Pernilla Fagergren poster abstract

Cocaine mediated dopamine transmission and behavior in depressed rats

P. Fagergren1, D.H. Overstreet2, Y.L. Hurd1

1Karolinska Institute, Department of Clinical Neuroscience, Psychiatry Section, Stockholm, Sweden; 2University of North Carolina

There is strong comorbidity between depression and drug abuse that suggest a shared genetic vulnerability and a similar underlying neurobiology. Therefore we studied the cocaine response on behavior and on mesolimbic dopamine transmission in the FSL rats, a genetic animal model of human depression, and their control FRL rats.

First, the reinforcing properties of cocaine examined by using a self-administration paradigm. We found no difference between the two lines in the ability to acquire cocaine self-administration; stable responding was reached within seven days of training.

Second, we examined locomotor behavior and in vivo mesolimbic dopamine transmission during novelty and after passive cocaine administration. The FSL rats had a reduced locomotor response to novelty and exhibited more cocaine-induced stereotyped behavior than their controls.

Microdialysis sampling from the amygdala and nucleus accumbens shell revealed no significant difference in the dopamine overflow between the rat lines during any condition studied.

These findings suggest that depression may not be an initial drive for cocaine seeking behavior and that depressed rats have impaired motor functions that are not correlated to mesolimbic dopamine overflow.

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