To eat or not to eat: Hippocampal involvement in meal onset.
Y. OGAWA1, G. P. SMITH3, A. VAZDARJANOVA4, M. B. PARENT2;
1Neurosci. Inst., 2Neurosci. Inst. and Dept. of Psychology, Georgia State Univ., Atlanta, GA; 3Psychiatry, Weill Cornell Med. Col., New York, NY; 4Neurol., Georgia Hlth. Sci. Univ., Augusta, GA
TL;DR: Dorsal hippocampal neurons expressed Arc 7min after feeding; inhibiting dHC after eating shortened the time before subsequent meal -> dHC might be involved in meal onset by forming a memory of a previous meal.
Across the animal kingdom, eating usually happens in bouts. Whether or not to start eating (or “meal onset”, in neuroscience lingo) might seem to be a simple decision; however, the neural mechanisms underlying the motivation to begin eating are surprisingly complex and poorly understood. So why do we begin eating?
Perhaps the simplest answer is because we feel hungry. Indeed, adipose (fatty) tissue and the gut can send out physiological signals relating to energy balance to the hypothalamus, which in turn regulates our feeding behaviour. Brain areas involved in decision making and emotion, such as the forebrain and amygdala, can also influence our motivation to start eating (hello dieting and emotional binging). Many exciting findings have come out of studies focusing on the above brain areas. However, recently a number of neuroscientists have turned to the hippocampus for more answers by asking the question: can the memory of consuming a meal influence the timing of our next meal?
How did the spotlight turn to the hippocampus (HC)? It is well known for its crucial role in learning and memory. Neuroanatomical tracings have found direct projections from hippocampal cell fields to brain regions that are known to be involved in feeding. In humans, functional magnetic resonance imaging show changes in HC activation in response to food stimulation and manipulations designed to increase interoceptive signals of satiety (the feeling of fullness). Maniputating the memory of a meal in healthy young women can affect how much they eat in a subsequent meal. Even more fascinating, patients with severe HC-related amnesia (who presumably can’t remember their last meal) show a reduced ability to suppress food intake when repeatedly given the opportunity to eat.
The question this current study asks is whether or not hippocampal neurons can form a memory of a meal and inhibit meal onset later on. The authors first trained rats to lick a sugar solution at specific times of the day. On testing day, after a sucrose meal, muscimol was directly injected into the dorsal hippocampus to inhibit its activity. Rats were subsequently monitored for 60 minutes to see if there are changes in eating behaviour. Compared to the controls, who received a vehicle injection, dHC-inactivated rats waited a shorter period of time before eating their next meal (as measured by the inter-meal interval), ate for a longer time during the next meal, thus overall displaying less satiety. Inactivation of the dHC also prevented a correlation between the size of the preceding meal and the onset of the next meal, meaning that how much the rats’ ate stopped influencing how much they later on ate. All these behaviour observations suggest by inactivating the dHC, rats don’t form a memory of a preceding meal, hence ate the next meal as if they hadn’t eaten not long ago.
In order for the dHC to be involved in meal onset, the neurons will have to be activated at the time (and shortly after) the rats started eating to code for this memory. This is what the paper next looked at. In the experimental group, the authors fasted the rats, then gave them a sucrose meal before sacrificing them to probe for Arc mRNA, an immediate early gene that points to neuronal activation. The control group were also fasted but did not receive the last meal. They found that an eating episode significantly increased the percentage of CA1 neurons that expressed Arc in the experimental group compared to their caged controls, suggesting that food consumption may induce synaptic plasticity in dHC neurons.
In all, this study suggests that dHC neuronal activity is involved in inhibiting meal onset. Granted, it’s a very preliminary study, but the results are fairly interesting. Some more controls are certainly needed. Is Arc activation coding for meal onset or the general context of feeding? Will it activate if control rats received a last meal of water instead of not getting anything? What happens if rats receive an injection of sucrose instead of voluntary eating? Can inhibiting dHC activation change an animal’s eating behaviour in the long run (60 minutes is a very short time)? How does the dHC-hypothalamus circuitry interact with other circuitries involved in feeding behaviour?
We’re a long way from the authors’ last conclusion that “impaired HC functioning may contribute to snacking and the development of obesity”, but it’s a cool field.
J Neurosci. 2007 Jun 13;27(24):6436-41.
Medial prefrontal cortex is necessary for an appetitive contextual conditioned stimulus to promote eating in sated rats.
Hippocampal Lesions Impair Retention of Discriminative Responding Based on Energy State Cues.