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1

Neural circuits in the central amygdala mediate socially transferred fear

100%
Rokosz K., Hamed A., Kondrakiewicz K., Knapska E.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
INTRODUCTION: Social complex behavior, like empathy, emerge over phylogeny from various precursors. One of the simplest is emotional contagion, i.e. sharing emotional states between individuals. Receiving signals of a potential danger may increase chances of survival, thus emotional contagion plays an important role in learning about external environment. The phenomenon is well described at the behavioral level, but the neural circuits necessary for sharing emotions are unknown. We designed a rat model of fear contagion and showed that a brief social interaction with a fearful cage mate promotes risk assessment behavior and activates the central amygdala (CeA) in an otherwise naïve rat. AIM(S): The purpose of this project was to elucidate the role of the CeA circuits involved in socially shared fear. METHOD(S): To investigate the functional outputs of the activated CeA neurons, we mapped neural circuits downstream from the CeA combining anterograde tracing with an imaging of activated neurons in transgenic “Venus” rats. To test the function of CeA “social fear” neurons, we optogenetically stimulated or inhibited subpopulation of CeA neurons activated by social interaction using c-fos-driven targeting of channelrhodopsin and halorhodopsin. RESULTS: In rats that socially shared fear of their partners, we observed strong activation of structures involved in anxiety and motor functions. Most of the activated cells received projections from the CeA. Optogenetic activation of the “social fear” neurons in a social context led to behavioral pattern resembling the one observed during social interaction with a fearful partner. Activation of neurons in non-social context induced exploration and risk assessment behavior (active fear). Inhibition of them had the opposite effects. CONCLUSIONS: The results suggest that the CeA neurons involved in socially transferred fear mediate active fear responses and anxiety-related behaviors in both social and non-social conditions.
2

Sex differences in fear extinction and renewal

88%
Mikosz M., Rokosz K., Szadzinska W., Kondrakiewicz K., Knapska E.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr Suppl.1
Posttraumatic stress disorder (PTSD) develops following exposure to a traumatic event, afflicting 7–12% of the population. Women are shown to be twice as likely as men to develop PTSD. Moreover, their susceptibility to PTSD following a trauma depending on the phase of menstrual cycle. Clarification of the biological mechanism underlying sex differences in the susceptibility to PTSD is necessary to design sexspecific therapies. We addressed this issue using an animal model of extinction and renewal of conditioned fear. We investigated the impact of estrus cycle phase on fear memory acquisition, extinction and recall. We hypothesized that hormonal status would influence memory formation and recall at all stages of the behavioral procedure. Therefore we employed a matrix design, carrying out fear conditioning, extinction and fear/extinction memory recall in either estrus or metaestrus. Males and gonadectomized have been trained at corresponding time intervals While estrus cycle phase during fear conditioning did not affect the retrieval of fear memory, hormonal status during both extinction and following fear/extinction memory recall affected animals’ freezing rates. Highest differences have been found in animals that have been tested in metaestrus and extinguished in estrus or metaestrus. Collectively, we claim that it is necessary to control the hormonal status of female animals used in experiments involving fear conditioning, extinction and renewal.
3

Presence of a companion alleviates fear response but does not equal fear extinction

88%
Gorkiewicz T., Rokosz-Andraka K., Kondrakiewicz K., Meyza K., Knapska E.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
|
nr Suppl.1
INTRODUCTION: Social support during exposure-based psychotherapy has been suggested to have an important influence on the course of exposure treatment, however some clinical trials show that individual therapy may be more effective than group therapy. The mechanisms of social influence on fear extinction remain unknown. METHOD(S): To study neuronal correlates of social buffering in fear extinction, we have developed a rat model. In our model, rats showed a significant lowering of fear response during fear extinction when exposed to fear‑associated stimuli with a companion. The buffering magnitude depended on familiarity and physical similarity of the tested animals but not on their emotional status; the fear‑conditioned partners were as effective as naïve ones. However, the effect was transient and disappeared when rats were tested individually the next day. To test whether social buffering shares neuronal mechanisms with fear extinction, we measured activation of fear regulating neuronal circuits. Lower fear response during exposure with a partner was associated with lower activation of the infralimbic (IL), prelimbic (PL), and anterior cingulate (ACC) cortices. However, although optogenetic blocking of the IL increased fear response in rats tested separately, it left the social buffering effect intact. RESULTS: Analyzing inputs to the cortex from the ventral hippocampus (vHIPP) and basolateral amygdala (BL), we found significantly more vHIPP innervated neurons activated in the PL but not IL or ACC of the socially buffered rats. CONCLUSIONS: The results show that fear memory suppression by the presence of a companion is transient and relies, at least partially, on different neuronal circuits than fear extinction.
4

C-Fos driven modulation of appetitive behavior in the central nucelus of amygdala

76%
Lebitko T., Madej H., Jaworski T., Beroun A., Kondrakiewicz K., Knapska E., Kaczmarek L.
Acta Neurobiologiae Experimentalis
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2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: The central nucleus of the amygdala (CeA) has primarily been studied as a structure involved in processing of aversive behaviors, whereas its role in appetitively-motivated learning is less understood. The published data show involvement of the basolateral amygdala (BL), which sends projections to the CeA, in encoding sensory‑specific features during appetitive learning. In contrast, the CeA was implicated in modulation of incentive motivation to pursue an associated external reward. Previously we reported that after appetitive, but not aversive learning, expression of c-Fos, a protein closely linked to synaptic plasticity, is significantly increased in the CeA. AIM(S): We aimed at testing the hypothesis that appetitive learning depends on c-Fos expressing neural circuits in the CeA. METHOD(S): We first compared c‑Fos expression pattern in the amygdala following place preference and place avoidance training and examined inputs from the BL on the activated CeA neurons. Then we used c-fos-driven targeting of channelrhodopsin and trained the animals in an operant conditioning task, in which they learned to associate auditory stimulus with food reinforcement. To further test the role of c-fos-expressing neurons in appetitive learning, we locally blocked behaviorally-induced c-fos expression using a shRNA. RESULTS: The c‑Fos expression in the CeA wassignificantly higher following place preference than place avoidance training, with over 90% of the c‑Fos positive cells receiving projections from the BL. Optogenetic stimulation of the neurons increased bar-pressing responses but only when the conditioned stimulus was present. Blocking c-fos expression resulted in impairment of appetitively but not aversively motivated discrimination learning and decreased motivation to seek reward. CONCLUSIONS: The results reveal that c-fos expression in the CeA neurons is necessary for appetitively but not aversively motivated learning, modulating of incentive motivation but not reward consumption. FINANCIAL SUPPORT: Tomasz Lebitko was supported by NCN grant Sonata UMO-2012/05/D/NZ3/02085 to Tomasz Jaworski.
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