University of Louisville
Localization of GABA within CRH- or SST-expressing Axon Terminals in the PBN
Institution
University of Louisville
Faculty Advisor/ Mentor
Robert F. Lundy, Jr.
Abstract
Corticotrophin-releasing hormone (CRH) is a hormone that increases short-term appetite, and somatostatin (SST) is a hormone that conflictingly increases or decreases short-term appetite based on dose and application site. Previous work has shown that these hormones project into the taste-sensitive area of the parabrachial nucleus (PBN); this project aimed to investigate synapses in the PBN that contain these hormones and determine if there is a correlation with expression of the inhibitory neurotransmitter GABA. SST or CRH terminals in the PBN were labeled by crossing SST-cre or CRH-cre mice with Ai9 TdTomato fluorescent reporter mice. In SST/TdTomato mouse tissue, seventy-five percent of SST synaptic terminals (27 of 36) in the PBN contained GABA. In contrast, only 8 of 28 (28%) CRH/TdTomato synaptic terminals in the PBN contained GABA. Additional experiments using viral delivery of fluorescent reporter identified SST cell types in the central nucleus of the amygdala (CeA) as a major source of GABAergic input to the PBN. In all cases, the majority of postsynaptic targets did not contain GABA, which likely reflects direct synaptic contacts on PBN projection neurons. These results indicate a mechanism whereby activation of SST CeA cell types can monosynaptically inhibit PBN neurons and gate the relay of taste signals through the PBN.
Localization of GABA within CRH- or SST-expressing Axon Terminals in the PBN
Corticotrophin-releasing hormone (CRH) is a hormone that increases short-term appetite, and somatostatin (SST) is a hormone that conflictingly increases or decreases short-term appetite based on dose and application site. Previous work has shown that these hormones project into the taste-sensitive area of the parabrachial nucleus (PBN); this project aimed to investigate synapses in the PBN that contain these hormones and determine if there is a correlation with expression of the inhibitory neurotransmitter GABA. SST or CRH terminals in the PBN were labeled by crossing SST-cre or CRH-cre mice with Ai9 TdTomato fluorescent reporter mice. In SST/TdTomato mouse tissue, seventy-five percent of SST synaptic terminals (27 of 36) in the PBN contained GABA. In contrast, only 8 of 28 (28%) CRH/TdTomato synaptic terminals in the PBN contained GABA. Additional experiments using viral delivery of fluorescent reporter identified SST cell types in the central nucleus of the amygdala (CeA) as a major source of GABAergic input to the PBN. In all cases, the majority of postsynaptic targets did not contain GABA, which likely reflects direct synaptic contacts on PBN projection neurons. These results indicate a mechanism whereby activation of SST CeA cell types can monosynaptically inhibit PBN neurons and gate the relay of taste signals through the PBN.