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Intra ventral tegmental area noradrenergic receptor signalling regulates CUE-induced fear memory retrieval

100%
Zajda K., Drwiega G., Wira P., Szklarczyk K., Solecki W. B.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
INTRODUCTION: Noradrenergic receptors (α‑AR) in the ventral tegmental area (VTA) regulate phasic dopamine release in the mesolimbic, but not in the mesocortical pathway. Accordingly, the α‑ARs modulate conditioned behaviours, such as acquisition of fear memories. Importantly, the role of the VTA noradrenergic signaling in fear memory retrieval remain unclear. AIM(S): The aim of the study was to investigate the role of α1‑AR and α2-AR in VTA in the retrieval of conditioned stimulus (CS)‑induced fear memories. In control studies, we investigate their role in the locomotor activity and anxiety‑like behaviour. METHOD(S): We performed fear conditioning and open field tests in adult male, Spraque‑Dawley rats combined with intra‑VTA microinfusions. The fear conditioning consisted of two phases: training during which CS was associated with footshock, and retrieval of the conditioned fear memory. Retrieval test was preceded by intra‑VTA administration of α1‑AR and α2-AR antagonist (terazosin 1 µg/side and RX 821002 2.7 µg/side) and conducted in a novel context in which presentation of CS induced fear responses. RESULTS: We demonstrated that α1-AR blockade in the VTA decreased freezing responses during retrieval of CS‑induced fear memory. In contrast, α2AR blockade had no effects. Furthermore, neither blockade of α1-AR and α2-AR had no effects on locomotor activity and anxiety‑like behavior. CONCLUSIONS: Here, we demonstrated a potential role of the VTA noradrenergic signaling in fear memory retrieval. These results indicate that the noradrenergic signalling in the VTA modulates CS-fear induced responses predominantly via α1‑AR.
2

Molecular and behavioral patterns associated to stress responsivity and PTSD risk

86%
Szklarczyk K., Smutek M., Korostynski M., Solecki W., Golda S., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
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nr S
Post-traumatic stress disorder (PTSD) is a chronic anxiety condition that develops as a result of a terrifying event. Clinical studies show that only about 10% of trauma-exposed people suffer from PTSD. Our research was focused on endophenotypes and molecular biomarkers of PTSD in an animal model. Differences in response to stress among inbred mouse strains (C57BL/6J, DBA/2J, SWR/J and 129P3/J) were compared: a single intense footshock was applied and ultrasonic vocalization during/after the stress was measured. Long-lasting effects were assessed 4-6 weeks after the traumatic event: conditioned and sensitized fear, social withdrawal, depressive-like behavior and susceptibility to drug addiction. SWR/J strain displayed the lowest conditioned fear, whereas sensitized fear was increased over time in C57BL/6J mice. Moreover, C57BL/6J strain exhibited increase in depressive-like behavior, while DBA/2J strain displayed increased social withdrawal. In addition, it was observed that exposition to traumatic stress increased sensitivity to rewarding properties of morphine in 129P3/J mice. Diverse long-lasting behavioral consequences of exposition to stress were associated with changes in basal and stress-induced profile of glucocorticoid receptor-dependent (GR) genes (e.g., Fkbp5 and Tsc22d3) in amygdala. Furthermore, our research showed that administration of GR antagonist disrupted reconsolidation of the traumatic event memory. Our research supports a model in which genetic factors are important for phenotypic variation in responsivity to stress. These genes may provide novel insight into mechanisms of stress-related disorders. This work was supported by Polish MSHE grants NN405 274137, N405 143238, IUVENTUS Plus and POIG De-Me-Ter 3.1
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