamic of recovery, tensor-based analysis of the fractional anisotropy (FA) was performed. Results revealed that in RLN the FA values were growing after the lesions but were stable in the RLT. We propose that the visual stimulation via intact peripheral retinae facilitates reestablishment of visual functions after lesion.

3. MSc Ilke Guntan

Laboratory of Epileptogenesis

Supervisor: Prof. Katarzyna Łukasiuk, PhD, DSc

Title: Characterisation of Zbtb14 protein in the hippocampus of naive and epileptic mice

Abstract

The role of Zbtb14 (Zfp161, Znf478, Zf5) is unclear in mammals. The research on this protein indicates that it coordinates the dorsal-ventral axis in Xenopus embryos with Zbtb21 (Takebayashi-Suzuki et al., 2018; Takebayashi-Suzuki et al., 2022), cooperates with aryl hydrocarbon receptor in dioxin response in silico analysis (Oshchepkova et al., 2020), and maintains replication fork stability with ATR/ATRIP complex (Kim et al., 2019). Our published data (Debski KJ et al., 2020) revealed that gene expression of several genes oscillates over the circadian cycle in the hippocampus of naive mice, which is disturbed in an experimental model of epilepsy - the pilocarpine model. Moreover, promoters of these genes show an interesting common feature: the overrepresentation of the ZF5 motif. Our goal was to characterise Zbtb14 protein expression in mice's hippocampus over the circadian cycle in naive and epileptic mice. Using immunostaining, Western blot, and immunoprecipitation techniques, we showed that Zbtb14 oscillates in the ventral hippocampus but not in the dorsal hippocampus and the somatosensory cortex of naive mice. Furthermore, the circadian rhythm of the Zbtb14 protein was disturbed in epileptic mice in a time-dependent manner.

This research is supported by the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie COFUND grant agreement No 665735 and Polish National Research Grant 2015/18/M/NZ3/00779.

4. MScMartyna Pekała

Laboratory of Neurobiology, Nencki-EMBL Center of Excellence for Neural Plasticity and

Brain Disorders – BRAINCITY

Supervisor: Dr. Katarzyna Kalita-Bykowska, PhD, DSc

Title: The role of lipocalin 2 in the regulation of brain development during prenatal infection

Abstract:

Epidemiological studies indicate that maternal infection during pregnancy is a risk factor for neurodevelopmental disorders; however, the mechanisms underlying this phenomenon remain unclear. One of the proteins highly expressed in the brain in response to infection is lipocalin 2 (Lcn2), an immune protein associated with neurogenesis and synaptic plasticity. Our studies aim to characterize the role of Lcn2 in the regulation of brain development during prenatal infection. We used a maternal immune activation (MIA) model to mimic maternal infection with i.p. lipopolysaccharide injections in pregnant mice. First, we evaluated Lcn2 mRNA expression in the fetal and adolescent hippocampus. To address how prenatal infection may influence the electrophysiological properties of neurons, we conducted excitability and miniature excitatory postsynaptic currents recordings from hippocampal CA1 neurons. We also performed behavioral experiments to assess anxiety levels and social behavior in MIA offspring. Our results indicate that Lcn2 mRNA is significantly upregulated in the hippocampus in response to prenatal  infection in the fetal and adolescent brain. Moreover, deletion of the Lcn2 gene led to abnormalities in the electrophysiological properties of neurons, and behavioral impairments, such as increased anxiety and decreased social behavior. Similar deficits were observed in wild-type MIA offspring. Interestingly, the effect caused by Lcn2 deletion was not exacerbated by maternal infection. These findings suggest that lipocalin 2 is an essential factor in regulating brain development, but it doesn’t play a protective role during prenatal infection.

This work was supported with NCN grant 2017/27/B/NZ4/01639.