Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-5-24
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4090-103
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11356897-Action Potentials, pubmed-meshheading:11356897-Amygdala, pubmed-meshheading:11356897-Animals, pubmed-meshheading:11356897-Apomorphine, pubmed-meshheading:11356897-Behavior, Animal, pubmed-meshheading:11356897-Dopamine, pubmed-meshheading:11356897-Dopamine Agonists, pubmed-meshheading:11356897-Dopamine Antagonists, pubmed-meshheading:11356897-Electric Stimulation, pubmed-meshheading:11356897-Electrodes, Implanted, pubmed-meshheading:11356897-Haloperidol, pubmed-meshheading:11356897-Injections, Intravenous, pubmed-meshheading:11356897-Interneurons, pubmed-meshheading:11356897-Male, pubmed-meshheading:11356897-Neural Inhibition, pubmed-meshheading:11356897-Neurons, pubmed-meshheading:11356897-Prefrontal Cortex, pubmed-meshheading:11356897-Rats, pubmed-meshheading:11356897-Rats, Sprague-Dawley, pubmed-meshheading:11356897-Reaction Time, pubmed-meshheading:11356897-Receptors, Dopamine, pubmed-meshheading:11356897-Sensory Thresholds, pubmed-meshheading:11356897-Temporal Lobe
pubmed:year
2001
pubmed:articleTitle
Dopamine attenuates prefrontal cortical suppression of sensory inputs to the basolateral amygdala of rats.
pubmed:affiliation
Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA. Rosenk@bns.pitt.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.