Literature DB >> 17120289

Postsynaptic targets of somatostatin-containing interneurons in the rat basolateral amygdala.

Jay F Muller1, Franco Mascagni, Alexander J McDonald.   

Abstract

The basolateral amygdala contains several subpopulations of inhibitory interneurons that can be distinguished on the basis of their content of calcium-binding proteins or peptides. Although previous studies have shown that interneuronal subpopulations containing parvalbumin (PV) or vasoactive intestinal peptide (VIP) innervate distinct postsynaptic domains of pyramidal cells as well as other interneurons, very little is known about the synaptic outputs of the interneuronal subpopulation that expresses somatostatin (SOM). The present study utilized dual-labeling immunocytochemical techniques at the light and electron microscopic levels to analyze the innervation of pyramidal cells, PV+ interneurons, and VIP+ interneurons in the anterior basolateral amygdalar nucleus (BLa) by SOM+ axon terminals. Pyramidal cell somata and dendrites were selectively labeled with antibodies to calcium/calmodulin-dependent protein kinase II (CaMK); previous studies have shown that the vast majority of dendritic spines, whether CAMK+ or not, arise from pyramidal cells. Almost all SOM+ axon terminals formed symmetrical synapses. The main postsynaptic targets of SOM+ terminals were small-caliber CaMK+ dendrites and dendritic spines, some of which were CaMK+. These SOM+ synapses with dendrites were often in close proximity to asymmetrical (excitatory) synapses to these same structures formed by unlabeled terminals. Few SOM+ terminals formed synapses with CaMK+ pyramidal cell somata or large-caliber (proximal) dendrites. Likewise, only 15% of SOM+ terminals formed synapses with PV+, VIP+, or SOM+ interneurons. These findings suggest that inhibitory inputs from SOM+ interneurons may interact with excitatory inputs to pyramidal cell distal dendrites in the BLa. These interactions might affect synaptic plasticity related to emotional learning. Copyright 2006 Wiley-Liss, Inc.

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Year:  2007        PMID: 17120289     DOI: 10.1002/cne.21185

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


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