Camilla Bellone (born c. 1975)[1] is an Italian neuroscientist and assistant professor in the Department of Basic Neuroscience at the University of Geneva, in Switzerland.
[2] In Di Luca's lab, Bellone studied protein-protein interactions and signalling pathways in the postsynaptic compartment as well as the role of PSD-95 in neuronal stability and homeostasis.
[4][5] Bellone stayed at the University of Milano to begin her graduate studies exploring the molecular biology and structural composition of the synapse.
[3] In Bellone's first author paper in 2005, she elucidate the mechanisms of long-term depression (LTD) in the glutamatergic synapses onto Ventral Tegmental Area (VTA) dopamine neurons.
[7] Bellone found that cocaine caused significant increases in AMPA:NMDA ratio, a sign of neuroplastic adaptation, as well as a recruitment of AMPARs to the synapse that lack GluR2.
[3] Shortly after joining the Nicoll Lab, Bellone published a first author paper in Neuron exploring the trafficking of NMDA receptors in hippocampal pyramidal cells in newborn mice.
[3] During her further training in the Lüscher Lab, Bellone explored the effects of drugs of abuse on synaptic plasticity and physiology in the dopaminergic reward system.
[10] In her paper published in Nature Neuroscience, Bellone showed that the glutamate receptor switch that occurs postnatally is delayed and mGluR1 function is impaired due to in utero cocaine exposure.
[3] Funded by the Swiss National Science Foundation, Bellone became an assistant professor in the Department of Fundamental Neuroscience at the University of Lausanne.
[3] Bellone sought to explore the connection between altered synaptic proteins and impaired social behaviors, merging her previous research experience with her new independent career interests.
[17] They found that mice exhibited impaired social preferences and abnormal excitatory transmission which reduced the output of VTA DA neurons.