Amygdala lesions block conditioned enhancement of the early component of the rat eyeblink reflex.
A tone conditioned stimulus (CS) previously paired with a grid shock unconditioned stimulus (US) can greatly enhance the early electromyographic (EMG) component (R1) of the rat eyeblink reflex. The hypothesis that the central nucleus of the amygdala (ACe) is an essential part of the circuitry mediating conditioned R1 enhancement was tested. After bilateral ACe lesions (L) or a sham operation (S), rats received paired presentations of the CS and US (P) or explicitly unpaired CS and US presentations (U), resulting in 4 groups: P/S, P/L, U/S, and U/L. ACe lesions completely prevented conditioned R1 enhancement, which was only exhibited in Group P/S. In the latter group, the "preextinction" conditioned enhancement effect was roughly a 2-fold increase in the R1 magnitude. Circuit-level mechanisms are discussed, and some advantages of the eyeblink EMG response in this general conditioning paradigm are considered.
Choi
J S
JS
Department of Psychology, Yale University, New Haven, Connecticut 06520-8205, USA.
Lindquist
D H
DH
Brown
T H
TH
D000161:Acoustic Stimulation; D000679:Amygdala / Q000293:injuries / Q000473:pathology / Q000502:physiology*; D000818:Animals; D001767:Blinking; D003214:Conditioning, Classical; D005108:Extinction, Psychological; D005239:Fear / Q000502:physiology*; D006185:Habituation, Psychophysiologic; D008297:Male; D008954:Models, Biological; D009415:Nerve Net; D051381:Rats; D017207:Rats, Sprague-Dawley