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The Journal of Neuroscience, January 15, 1999, 19(2):836-844
Reciprocal Changes in the Firing Probability of Lateral and
Central Medial Amygdala Neurons
Dawn R.
Collins and
Denis
Paré
Laboratoire de Neurophysiologie, Département de Physiologie,
Faculté de Médecine, Université Laval,
Québec, Canada G1K 7P4
The amygdala is essential for classical fear conditioning.
According to the current model of auditory fear conditioning, the lateral nucleus is the input station of the amygdala for conditioned auditory stimuli, whereas the central nucleus is the output station for
conditioned fear responses. Yet, the lateral nucleus does not project
to the central medial nucleus, where most brainstem projections of the
amygdala originate. The available evidence suggests that the basal
nuclei could transmit information from the lateral to the central
medial nucleus. However, interposed between the basolateral complex and
the central nucleus are clusters of GABAergic cells, the intercalated
neurons, which receive inputs from the lateral and basal nuclei and
contribute a massive projection to the central medial nucleus. Because
it is impossible to predict the consequences of these
connections, we correlated the spontaneous and auditory-evoked activity
of multiple simultaneously recorded neurons of the lateral, basal, and
central nuclei. The spontaneous activity of lateral and basolateral
neurons was positively correlated to that of central lateral cells but
negatively correlated to that of central medial neurons. In response to
auditory stimuli, the firing probability of lateral and central medial
neurons oscillated in phase opposition, initially being excited and
inhibited, respectively. In light of previous anatomical findings, we
propose that the lateral nucleus exerts two indirect actions on central
medial neurons: an excitation via the basal nuclei and an inhibition via intercalated neurons.
Key words:
amygdala; fear conditioning; multisite recording; lateral
amygdala; intra-amygdaloid pathways; intercalated cell masses
Copyright © 1999 Society for Neuroscience 0270-6474/99/192836-09$05.00/0
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