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Wezik Marcelina Olga, Coimbra Barbara, Correia Raquel, Gaspar Rita, Vieitas-Gaspar Natacha, Goncalves Ricardo, Terrier Claire, Soares-Cunha Carina, Rodrigues Ana Joao
Life and Health Sciences Research Institute (ICVS), Universidade do Minho, Braga, Portugal
Abstract: Many brain regions have been associated with positive and negative valence encoding, this is, the attribution of subjective value to sensory stimuli which determines subsequent appropriate behavior. Since dysfunction occurring in one or several of these brain regions is associated with mental disorders such as addiction or depression, it is essential to understand in detail what are all the components of this circuitry and what is their contribution for valence encoding. The main aim of this work was to perform a brain-wide identification of neuronal ensembles responsive to positive (cocaine) or negative (foothshock) valence stimuli. Taking advantage of permanent genetic access to transiently active neurons via TRAP, the recruited neuronal ensembles for valence-specific stimuli were quantified using a semi-automatized histological data analysis and generation of 3 dimensional models of the whole brain. Our data shows that brain regions of the reward circuit, such as the basolateral amygdala, the nucleus accumbens and the laterodorsal tegmental area, among other limbic and non-limbic regions, are particularly involved in positive and/or negative valence encoding. In conclusion, here we describe a brain-wide and region-specific involvement in valence encoding, with unprecedented detail.
Funding: This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No 101003187). The project leading to these results have received funding from “la Caixa” Foundation (ID 100010434), under the agreement LCF/PR/HR20/52400020. This work was funded by FCT under the scope of the project PTDC/MED-NEU/29071/2017(REWSTRESS), PTDC/MED-NEU/4804/2020 (ENDOPIO) and PTDC/SAU-TOX/6802/2020 (REMIND). This work has been funded by National funds, through the Foundation for Science and Technology (FCT) - project UIDB/50026/2020 and UIDP/50026/2020.
RoszkowskaN.1, Nikolaev T.2,Meyza K.2
1Faculty of Biology and Environmental Sciences, UKSW, Warsaw, Poland
2Laboratory of Neurobiology of Emotions, Nencki Institute of Experimental Biology, Warsaw, Poland
Abstract: To study how negative emotions are transferred in mice, particularly in the amygdala and prefrontal cortex, the Remote Transfer of Fear behavioural paradigm was employed. This involved housing pairs of mice (Observer and Demonstrator) for three weeks before the Demonstrator was removed from the home cage and subjected to adverse stimuli (10 foot shocks - 1s long, 0.6mA).
Once the Demonstrator had been returned to the home cage, the first ten minutes of interaction were recorded. After another eighty minutes, the mice were sacrified for immunohistochemical staining purposes. Sst-IRES-Cre mouse strains were used, as they expressed fluorescence marker (dTomato) through viral tagging. Combined with immunochemistry against c-Fos (a standard neuronal novelty marker), this enabled checking for somatostatin interneuron activity.
The first ten minutes of interaction show higher levels of anogenital sniffing, body sniffing and self-grooming behaviour for Observers (Control group). Meanwhile, exploratory behaviour was higher for both Demonstrator and Observer mice (Experimental group).
This altered behaviour within the Experimental group, combined with increased neuronal activation (higher c-Fos levels for both amygdala and prefrontal cortex), confirms that emotional contagion occurred. Changes in somatostatin cell activity within amygdala region (Observers; both groups) likewise indicate their role in the emotional contagion regulatory circuit.
Funding: Grant number 2019/35/N/NZ4/01948.
