Dr. Min Lin

The major goals of my projects with either wild-type, methamphetamine (METH) treatment, α-syn overexpression or transgenic animal models are to understand 1) the role of dopamine transporter in neuronal excitabilities 2) the underlying mechanism of regulating the neuronal excitabilities by METH-or α-syn induces the release of inflammatory mediators such as cytokines. 3) the mechanism of α-syn-mediated neuronal dysfunction. 4) networking and modulating midbrain dopamine neurons and vagus nerve circuits.

To investigate METH, cytokines, or α-syn impacts dopaminergic neurophysiological and pathological activities, I routinely employ two-photon confocal microscope, total internal reflection fluorescence microscopy, and digital mirror device-based pattern illuminator to detect the neural calcium homeostasis, dopamine receptor or transporter expression, and dopamine release. Using various electrophysiological techniques including single channel, field signal, current and voltage clamp recordings, I am investigating the property of ion channels or dopamine receptors, and the excitative regulation of dopamine neurons by α-syn overexpression, methamphetamine exposure, or inflammatory mediators in dopamine neurons. On the other hand, I am using microinjection to treat or label the dopamine neuron using adeno-associated virus and conduct in vivo imaging and behaviors following vagus nerve stimulation or systemic drug application to identify the role of the parasympathetic or sensory vagal components in the regulation of dopamine neuronal activities in the methamphetamine exposure, α-syn overexpression or transgenic animal models.

CV