Flexible control of social and non-social behaviors by zebrafish oxytocin circuitry


March 30, 2016 - 1:00pm
Northwest 243
About the Speaker
Caroline Wee (Engert Lab)

Neuromodulators often exert widespread effects on brain circuits and behavior, making them a challenge to fully understand. The neuropeptide oxytocin is no exception, having been implicated in numerous functions such as social behavior, pain, and appetite. For example, loss of oxytocin neurons in Prader-Willi syndrome is characterized by a diverse set of symptoms including severe overeating, social deficits and a high pain tolerance. Here, we leverage the accessible neural circuitry and genetics of the larval zebrafish to explore the evolutionary logic underlying oxytocin’s broad effects on behavior. By using an unbiased brain-wide activity mapping approach, we pinpoint hypothalamic oxytocin neurons as a key hub for the control of defensive behaviors against pain. We show that oxytocin neurons integrate multiple noxious stimuli, particularly input from TRPA1 damage-sensing receptors, to drive pain avoidance behavior via the co-release of oxytocin and glutamate in the hindbrain and spinal cord. Interestingly, we discover that oxytocin neurons also increase their activity during social isolation, which correlates with a profound reduction in food intake, and manipulating oxytocin signaling can reverse this effect. Thus, oxytocin neurons can integrate information about an animal’s social context to control multiple homeostatic drives. Our results not only recapitulate oxytocin-related phenotypes in mammals, but also provide insights into how a single neuromodulator can exert flexible, state-dependent control over diverse social and non-social behaviors.