Researchers from the university that form part of CIBER Physiopathology of Obesity and Nutrition (CIBEROBN), who are working in collaboration with the Universitat Autònoma de Barcelona, the University of California (USA) and Ibaraki University (Japan), have discovered that the CPT1C protein acts as a sensor for detecting neuron energy levels and regulating synaptic plasticity processes, which are key for learning and retaining information. 

The Journal of Cell Biology has recently published this study titled “Sensing of nutrients by CPT1C controls SAC1 activity to regulate AMPA receptor trafficking”. The project offers a greater understanding of the molecular mechanisms that regulate the transportation of AMPA receptors in neurons, responsible for controlling brain activity and neuroplasticity. 

Dr Núria Casals, head of the NeuroLipid Research Group, explained that “until now, we thought that our energy levels conditioned our cognitive ability, such as our attention span or how well we retain information when we’re hungry, or following a meal that is too rich in fats. However, it turns out we knew very little about the mechanisms involved in these processes”. “Thanks to our recent study, we have been able to demonstrate that there is a protein called CPT1C that acts as a switch, blocking the transmission of information between neurons in states of fasting or metabolic stress”. 

The group of UIC Barcelona researchers has shown how CPT1C controls synaptic transmission using another protein, SAC1, which is also involved in other processes such as cholesterol metabolism and tumour growth.  “This new CPT1C-SAC1 focus could be key to explaining the impact nutrients have on different pathologies, such as Alzheimer's disease, obesity or cancer”, highlighted Dr Rut Fadó, one of the study’s principal investigators.