title: Effects of basolateral amygdala dopamine depletion on the nucleus accumbens and medial prefrontal cortical dopamine responses to stress.
abstract: In vivo voltammetry was used to study the effects of basolateral amygdala dopamine depletion on stress-induced dopamine release in the nucleus accumbens and medial prefrontal cortex. Male Long-Evans rats received bilateral microinjections of 6-hydroxydopamine or vehicle into the basolateral amygdala. Changes in dopamine signal were monitored in the nucleus accumbens and in the right and left hemispheres of medial prefrontal cortex, in lesioned animals and shams. Animals were subjected to a physical stressor (tail pinch) and a species-typical threat (fox odour); each stressor was presented twice over four consecutive daily sessions. The results indicate that the nucleus accumbens dopamine responses to both stressors are significantly potentiated by dopamine-depleting lesions to basolateral amygdala. In contrast, while the dopamine stress response in the left medial prefrontal cortex did not differ between lesioned animals and shams, the right medial prefrontal cortical dopamine response to tail pinch, but not fox odour stress, was significantly attenuated in lesioned animals. Therefore, basolateral amygdala dopamine depletion had opposite effects on the nucleus accumbens and medial prefrontal cortical dopamine responses to stress, although the effect on the latter is lateralized to the right hemisphere in a stressor-specific manner. These data indicate that stress-induced activation of meso-amygdaloid dopamine exerts an inhibitory influence on the nucleus accumbens dopamine response to stress. They also suggest the possibility that meso-amygdaloid dopamine influences the nucleus accumbens dopamine response to stress indirectly by modulating stress-induced dopamine release in medial prefrontal cortex. These findings add to a growing body of evidence of a preferential involvement of right medial prefrontal cortical dopamine in a wide range of physiological responses to stress.
authors.affiliation: Douglas Hospital Research Centre, McGill University, 6875 Boulevard LaSalle, Montréal, Québec, Canada H4H 1R3.
authors.forename: C W
authors.initials: CW
authors.lastname: Stevenson
authors.forename: R M
authors.initials: RM
authors.lastname: Sullivan
authors.forename: A
authors.initials: A
authors.lastname: Gratton
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D004298:Dopamine / Q000378:metabolism*; D004563:Electrochemistry; D007839:Functional Laterality; D008297:Male; D009410:Nerve Degeneration / Q000139:chemically induced; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism; D009714:Nucleus Accumbens / Q000378:metabolism*; D016627:Oxidopamine; D017397:Prefrontal Cortex / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D013315:Stress, Psychological; D013565:Sympatholytics
chemical_list: D013565:Sympatholytics; D016627:Oxidopamine; D004298:Dopamine; D009638:Norepinephrine