Olga Gulka,Anita Cybulska-Kłosowicz, Ewelina Knapska
Laboratory of Emotions Neurobiology, Nencki Institute of Experimental Biology of the Polish Academy of Science, Warsaw, Poland
Abstract: The corticotropin-releasing factor (CRF) is a neuropeptide responsible for controlling stress responses. The CRF-expressing neurons in the central amygdala (CeA) are activated by the social transfer of fear. We investigated the role of CRF neurons localized in the CeA in the remote threat paradigm, in which a non-stressed rat – the observer – is paired with a partner that experienced aversive foot-shocks (the demonstrator). We employed PSAM/PSEM chemogenetics to activate CRF neurons in male CRF-Cre observer rats. We analyzed observer rats' behaviors, including rearing, cage exploration, and social interactions, to explore the effect of CRF neurons stimulation on socially transfer fear. Activation of the CeA CRF neurons decreased cage exploration and rearing in the observers paired with shocked demonstrators compared to the animals without blocking or paired with the control (non-shocked) demonstrators. Regardless of CRF blocking, the observers paired with the shocked demonstrators interacted with them longer than those paired with the non-shocked demonstrators. The data shows that activation of the CeA CRF cells results in significant behavioral changes, which suggests a pivotal role of these neurons in socially transferred fear and emotional contagion.
Funding: European Research Council starting grant (H 415148 to E. Knapska)
Karolina Protokowicz, Iwona Sirocka, Leszek Kaczmarek
BRAINCITY, Laboratory of Neurobiology, Nencki Institute, Poland
Abstract: Disorders that affect nervous system development are called neurodevelopmental disorders (NDDs). NDDs characterized by altered psychosocial behavior, such as Autism spectrum disorder or schizophrenia are considered to have a multifactorial etiology. It is, however, believed that inflammatory reactions may be one of the causes.
The aim of this study was to evaluate changes in psychosocial behavior of adult mice treated with bacterial lipopolysaccharide (LPS) in early life. In terms of onset of exuberant synaptogenesis, postnatal day 7 (P7) in mice corresponds with the second trimester of pregnancy in humans. On P7, mice pups were injected either with LPS or physiological saline. After 3 weeks marble burying test, elevated plus maze, three chamber test, Eco-HAB® sociability test, and appetitive training in Intellicage were conducted. Mice after LPS treatment were less anxious and less active. The LPS-treated group spent more time together in the course of the social test. Interestingly, males avoided social stimulus from unknown animals, whilst females were more interested in social stimulus than the control group. Additionally, animals injected with LPS needed more time to learn new conditions. Therefore presented results suggest, that immune activation during neurodevelopment induces alterations of behavior that resemble symptoms observed in human NDD patients.
Patryk Sambak,Gabriela Stopka, Anna Blasiak
Department of Neurophysiology and Chronobiology, Institute of Zoology and Biomedical Research,
Jagiellonian University, Krakow, Poland
Abstract: Correct response to novel stimuli is crucial for animals to adapt to ever-changing environment, and such responsiveness is disrupted in many neuropsychiatric diseases. One of the key nodes in familiarity signalling and expression of novelty preference is midbrain interpeduncular nucleus (IPN). IPN is strongly innervated by nucleus incertus (NI), a highly stress sensitive component of an ascending arousal network. However, the nature of the NI-IPN interactions remains largely unknown.
We showed that the NI innervation of IPN is predominantly monosynaptic, using intra NI injections of viral vectors carrying channelrhodopsin-2 and YFP male rats, leading to expression fluorescence protein. During whole-cell patch-clamp ex vivo experiments electrical activity of IPN neurons was recorded, while NI originating fibers were optically stimulated. Both outward and inward light-evoked postsynaptic currents (le-PSCs) were observed. Inward le-PSCs were blocked by glutamate receptors antagonists whereas outward le-PSCs were inhibited by GABAA receptor antagonist, what confirmed their glutamatergic and GABA-ergic nature, respectively. Interestingly, we observed IPN neurons, that had both excitatory and inhibitory inputs from NI, as well as those, which were innervated directly and indirectly by NI.
Our data show that the NI-IPN axis may constitute an important neuronal element involved in adapting novelty preference to stressful conditions.
Funding: This research was supported by research grant from the National Science Centre, Poland (UMO-2018/30/E/NZ4/00687).
