title: Selective suppression of plasticity in amygdala inputs from temporal association cortex by the external capsule.
abstract: GABAergic neurons in the external capsule (EC) provide feedforward inhibition in the lateral amygdala (LA), but how EC affects synaptic transmission and plasticity in inputs from specific cortical areas remains unknown; this is because axonal fibers from different cortical areas are intermingled in the amygdala and cannot be activated selectively using conventional electrical stimulation. Here, we achieved selective activation of fibers from the temporal association cortex (TeA) or the anterior cingulate cortex (ACC) by using channelrhodopsin-2. Long-term potentiation (LTP) in the TeA-LA pathway, which runs through EC, was enabled by cutting connections between EC and LA or by blocking GABA(A) receptor-mediated transmission. In contrast, LTP in the ACC-LA pathway, which bypasses EC, was GABA(A) receptor independent. The EC transection shifted balance between inhibitory and excitatory responses in the TeA-LA pathway toward excitation, but had no effect on the ACC-LA pathway. Thus, EC provides pathway-specific suppression of amygdala plasticity.
authors.affiliation: Unit on Behavioral Genetics, Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: Alexei
authors.initials: A
authors.lastname: Morozov
authors.forename: Daniel
authors.initials: D
authors.lastname: Sukato
authors.forename: Wataru
authors.initials: W
authors.lastname: Ito
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology*; D000679:Amygdala / Q000166:cytology / Q000502:physiology*; D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology / Q000502:physiology*; D000075402:Channelrhodopsins; D000229:Dependovirus / Q000235:genetics; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000235:genetics / Q000502:physiology; D018756:GABA Antagonists / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000235:genetics; D005968:Glutamate Decarboxylase / Q000235:genetics; D049452:Green Fluorescent Proteins / Q000235:genetics; D066298:In Vitro Techniques; D008164:Luminescent Proteins / Q000235:genetics; D008297:Male; D008564:Membrane Potentials / Q000235:genetics / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009473:Neuronal Plasticity / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D010775:Photic Stimulation / Q000379:methods; D010852:Picrotoxin / Q000494:pharmacology; D013997:Time Factors; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D000075402:Channelrhodopsins; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D005968:Glutamate Decarboxylase; D049452:Green Fluorescent Proteins; D008164:Luminescent Proteins; D010852:Picrotoxin; D014633:Valine; C056639:2-amino-5-phosphopentanoic acid; C402565:glutamate decarboxylase 1