Nicole Vittoz Nearly-Finished Graduate Student 
Biological Area Group 


University of Wisconsin
Department of Psychology 
W. J. Brogden Building 
1202 West Johnson Street 
Madison, WI 53706 

Phone: (608)265-0058
           (608)265-8722 
Fax:    (608)262-4029 
Email:nmvittoz@students.wisc.edu

Curriculum Vita 

Faculty advisor's page 

Lab Web Page

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Extensive research has has established that the neuropeptide hypocretin/orexin exerts robust arousal-promoting effects, in part via its actions on a broad array of neuromodulatory and neuroendocrine systems. Among these, the dopamine system is known to play a role in the modulation of behavioral state and state-dependent processes, particularly under high-arousal appetitive and aversive conditions such as stress and reward. Given recent evidence suggesting the particular involvement of hypocretin in high-arousal states, including stress and reward, the actions of hypocretin on dopamine systems are of particular interest.

Intriguingly, when applied in vitro, hypocretin activates only a subset of dopamine neurons. To date, however, it is unclear to which terminal fields hypocretin-activated dopamine neurons project. The first project I completed in the Berridge lab addressed this question and found that hypocretin administration increases dopamine levels within the prefrontal cortex but not within the core division of the nucleus accumbens. The prefrontal cortex is a brain area that mediates a variety of higher cognitive and affective processes. Moreover, when released within the prefrontal cortex, dopamine acts to modulate a subset of these processes, such as attention and working memory. Thus, the hypocretin system is well-situated to influence prefrontal cortex activity and function both directly and indirectly via actions on neuromodulatory (i.e. dopamine) systems. To date, however, very little is known about the extent to which hypocretin may impact prefrontal cortex-dependent cognitive processes. My second project in the lab demonstrated that hypocretin, perhaps in part via its selective increase in dopamine efflux within the prefrontal cortex, produces a stress-like impairment in working memory.

When administered directly into the ventral tegmental area, hypocretin preferentially increases rates of dopamine neurotransmission within the prefrontal cortex and not the nucleus accumbens core. It is unclear whether these observations reflect the selective activation of prefrontal cortex-projecting over nucleus accumbens-projecting dopamine neurons within the ventral tegemental area. To address this question, the third project I have completed in the lab examined the topographical location and projection targets of hypocretin-activated dopamine neurons. Altogether, the current studies provide valuable information about hypocretin-dopamine interactions and the implications thereof for the modulation of higher cognitive processes.


Publications


Vittoz, NM, Berridge, CW. (2006) Hypocretin/Orexin Selectively Increases Dopamine Efflux within the Prefrontal Cortex: Involvement of the Ventral Tegmental Area. Neuropsychopharmacology, 31(2) 384-395.

Day H.E.W., Vittoz N.M., Oates M.M., Badiani A., Watson, S.J., Jr., Robinson T.E., Akil H. (2002) A 6-Hydroxydopamine lesion of the mesostriatal dopamine system decreases the expression of corticotropin releasing hormone and neurotensin mRNAs in the amygdala and bed nucleus of the stria terminalis. Brain Research, 945(2), 151-159.

Day, H.E.W., Badiani, A., Uslaner, J.M., Oates, M.M., Vittoz, N.M., Robinson, T.E., Watson, S.J., Jr., Akil, H. (2001) Environmental novelty differentially affects amphetamine-induced c-fos mRNA expression in the bed nucleus of the stria terminalis and amygdala. Journal of Neuroscience, 21(2), 732-740.


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Last Modified 6.15.05