title: Blockade of glutamatergic transmission in the primate basolateral amygdala suppresses active behavior without altering social interaction.
abstract: The amygdala is an integrator of affective processing, and a key component of a network regulating social behavior. While decades of lesion studies in nonhuman primates have shown alterations in social interactions after amygdala damage, acute manipulations of the amygdala in primates have been underexplored. We recently reported (Wellman, Forcelli, Aguilar, & Malkova, 2016) that acute pharmacological inhibition of the basolateral complex of the amygdala (BLA) or the central nucleus of the amygdala increased affiliative social interactions in experimental dyads of macaques; this was achieved through microinjection of a GABA-A receptor agonist. Prior studies in rodents have shown similar effects achieved by blocking NMDA receptors or AMPA receptors within the BLA. Here, we sought to determine the role of these receptor systems in the primate BLA in the context of social behavior. In familiar dyads, we microinjected the NMDA receptor antagonist 2-amino-7-phosphonoheptanoic acid (AP7) or the AMPA receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) and observed behaviors and social interactions in the immediate postinjection period. In striking contrast with our prior report using GABA agonists, and in contrast with prior reports in rodents using glutamate antagonists, we found that neither NMDA nor AMPA blockade increase social interaction. Both treatments, however, were associated with decreases in locomotion and manipulation and increases in passive behavior. These data suggest that local blockade of glutamatergic neurotransmission in BLA is not the functional equivalent of local activation of GABAergic signaling, and raise interesting questions regarding the functional microcircuitry of the nonhuman primate amygdala in the context of social behavior. (PsycINFO Database Record
authors.affiliation: Department of Pharmacology and Physiology, Georgetown University.
authors.forename: Patrick A
authors.initials: PA
authors.lastname: Forcelli
authors.affiliation: Department of Pharmacology and Physiology, Georgetown University.
authors.forename: Laurie L
authors.initials: LL
authors.lastname: Wellman
authors.affiliation: Department of Pharmacology and Physiology, Georgetown University.
authors.forename: Ludise
authors.initials: L
authors.lastname: Malkova
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000008:administration & dosage / Q000031:analogs & derivatives; D000818:Animals; D066272:Basolateral Nuclear Complex / Q000502:physiology*; D001522:Behavior, Animal; D018691:Excitatory Amino Acid Antagonists / Q000008:administration & dosage; D005260:Female; D018698:Glutamic Acid / Q000502:physiology; D007398:Interpersonal Relations; D008254:Macaca nemestrina; D008297:Male; D009043:Motor Activity; D011810:Quinoxalines / Q000008:administration & dosage; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology*; D012919:Social Behavior; D009435:Synaptic Transmission
chemical_list: D018691:Excitatory Amino Acid Antagonists; D011810:Quinoxalines; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D018698:Glutamic Acid; D015763:2-Amino-5-phosphonovalerate; C031231:2-amino-7-phosphonoheptanoic acid