ePoster · Neuroscience
Milica Prvulovic, Smilja Todorovic, Desanka Milanovic, Valentina Simeunovic, Andjela Vukojevic, Milena Jovic, Srdjan Sokanovic, Aleksandra Mladenovic · FENS Forum 2024
Calorie restriction (CR) is recognized for its potential to delay age-related changes; however, its effectiveness can vary based on factors such as duration, age, and sex. Implementing CR later in life may not only diminish its protective potential but could also have detrimental effects. Herein, we aimed to investigate the effect of CR on short-term (STM) and long-term (STM) memory and explore the potential role of the mTOR signaling pathway as an underlying molecular mechanism. Female Wistar rats of different ages (adult, middle-aged, and old) were exposed to CR (60% of ad libitum (AL)) to s
ePoster · Neuroscience
Auriane Gerbelot-Barrillon, Martin Kriebel, Ingrid Ehrlich, Regina Sullivan, Hans-Jürgen Volkmer, Valérie Doyère, Heather McLean · FENS Forum 2024
Several anxiety-related neuropsychiatric disorders are associated with amygdala dysfunction during early periods of postnatal development, and adolescence is a particularly vulnerable emotional period. Among the cellular mechanisms involved in changes in the activity of individual neurons and their synaptic connections, the mTOR signaling pathway has been proposed as a molecular regulator of emotional memories and could thus constitute a common mechanistic source of the emergence of anxiety symptoms in these disorders. We hypothesize that amygdala mTOR dysfunction during infancy can initiate a
ePoster · Neuroscience
Adam Bogdanovič, Bohdana Hrušková, Nikola Vršková, Diana Pfeiferová, Monika Řehořová, Jan Kudláček, Přemysl Jiruška, Helena Pivoňková · FENS Forum 2024
Focal cortical dysplasia (FCD) is a regional malformation of cortical development frequently associated with pharmacoresistant epilepsy. It is caused by somatic mutations affecting the mTOR signaling pathway within excitatory neurons. At the cellular level, FCD manifests as the emergence of dysmorphic neurons, disrupted neuronal migration, and consequent alterations in neuronal circuitry, accompanied by seizure occurrence. It has been demonstrated that physiological neuronal activity stimulates oligodendrocyte lineage cells (OLCs) to proliferate, differentiate, and myelinate. We hypothesize th