title: Dopamine attenuates prefrontal cortical suppression of sensory inputs to the basolateral amygdala of rats.
abstract: The basolateral complex of the amygdala (BLA) plays a significant role in affective behavior that is likely regulated by afferents from the medial prefrontal cortex (mPFC). Studies suggest that dopamine (DA) is a necessary component for production of appropriate affective responses. In this study, prefrontal cortical and sensory cortical [temporal area 3 (Te3)] inputs to the BLA and their modulation by DA receptor activation was examined using in vivo single-unit extracellular recordings. We found that Te3 inputs are more capable of driving BLA projection neuron firing, whereas mPFC inputs potently elicited firing from BLA interneurons. Moreover, mPFC stimulation before Te3 stimulation attenuated the probability of Te3-evoked spikes in BLA projection neurons, possibly via activation of inhibitory interneurons. DA receptor activation by apomorphine attenuated mPFC inputs, while augmenting Te3 inputs. Additionally, DA receptor activation suppressed mPFC-induced inhibition of Te3-evoked spikes. Thus, the mPFC may attenuate sensory-driven amygdala-mediated affective responses via recruitment of BLA inhibitory interneurons that suppress sensory cortical inputs. In situations of enhanced DA levels in the BLA, such as during stress and after amphetamine administration, mPFC regulation of BLA will be dampened, leading to a disinhibition of sensory-driven affective responses.
authors.affiliation: Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA. Rosenk@bns.pitt.edu
authors.forename: J A
authors.initials: JA
authors.lastname: Rosenkranz
authors.forename: A A
authors.initials: AA
authors.lastname: Grace
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000679:Amygdala / Q000166:cytology / Q000502:physiology*; D000818:Animals; D001058:Apomorphine / Q000008:administration & dosage; D001522:Behavior, Animal / Q000502:physiology; D004298:Dopamine / Q000378:metabolism* / Q000494:pharmacology; D018491:Dopamine Agonists / Q000008:administration & dosage; D018492:Dopamine Antagonists / Q000008:administration & dosage; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D006220:Haloperidol / Q000008:administration & dosage; D007275:Injections, Intravenous; D007395:Interneurons / Q000187:drug effects / Q000502:physiology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D017397:Prefrontal Cortex / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D011954:Receptors, Dopamine / Q000378:metabolism; D012684:Sensory Thresholds / Q000187:drug effects; D013702:Temporal Lobe / Q000502:physiology
chemical_list: D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D011954:Receptors, Dopamine; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine