Prefrontal cortex deletion affects the dopaminergic neural firing complexity in nicotine-treated ventral tegmental area

Abstract

Nicotine, an addictive substance in cigarette, triggers glutamatergic synaptic plasticity on ventral tegmental area (VTA) dopamine (DA) neurons. The functional coupling between prefrontal cortex (PFC) and VTA has been demonstrated, but little is known how PFC mediates nicotinic modulation in VTA DA neurons. In this study, we tested the hypothesis that systemic exposure to nicotine significantly increases the VTA DA neuron's complexity of firing. The complexity of the neural firing of VTA DA neurons was significantly increased in PFC intact subjects, as determined using the advanced nonlinear dynamic method based on the Lempel-Ziv estimator. To further understand the functional coupling between PFC and VTA, we used LZ complexity method to estimate the complexity of firing of PFC transected subjects. Interestingly, without the input from PFC, the change in complexity estimated from VTA for PFC transected subjects is not significant. The results suggest PFC plays an important role in mediating VTA activity and that the LZ complexity method is a useful tool for the characterization of the dynamical changes in VTA DA neurons firing activities.