The vasopressin 1b receptor has been consistently implicated as a key factor in the regulation of social behavior;however, the precise region of the brain where the vasopressin 1b receptor is acting has not been identified. The objective in this application is to identify neural substrates on which vasopressin acts via the vasopressin 1b receptor to affect social behavior in an experimental animal model. Specifically, the proposed experiments have been designed to test the central hypothesis that vasopressin 1b receptor mediated-signaling, specifically within the CA2 region of the hippocampus, contributes to normal displays of social behavior. The rationale for these studies is that identification of the neuroanatomical substrate upon which vasopressin acts via the vasopressin 1b receptor to impact social behavior will potentially further our understanding of aberrant social behavior. This knowledge is relevant to the NIH's mission in that it will potentially provide new targets for psychiatric disease treatment in humans.
The specific aim of this proposal is to determine the contribution of the vasopressin 1b receptor within the CA2 region of the hippocampus to social behavior. This will be achieved by coupling experimental animal behavioral studies with targeted, site-specific, gene knockdown to identify pathways important to the regulation of behavior. It is expected that completion of this research will lead to the identification of one of the important neural substrates contributing to the vasopressin 1b receptor's regulation of social behavior. The proposed research is significant because the findings of this work will serve as a foundation for a more focused examination of the interaction between vasopressin and other neurotransmitter systems;ultimately resulting in a more complete understanding of the regulation of social behavior.

Public Health Relevance

The proposed studies are important because they have the potential to identify one of the key neural substrates that likely contributes to manifestations of aberrant social behavior. The proposed research has relevance to public health, because the neurochemicals, neurosubstrates, and circuits that underlying the regulation of behavior are evolutionarily conserved. Thus, the findings are ultimately expected to be applicable to the health of human beings.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Exploratory/Developmental Grants (R21)
Project #
5R21MH083963-02
Application #
7835637
Study Section
Neuroendocrinology, Neuroimmunology, and Behavior Study Section (NNB)
Program Officer
Simmons, Janine M
Project Start
2009-05-07
Project End
2012-04-30
Budget Start
2010-05-01
Budget End
2012-04-30
Support Year
2
Fiscal Year
2010
Total Cost
$176,382
Indirect Cost
Name
Kent State University at Kent
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
041071101
City
Kent
State
OH
Country
United States
Zip Code
44242
Witchey, Shannah K; Stevenson, Erica L; Caldwell, Heather K (2016) Genotypic differences in intruder-evoked immediate early gene activation in male, but not female, vasopressin 1b receptor knockout mice. BMC Neurosci 17:75
Stevenson, Erica L; Caldwell, Heather K (2014) Lesions to the CA2 region of the hippocampus impair social memory in mice. Eur J Neurosci 40:3294-301
Caldwell, Heather K (2012) Neurobiology of sociability. Adv Exp Med Biol 739:187-205
Stevenson, Erica L; Caldwell, Heather K (2012) The vasopressin 1b receptor and the neural regulation of social behavior. Horm Behav 61:277-82