I have come to Stanford University to increase my knowledge and acquire new skills in neuroscience and synaptic plasticity. My interest in the brain arises from its unique complexity and malleability to shape different behavioral outcomes. My PhD was aimed at studying the modulation of voltage-gated calcium channels in primary neuronal cultures and brain slices by a GPCR involved in energy homeostasis and memory. At this stage I am willing to use my expertise in electrophysiology and subcellular neuroscience to explore the plasticity of inhibitory afferents into the VTA and its relation with stress-induced relapse.

I also believe that science is a powerful tool to explore and change the world, and hence I am highly interested in the ideas behind science policies as well as in understanding how science shapes the reality we live in, and the responsibility we have as scientists.

Professional Education

  • Doctor of Philosophy, Universidad Nacional de La Plata - Buenos Aires - Argentina, Impact of presynaptic voltage-gated calcium channels modulation by GHSR constitutive activity in hippocampal inhibitory transmission (2014)
  • Bachelor in Biotechnology, Universidad Nacional de La Plata - Buenos Aires - Argentina (2009)

Stanford Advisors

All Publications

  • Periaqueductal Gray and Rostromedial Tegmental Inhibitory Afferents to VTA Have Distinct Synaptic Plasticity and Opiate Sensitivity. Neuron St Laurent, R. n., Martinez Damonte, V. n., Tsuda, A. C., Kauer, J. A. 2020


    The ventral tegmental area (VTA) is a major target of addictive drugs and receives multiple GABAergic projections originating outside the VTA. We describe differences in synaptic plasticity and behavior when optogenetically driving two opiate-sensitive GABAergic inputs to the VTA, the rostromedial tegmental nucleus (RMTg), and the periaqueductal gray (PAG). Activation of GABAergic RMTg terminals in the VTA in vivo is aversive, and low-frequency stimulation induces long-term depression in vitro. Low-frequency stimulation of PAG afferents in vitro unexpectedly causes long-term potentiation. Opioid receptor activation profoundly depresses PAG and RMTg inhibitory synapses but prevents synaptic plasticity only at PAG synapses. Activation of the GABAergic PAG terminals in the VTA promotes immobility, and optogenetically-driven immobility is blocked by morphine. Our data reveal the PAG as a source of highly opioid-sensitive GABAergic afferents and support the idea that different GABAergic pathways to the VTA control distinct behaviors.

    View details for DOI 10.1016/j.neuron.2020.02.029

    View details for PubMedID 32191871