Paraventricular oxytocin neurons impact energy intake and expenditure: projections to the bed nucleus of the stria terminalis reduce sucrose consumption.

BACKGROUND

The part played by oxytocin and oxytocin neurons in the regulation of food intake is controversial. There is much pharmacological data to support a role for oxytocin notably in regulating sugar consumption, however, several recent experiments have questioned the importance of oxytocin neurons themselves.

METHODS

Here we use a combination of histological and chemogenetic techniques to investigate the selective activation or inhibition of oxytocin neurons in the hypothalamic paraventricular nucleus (Oxt). We then identify a pathway from Oxt neurons to the bed nucleus of the stria terminalis using the cell-selective expression of channel rhodopsin.

RESULTS

Oxt neurons increase their expression of cFos after both physiological (fast-induced re-feeding or oral lipid) and pharmacological (systemic administration of cholecystokinin or lithium chloride) anorectic signals. Chemogenetic activation of Oxt neurons is sufficient to decrease free-feeding in mice, while inhibition in mice attenuates the response to administration of cholecystokinin. Activation of Oxt neurons also increases energy expenditure and core-body temperature, without a significant effect on locomotor activity. Finally, the selective, optogenetic stimulation of a pathway from Oxt neurons to the bed nucleus of the stria terminalis reduces the consumption of sucrose.

CONCLUSION

Our results support a role for oxytocin neurons in the regulation of whole-body metabolism, including a modulatory action on food intake and energy expenditure. Furthermore, we demonstrate that the pathway from Oxt neurons to the bed nucleus of the stria terminalis can regulate sugar consumption.