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Amygdala inputs drive feedforward inhibition in the medial prefrontal cortex
- Publication Year :
- 2013
- Publisher :
- American Physiological Society, 2013.
-
Abstract
- Although interactions between the amygdala and prefrontal cortex (PFC) are critical for emotional guidance of behavior, the manner in which amygdala affects PFC function is not clear. Whereas basolateral amygdala (BLA) output neurons exhibit many characteristics associated with excitatory neurotransmission, BLA stimulation typically inhibits PFC cell firing. This apparent discrepancy could be explained if local PFC inhibitory interneurons were activated by BLA inputs. Here, we used in vivo juxtacellular and intracellular recordings in anesthetized rats to investigate whether BLA inputs evoke feedforward inhibition in the PFC. Juxtacellular recordings revealed that BLA stimulation evoked action potentials in PFC interneurons and silenced most pyramidal neurons. Intracellular recordings from PFC pyramidal neurons showed depolarizing postsynaptic potentials, with multiple components evoked by BLA stimulation. These responses exhibited a relatively negative reversal potential (Erev), suggesting the contribution of a chloride component. Intracellular administration or pressure ejection of the GABA-A antagonist picrotoxin resulted in action-potential firing during the BLA-evoked response, which had a more depolarized Erev. These results suggest that BLA stimulation engages a powerful inhibitory mechanism within the PFC mediated by local circuit interneurons.
- Subjects :
- Male
Physiology
Prefrontal Cortex
Stimulation
Neurotransmission
Inhibitory postsynaptic potential
Rats, Sprague-Dawley
Postsynaptic potential
Interneurons
Neural Pathways
medicine
Animals
Prefrontal cortex
Chemistry
General Neuroscience
Pyramidal Cells
Neural Inhibition
Articles
Amygdala
Rats
Electrophysiology
medicine.anatomical_structure
nervous system
Excitatory postsynaptic potential
Neuroscience
Basolateral amygdala
Subjects
Details
- Language :
- English
- Database :
- OpenAIRE
- Accession number :
- edsair.doi.dedup.....3559f467a1171fa6877f65e993bce09d