{"id":861,"date":"2018-12-20T01:38:30","date_gmt":"2018-12-20T01:38:30","guid":{"rendered":"https:\/\/wp.uthscsa.edu\/pharmacology\/?page_id=861"},"modified":"2018-12-20T01:38:30","modified_gmt":"2018-12-20T01:38:30","slug":"stephanie-perez","status":"publish","type":"page","link":"https:\/\/lsom.uthscsa.edu\/pharmacology\/stephanie-perez\/","title":{"rendered":"Stephanie Perez"},"content":{"rendered":"

Postdoctoral Fellow<\/span><\/h3>\n

Ph.D., Neuroscience<\/span>
\nUT Health San Antonio<\/span>
\nSan Antonio, Texas<\/span>
\nLab: 210-567-4273<\/span>
\nEmail: perezsm@uthscsa.edu<\/span>
\nLab Association:<\/span> Daniel Lodge, Ph.D.<\/span><\/a>
\nResearch Interests<\/b><\/p>\n\n\n\n\n\n
\u2022 schizophrenia \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0<\/span><\/td>\n\u2022 dopamine<\/span><\/td>\n<\/tr>\n
\u2022 hippocampus<\/span><\/td>\n\u2022 neuroscience<\/span><\/td>\n<\/tr>\n
\u2022 electrophysiology<\/span><\/td>\n\u2022 optogenitcs<\/span><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Research Summary<\/b>
\nEvidence supports the hypothesis that a pathological increase in hippocampal output drives hyperactivity of the mesolimbic dopamine system in rodent models of schizophrenia. Previously, we have demonstrated that aberrant dopamine system function and associated behaviors can be restored with cell based therapies, as well as, by directly (TTX inactivation, deep brain stimulation) and indirectly (vagal nerve stimulation) targeting the ventral hippocampus. We are now utilizing an optogenetic approach combined with electrophysiology to determine whether afferents differentially regulate discrete populations of VTA dopamine neurons and whether these discrete subpopulations are differentially regulated in rodent models of schizophrenia and drug sensitization. We believe that dopamine neuron subpopulations are differentially affected by afferent modulation in various disease states, possibly explaining the differences we observe in symptomology of diseases that exhibit hyperactivity of the mesolimbic dopamine system. We believe these data will help us to better understand subtle differences in discrete dopamine neuron subpopulations that contribute to the symptoms of schizophrenia and drug sensitization, ultimately, establishing better, more targeted therapies for various disease states.<\/span>
\n 
\n Accomplishments, Awards and Honors\u00a0<\/b><\/p>\n