Regulation of stress and metabolism in neonates

Focused on the developmental regulation of the stress axis and metabolism in neonates, the basic and clinical studies are oriented towards understanding the long-term physiological and behavioral consequences for the brain of early perinatal and neonatal exposure to stressors.

Conditions such as altered nutrition and fat intake in particular are known to affect a number of critical developmental brain processes in humans and animals.

Other stressors such as repeated pain in early development can also have multiple long-term consequences in both species. The lab is interested to determine whether maternal care can be effective at preventing some of the negative aspects of pain in neonates.

Research projects

To determine the role of neonatal fat intake and leptin, the “anti-obesity” protein secreted by the adipose tissue on hippocampal development, including aspects relating to neurogenesis and synaptogenesis, long-term potentiation and expression of specific receptors in the hippocampus. The lab hypothesis is that elevated leptin levels observed during neonatal development enhance the development of hippocampal function. This project will continue to investigate the effects of metabolic effectors (insulin, ghrelin, leptin, fatty acids) on the development of the dopaminergic system in relation to the rewarding properties of food in adulthood.
Funding: CIHR 2002-2007, renewed in 2007.

The lab is also testing whether differential hypothalamic sensitivity to leptin in developing neonates determines the pattern of neuropeptide development (NPY, POMC, CART, MSH) that controls food intake and energy balance. This project is continued by the investigation of the specific role of endocannabinoids, derived from lipid precursors, on the regulation of the stress response during development
Funding: NSERC, 2006-2011.

To determine the effect or neonatal repeated pain on neuroendocrine and neuronal circuits implicated in stress and pain responses and to compare various modalities of maternal comfort behavior in preventing specific pain-induced neuronal activation in brain areas associated with pain, emotion and learning. The lab hypothesis is that enhanced maternal care at the time of pain in developing neonates will promote a better recovery of stress hormones and neuronal activation, and thus reduce the long-term effects of early pain on later physiological stability and pain sensitivity.

These studies may contribute theoretically to the underlying mechanisms of long term effects of maternal comfort in the presence of pain. They are done in collaboration with Dr Celeste Johnston (School of Nursing, McGill University) who is leading the clinical portion of this project
Funding: CIHR, 2003-2008