Table 3.

Modulators of social avoidance in animals

Modulator	Regulation pro social avoidance	Regulation contra social avoidance
Glucocorticoids and HPA axis	↓CORT (juvenile), specific ↑CORT (adult), non-specific ↑CRH in HT ↓GR in HT and HPC ↑GR-signaling in mPFC Systemic CORT application (adult)	Systemic CORT application (juvenile) Systemic inhibition of the GR (adult) Imipramine: ↓CRH in HT Escitalopram: ↓CORT, ↑GR in HPC Icariin: ↓CRH in HT, ↑GR in HPC
Testosterone	↓ testosterone (males only)?	↓ vHPC-NAc activity via testosterone?
BDNF	↑ BDNF in NAc and/or VTA ↓ BDNF in FC, HPC, HT Local infusion of BDNF in NAc Increase of BDNF-signaling in HPC Systemic TrkB antagonism	↓ BDNF in NAc and/or VTA Inhibition of TrkB signaling in NAc and/or VTA Inhibition of CRH-receptors in NAc by prevention of BDNF-increase Increase of BDNF-signaling in HPC Systemic TrkB agonism SNP Val66Met with ↓BDNF in NAc
Dopamine	↑ in VTA and NAc (via D2 receptors) ↓ in mPFC and DRN ↓ D1 receptor in mPFC ↑ DA-signaling via D1 in AMY knock-out of D1 receptor in mPFC	DA antagonism in NAc (males)
5-HT	↑5-HT in brain and plasma 50% reduced expression of 5-HTT ↓5HT in the frontal cortex ↓5-HT1A receptor expression and disinhibition of 5-HT neurons (P14-30) Citalopram: ↑5-HT transmission	Imipramine: restores properties of 5-HT neurons
Oxytocin	↑ OXT-R density in NAc and dLS ↑ OXT-R binding in AMY, HPC, dLS OXT-R overexpression in dLS Inhibition of OXT signaling in VTA Inhibition/deletion of OXT-R in NAc Inhibition of OXT-R in DNR OXT-R antagonist in BNST (females) Intranasal OXT (females) i.c.v. OXT-R antagonist Systemic OXT-R antagonist	Local injection of OXT into dLS Knock-out of OXT-R in dLS i.c.v. OXT Intranasal OXT (females)
Endocannabinoids	Activation of CB1 in HPC Inhibition of CB1 signaling knock-out of DAGLa knock-out -OUT of CB1	Systemic increase in 2-AG Inhibition of 2-AG degradation