title: Complexity of VTA DA neural activities in response to PFC transection in nicotine treated rats.
abstract: BACKGROUND
  The dopaminergic (DA) neurons in the ventral tegmental area (VTA) are widely implicated in the addiction and natural reward circuitry of the brain. These neurons project to several areas of the brain, including prefrontal cortex (PFC), nucleus accubens (NAc) and amygdala. The functional coupling between PFC and VTA has been demonstrated, but little is known about how PFC mediates nicotinic modulation in VTA DA neurons. The objectives of this study were to investigate the effect of acute nicotine exposure on the VTA DA neuronal firing and to understand how the disruption of communication from PFC affects the firing patterns of VTA DA neurons.
  
  
  METHODS
  Extracellular single-unit recordings were performed on Sprague-Dawley rats and nicotine was administered after stable recording was established as baseline. In order to test how input from PFC affects the VTA DA neuronal firing, bilateral transections were made immediate caudal to PFC to mechanically delete the interaction between VTA and PFC.
  
  
  RESULTS
  The complexity of the recorded neural firing was subsequently assessed using a method based on the Lempel-Ziv estimator. The results were compared with those obtained when computing the entropy of neural firing. Exposure to nicotine triggered a significant increase in VTA DA neurons firing complexity when communication between PFC and VTA was present, while transection obliterated the effect of nicotine. Similar results were obtained when entropy values were estimated.
  
  
  CONCLUSIONS
  Our findings suggest that PFC plays a vital role in mediating VTA activity. We speculate that increased firing complexity with acute nicotine administration in PFC intact subjects is due to the close functional coupling between PFC and VTA. This hypothesis is supported by the fact that deletion of PFC results in minor alterations of VTA DA neural firing when nicotine is acutely administered.
authors.affiliation: Department of Biomedical Engineering, Cullen College of Engineering, University of Houston, Houston, TX 77204, USA.
authors.forename: Ting Y
authors.initials: TY
authors.lastname: Chen
authors.forename: Die
authors.initials: D
authors.lastname: Zhang
authors.forename: Andrei
authors.initials: A
authors.lastname: Dragomir
authors.forename: Yasemin M
authors.initials: YM
authors.lastname: Akay
authors.forename: Metin
authors.initials: M
authors.lastname: Akay
mesh_terms: D000818:Animals; D019771:Axotomy; D004298:Dopamine / Q000378:metabolism*; D004594:Electrophysiology; D008297:Male; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D017397:Prefrontal Cortex / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017557:Ventral Tegmental Area / Q000187:drug effects* / Q000502:physiology*
chemical_list: D018722:Nicotinic Agonists; D009538:Nicotine; D004298:Dopamine