Ferdinand Althammer

This study shows that Magel2 deficiency in a mouse model of Prader-Willi syndrome causes microglial structural changes and increased synaptic engulfment, altering neuron-microglia interactions and hypothalamic circuit function.

The paper identifies FOXP1 as a key regulator of oxytocin neuron differentiation and shows its role in reducing AVP and OXT neuron abundance in knockout mice.

This study identifies a circuit in the medial prefrontal cortex where oxytocin modulates interneurons to promote social behavior in female rats, even under physiological stress.

This study shows that Angiotensin-II increases microglia-vascular interactions in rat heart failure models, leading to neuroinflammation that can be mitigated by blocking AngII receptors.

The paper shows that oxytocin-induced astrocyte process retraction in the amygdala modulates freezing behavior during stress by enhancing neuronal sensitivity to potassium.

This study investigates changes in the oxytocinergic circuit in the central amygdala of rats with chronic heart failure, finding impaired OT release and receptor function.

This study examines the oxytocin system and OTR-expressing astrocytes in a mouse model of PWS, finding reduced oxytocin cells and OTR-expressing astrocytes in specific brain regions with sex-specific differences.

The paper investigates changes in the PVN-to-CA2 oxytocin pathway in heart failure rats, finding altered oxytocinergic innervation and reduced OTR-expressing astrocytes.

The paper identifies a novel analgesic pathway involving parvocellular oxytocin neurons projecting to the vlPAG, which suppresses spinal cord sensory neuron activity and alleviates pain.

This study shows that oxytocin acts on astrocytes in the central amygdala to promote a positive emotional state, challenging the notion that oxytocin only affects neurons.

This study identifies molecular mechanisms of cognitive and mood deficits in rats with heart failure by analyzing synaptic plasticity gene expression in multiple brain regions.