SOCIAL REGULATION OF THE THALAMIC PARATHYROID HORMONE TYPE II (PTH2) NEUROPEPTIDE IN ZEBRAFISH (DANIO RERIO)

Abstract

Social dominance is prevalent among social species. It allows group members to divide limited resources according to social rank. However, social dominance is often accompanied by aggression, stress and anxiety as group members establish their social relationships. These social stressors often lead to behavioral and neurophysiological consequences. This study examined the physiological effects of social dominance on the thalamic parathyroid system. Parathyroid Hormone Type II (PTH2) is a neuropeptide within the vertebrae thalamus serving as a sensory integration and relay center for stress responses. Studies using zebrafish (Danio rerio) as an organismal model of study reveal how behavioral decisions impact social relationships while highlighting the brain regions that are modulated by social behavior. Though PTH2 is expressed within the thalamic nucleus of zebrafish, the neurological mechanisms examining the role of PTH2 in information processing and stress responses to social behaviors remain poorly understood. Based on the idea that the presence of PTH2 affects behavior on a phenotypic level, I hypothesized that the thalamic PTH2 nucleus morphological and functional organization could be socially regulated. Using phosphorylated ribosomal S6 expression as a measure of cellular activity, I hypothesized that morphological differences in the PTH2 system leads to physiological changes. Moreover, I hypothesized that changes in the social environment because of social rise and social fall or social isolation will lead to a corresponding plasticity in the structural and functional organization of the PTH2 system. My results reveal that social dominance influences the number of PTH2 expressing cells: After one week of social interactions the number of PTH2 cells is higher in dominants compared to subordinates and communals (control), but this difference is abolished after two-weeks of interactions. Secondly, I show that PTH2 neurons expression of PS6, a marker of cellular activity is significantly upregulated in dominants compared to subordinates after one week of social interactions. Thirdly, social rise and fall in rank shifts the expression of PS6 and PS6 fluorescence intensity to reflect the animals’ current social status, but social reversal has limited effect on the number of PTH2 cells. Finally, social isolation or re-isolation of dominant animals show decreased PTH2 cell count and PS6 cellular activity, suggesting that re-isolation further modulates the molecular plasticity of the PTH2 neuropeptide circuit. These results provide new insights of how social isolation and aggressive interactions influence the plasticity of the PTH2 system in the context of social anxiety and stress.