Properties of the pathways from the lateral amygdal nucleus to basolateral nucleus and amygdalostriatal transition area.

Published

Journal Article

Studies have revealed that the amygdala formation is involved in emotional learning, attention, and autonomic functions. Although intra-amygdala connections have been described anatomically, the functional characteristics of these connections are not well understood. We used a rat brain slice preparation with a voltage-sensitive imaging system to compare the electrophysiological characteristics of intra-amygdala pathways. Electrical stimuli delivered to the lateral nucleus (La) caused the optical signal to propagate to basolateral nucleus (BL) and amygdalostriatal transition area (AStr), but not the central nucleus (Ce), consistent with previous anatomical studies, including the recently characterized projections from La to AStr. The velocity of propagation of the evoked potential along the La-AStr pathway was significantly faster than that along the La-BL pathway. In addition, the efficiency of the signal transmission (determined by the rate of decay) along the La-AStr pathway was higher than that along the La-BL pathway. Also, AStr possessed a distinct property of temporal summation of La signals. On the other hand, the La-BL pathway possessed a significantly higher sensitivity to bicuculline/picrotoxin and a stronger paired-pulse inhibition than the La-AStr pathway. Furthermore, the La-BL pathway expressed a higher D-2-amino-5-phosphonovaleric acid (a NMDA blocker) sensitivity than the La-AStr pathway. These results suggest that the La-AStr pathway, which conducts signals with high velocity and less attenuation, may be involved in rapid reflexive responses during fear-induced behavior, whereas the La-BL pathway facilitates signal integration and learning.

Full Text

Duke Authors

Cited Authors

  • Wang, C; Kang-Park, M-H; Wilson, WA; Moore, SD

Published Date

  • May 2002

Published In

Volume / Issue

  • 87 / 5

Start / End Page

  • 2593 - 2601

PubMed ID

  • 11976395

Pubmed Central ID

  • 11976395

International Standard Serial Number (ISSN)

  • 0022-3077

Digital Object Identifier (DOI)

  • 10.1152/jn.2002.87.5.2593

Language

  • eng

Conference Location

  • United States