title: Immunohistochemical characterization of parvalbumin-containing interneurons in the monkey basolateral amygdala.
abstract: Interneurons expressing the calcium-binding protein parvalbumin (PV) are a critical component of the inhibitory circuitry of the basolateral nuclear complex (BLC) of the mammalian amygdala. These neurons form interneuronal networks interconnected by chemical and electrical synapses, and provide a strong perisomatic inhibition of local pyramidal projection neurons. Immunohistochemical studies in rodents have shown that most parvalbumin-positive (PV+) cells are GABAergic interneurons that co-express the calcium-binding protein calbindin (CB), but exhibit no overlap with interneuronal subpopulations containing the calcium-binding protein calretinin (CR) or neuropeptides. Despite the importance of identifying interneuronal subpopulations for clarifying the major players in the inhibitory circuitry of the BLC, very little is known about these subpopulations in primates. Therefore, in the present investigation dual-labeling immunofluorescence histochemical techniques were used to characterize PV+ interneurons in the basal and lateral nuclei of the monkey amygdala. These studies revealed that 90-94% of PV+ neurons were GABA+, depending on the nucleus, and that these neurons constituted 29-38% of the total GABAergic population. CB+ and CR+ interneurons constituted 31-46% and 23-27%, respectively, of GABAergic neurons. Approximately one quarter of PV+ neurons contained CB, and these cells constituted one third of the CB+ interneuronal population. There was no colocalization of PV with the neuropeptides somatostatin or cholecystokinin, and virtually no colocalization with CR. These data indicate that the neurochemical characteristics of the PV+ interneuronal subpopulation in the monkey BLC are fairly similar to those seen in the rat, but there is far less colocalization of PV and CB in the monkey. These findings suggest that PV+ neurons are a discrete interneuronal subpopulation in the monkey BLC and undoubtedly play a unique functional role in the inhibitory circuitry of this brain region.
authors.affiliation: Department of Pharmacology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
authors.forename: F
authors.initials: F
authors.lastname: Mascagni
authors.forename: E C
authors.initials: EC
authors.lastname: Muly
authors.forename: D G
authors.initials: DG
authors.lastname: Rainnie
authors.forename: A J
authors.initials: AJ
authors.lastname: McDonald
mesh_terms: D000679:Amygdala / Q000166:cytology*; D000818:Animals; D064032:Calbindin 2; D064026:Calbindins; D002452:Cell Count / Q000379:methods; D002766:Cholecystokinin / Q000378:metabolism; D005260:Female; D007395:Interneurons / Q000378:metabolism*; D008253:Macaca mulatta; D008254:Macaca nemestrina; D008297:Male; D010320:Parvalbumins / Q000378:metabolism*; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D013004:Somatostatin / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: C576512:Calb2 protein, rat; D064032:Calbindin 2; D064026:Calbindins; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G; D013004:Somatostatin; D005680:gamma-Aminobutyric Acid; D002766:Cholecystokinin