RESEARCH GROUPS
Laboratory of Neuronal Plasticity
One of the brain’s most unique features is its ability to constantly change and adapt to its environment. The capacity to create or loose connections and strengthen or weaken them in response to the surrounding world is the cellular basis of learning. During the development, when brain circuits rapidly rewire, one of the cellular mechanisms of the increased capacity to learn is the existence of silent synapses.These are immature connections that do not participate in basal synaptic transmission (hence the term “silent”) but are easily recruited during learning processes. Thus, silent synapses are the substrates for enhanced learning. Yet, their function does not end in early life. Our research on cocaine addiction shows that silent synapses transiently reappear during addiction-related learning, which is considered as a pathological, extremely durable form of memory. We showed that these synapses are likely to be newly formed synaptic contacts that later, during drug withdrawal, become fully functional connections and contribute to the development of addiction-related behaviours. Our findings, therefore, prove that the brain preserves the ability to silence and unsilence synapses throughout adulthood but the mechanisms that drive the formation of silent synapses in various forms of learning is yet to be explained. Our research aims to bridge the knowledge gap between the phenomenon of silent synapse existence in adult brains and their actual function in learning and memory.
- Salamian A, Legutko D, Nowicka K, Badyra B, Kaźmierska-Grębowska P, Caban B, Kowalczyk T, Kaczmarek L, Beroun A. Corrigendum to: Inhibition of Matrix Metalloproteinase 9 Activity Promotes Synaptogenesis in the Hippocampus. Cereb Cortex. 2021 May 10;31(6):3161-3163. doi: 10.1093/cercor/bhab105
- Beroun A, Nalberczak-Skóra M, Harda Z, Piechota, M Ziółkowska, M Cały, A, Pagano R, Radwanska K. (2018) Generation of silent synapses in dentate gyrus correlates with development of alcohol addiction. Neuropsychopharmacol. 43: 1989-1999.
- Shukla A, Beroun A, Panopoulou M, Neumann PA, Grant SG, Olive MF, Dong Y, Schlüter OM. (2017) Calcium-permeable AMPA receptors and silent synapses in cocaine-induced place preference. EMBO J. 36: 458-474.
- Stefaniuk M, Beroun A, Lebitko T, Markina O, Leski S, Meyza K, Grzywacz A, Samochowiec J, Samochowiec A, Radwanska K, Kaczmarek L. (2017) Matrix metalloproteinase-9 and synaptic plasticity in the central amygdala in control of alcohol-seeking behavior. Biol. Psychiatry 81: 907-917.
- Suska (Beroun) A, Lee BR, Huang YH, Dong Y, Schlüter OM. (2013) Selective presynaptic enhancement of the prefrontal cortex to nucleus accumbens pathway by cocaine. PNAS. 110: 713-718.
- Lee BR, Ma YY, Huang YH, Wang X, Otaka M, Ishikawa M, Neumann PA, Graziane NM, Brown TE, Suska (Beroun) A, Guo C, Lobo MK, Sesack SR, Wolf ME, Nestler EJ, Shaham Y, Schlüter OM, Dong Y. (2013) Maturation of silent synapses in amygdala-accumbens projection contributes to incubation of cocaine craving. Nat. Neurosci. 16: 1644-1651.
- 2023 - 2027 National Science Centre OPUS 24 | Unraveling the Enigmatic Silent Synapses (dr. hab Anna Beroun)
- 2024 - 2029 National Science Centre Sonata BIS |Tracing Decisions: Central Amygdala's Role in Reward Learning (dr. hab Anna Beroun)
- 2025 - 2029 The Foundation for Polish Science |BRAINCITY – Centre of Excellence for Neural Plasticity and Brain Disorders
- 2016 The Fundation for Polish Science, HOMING | Addicted brain: mapping neural correlates of alcohol relapse (dr Anna Beroun)
- 2021-2021 National Science Centre PRELUDIUM 19 | In vivo and ex vivo tracking the cocaine"s mechanism of action in the medial part of the central amygdala (Łukasz Bijoch)
- 2018-2023 The Foundation for Polish Science |BRAINCITY – Centre of Excellence for Neural Plasticity and Brain Disorders, Strategic foreign partner European Molecular Biology Laboratory (EMBL)
Addiction is a big social problem in the whole Europe. According to the statistical data of European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) intake of drugs-of-abuses is increasing every year. Such tendency is observed also in the usage of so-called “hard drugs”, which are extremely addictive. Treatment costs of addicted people consume large part of public health funds. Moreover, addiction is a tragedy to addicts and their families. It is important to point that addiction is not a case of weakness, as some people might claim. It is a chronic, relapsing brain disease characterised in the revision ICD-10 by International Statistical Classification of Diseases and Related Health Problems. Drugs-of-abuse usage causes long-lasting changes in addicts’ brains, which are severe obstacles on their
way to healthiness. It is important that even single exposure to such substances cause long-lasting changes in the physiology of the brain.
Mechanisms involved in the addiction formation are similar to physiological processes underlying memory formation. They both cause neuroplasticity, characterized by for example changes on connections between neurons (synapses) in specific brain regions. Addictive substances engage regions called the reward system. This brain system is involved in processing emotions of positive valence. Such feelings are a result of for example eating sweet food or taking drugs-of-abuse. Both of them cause increased production of the “happiness hormone”, the dopamine.
Cocaine has a special ability in stimulating the reward system of the brain. It causes not only release of the dopamine but it also pharmacologically blocks its reuptake from synapses. This is accompanied with euphoria sensation, which is a reason why people so willingly use cocaine again. Unfortunately, increased dopamine level long-lastingly plastic changes in neurons in the reward system. This is a neuronal base of the addiction, which affect the processing by the brain also other pleasant stimuli.
The goal of our studies is to find exactly what is the neuroplastic modifications after cocaine usage and how it affects the activity of the brain. We are performing our studies on mice, as they have similar brain architecture as human brain does. We are studying an important part of the reward system of the brain – the amygdala, where we found neuronal populations sensitive to the dopamine. We are comparing effects of two substances causing positive experiences: sucrose and cocaine. Cocaine additionally is highly addictive due to its pharmacological properties.
We are expecting to broad our knowledge about molecular bases of addiction and effects of the drugs-of-abuse usage on the brain activity. We hope that such knowledge will help in bringing back the physiological brain activity of addicts.