Serdecznie zapraszamy na Seminarium Doktorantów, które odbędzie się 12 czerwca 2026 r. o godz. 10.30 w Sali Konorskiego (II piętro). W programie przewidziane są 3 prezentacje.

Informacje dotyczące prelegentów wraz z abstraktami znajdują się poniżej.

MSc: Mehdi Borjkhani
International Centre for Translational Eye Research (ICTER), Institute of Physical Chemistry, PAS, Warsaw
Supervisor: Prof. Daniel Wójcik, PhD, DSc.
Title:  Multiscale Computational Modeling of Addiction-Related Memory Formation: From Synaptic Plasticity to Network Dynamics

Abstract:

Addiction is sustained by persistent, relapse-prone memories formed when drugs of abuse hijack normal mechanisms of learning-related plasticity. This seminar presents a multiscale computational framework linking molecular events to circuit dynamics in addiction-related memory formation, from astrocyte-regulated synaptic plasticity and single-neuron excitability to synaptic-population behavior. Biophysically detailed models of dendritic spines and tripartite synapses show how opioids can induce long-term potentiation under conditions where normal potentiation fails, through enhanced NMDA conductance, calcium influx, and CaMKII phosphorylation. Astrocytic glutamate regulation emerges as a key control point and potential intervention target. Extensions to hippocampal microcircuitry connect these cellular mechanisms to oscillatory dynamics, while parallel modeling shows that cocaine-induced reduction of potassium current can destabilize intrinsic excitability and generate chaotic firing. At the receptor level, modulation of NMDA receptor activation duration identifies distinct routes to firing irregularity and aberrant CaMKII activation, with GABAergic inhibition stabilizing dynamics in a frequency-selective manner. At the population level, a four-synapse-state model formalizes cocaine-induced neural rejuvenation, capturing silent-synapse generation, maturation during withdrawal, subunit switching, and craving incubation.
Together, these results identify astrocytic regulation, intrinsic excitability, NMDA kinetics, and synaptic-population transitions as cross-scale controllers of pathological memory formation and therapeutic targets.

MSc. Sajjad Iqbal
Dioscuri Center for Chromatin Biology and Epigenomics
Supervisor: Dr. Aleksandra Pękowska, PhD, DSc, prof. of the Nencki Institute
Title: ATP Modulates Nuclear Proteins Dynamics in Embryonic Stem Cells

Abstract:

ATP is the main cellular energy carrier and is present at 8–12 mM, exceeding the amount required for energetic processes. Patel et al. showed that ATP also has hydrotrope-like properties preventing protein aggregation. Transcription and DNA repair occur in subnuclear compartments, but how these assemblies form and disassemble remains unclear. Many gene regulatory proteins contain unstructured regions that support formation of biomolecular condensates (BCs). We hypothesized that ATP influences the formation and dynamics of nuclear BC-forming proteins. We depleted ATP with oligomycin and 2-deoxyglucose in mouse ES cells and assessed nuclear ultrastructure, TF condensate formation, and TF-DNA interactions using FRAP and chromatin accessibility (ATAC-seq). Live-dead assay showed that ES cells remained viable. ATP depletion caused factor-specific effects: Oct4 and Med7 showed markedly reduced mobility; Sox2, Brd4, and CTCF showed moderate mobility loss with cluster formation; JunD was unaffected. Although RNA production was shut down after ATP loss, genome-wide transposase accessibility was largely preserved, indicating that altered TF biophysical properties were not explained by impaired DNA accessibility. After inhibitor washout, ATP recovered within four hours, coinciding with restored TF-DNA interactions and dissolution of nuclear clusters. These findings indicate that ATP reversibly controls nuclear condensate dynamics and TF mobility, shaping transcriptional regulation.

MSc. Justyna  Wiśniewska
Laboratory of Neuronal Plasticity
Supervisor:  Dr. Anna Beroun, PhD, DSc.
Title: NR2B-Dependent Synaptic Plasticity in the Central Amygdala during Appetitive Learning

Abstract:
The brain is a highly dynamic structure capable of adapting to environmental changes and encoding experiences as memories. Learning involves activity-dependent modifications of synaptic connectivity, including the formation of new synapses through long-term potentiation (LTP) and the elimination of existing ones via long-term depression (LTD). Both processes can transiently produce glutamatergic synapses that are functionally silent, characterized by the presence of NMDA receptors and the absence of AMPA receptors. Our previous work demonstrated the formation of silent synapses in the central nucleus of the amygdala (CeA) during appetitive learning in mice. However, the underlying mechanisms—specifically whether these synapses result from LTP or LTD—remain unclear. This study aimed to evaluate the role of LTP in appetitive learning by selectively knocking out the NR2B subunit of the NMDA receptor in the CeA, thereby impairing LTP. Behavioral assay and electrophysiological patch-clamp recordings were performed on NR2B knockout mice. Our results indicate a significant alteration in neuronal functional activity.

Z pozdrowieniami,
Anna Filipek & Anna Nowicka