Memory of a recently eaten meal can serve as a powerful mechanism for controlling future eating behavior because it provides a record of intake that likely outlasts most physiological signals generated by the meal. In support, impairing the encoding of a meal in humans increases the amount ingested at the next eating episode. However, the brain regions that mediate the inhibitory effects of memory on future intake are unknown.


  1. How do brain regions involved in memory control eating behavior?
  2. Does impaired memory/hippocampal function cause the development and/or maintenance of diet induced obesity? 

We approach our questions with two general strategies:

  1. Manipulate neural activity e.g., with drug infusions or optogenetics
  2. Measure the impact of ingestion on brain and behavior e.g., measures of synaptic plasticity

Our research typically involves obtaining measures of learning and memory, synaptic plasticity, energy intake, body weight, body fat, and biochemical measures from brain, blood, and peripheral organs such as the liver.

We currently focus on how hippocampal activity, which is traditionally associated with episodic memory, modulates energy intake in rodents. We hypothesize that hippocampal neurons form a memory of a meal and inhibit future intake, both in terms of delaying the initiation of the next meal and limiting the amount consumed during that meal. For more details regarding this hypothesis read our recent review (Parent et al 2014; Parent 2016; Parent 2016)

To the best of our knowledge, we are the first to implicate dorsal and ventral hippocampal neurons in energy intake during the period following a meal (Henderson et al 2013; Hannapel et al 2017). These findings indicate that manipulations that specifically impair hippocampal function increase energy intake. In life, many situations such as stress and illness impair hippocampal function. For example, we have found that one episode of pain on the day of birth produces long-lasting deficits in hippocampal function that last at least until middle-age (Henderson et al 2015; Henderson et al 2017). We have also shown that overeating fat and sugar and non-alcoholic fatty liver disease impair hippocampal-dependent memory (Darling et al 2013; Ross et al 2009; Ross et al 2012; Ross et al 2013).

Collectively, these findings have led us to further hypothesize that life events, such as stress or overeating, impair hippocampal function, which in turn causes more eating. For more details about this vicious cycle read our recent review (Parent et al 2014; Parent 2016; Parent 2016).


This research is supported by the National Science Foundation and the Georgia State University Brains & Behavior Program.

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