Abstract
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. In the present study, we tested the hypothesis that dorsal (dHC) and ventral hippocampal (vHC) glutamatergic pyramidal neurons play a critical role in the inhibition of energy intake during the postprandial period by optogenetically inhibiting these neurons at specific times relative to a meal. Male Sprague-Dawley rats were given viral vectors containing CaMKIIα-eArchT3.0-eYFP or CaMKIIα-GFP and fiber optic probes into dHC of one hemisphere and vHC of the other. Compared to intake on a day in which illumination was not given, inhibition of dHC or vHC glutamatergic neurons after the end of a chow, sucrose, or saccharin meal accelerated the onset of the next meal and increased the amount consumed during that next meal when the neurons were no longer inhibited. Inhibition given during a meal did not affect the amount consumed during that meal or the next one but did hasten meal initiation. These data show that dHC and vHC glutamatergic neuronal activity during the postprandial period is critical for limiting subsequent ingestion and suggest that these neurons inhibit future intake by consolidating the memory of the preceding meal.
Significance statement Memory of a recently eaten meal provides a lasting record of recent intake and limits subsequent ingestion; however, the neural mechanisms underlying these mnemonic effects remain unknown. Here, we show that optogenetic inhibition of dorsal or ventral hippocampal pyramidal neurons induced after the end of a sucrose, chow or saccharin meal, when the memory of the meal would be undergoing consolidation, accelerated the initiation of the next meal and, importantly, increased the amount consumed during that next meal when the neurons were no longer inhibited. These findings show that principal hippocampal neurons limit future intake and suggest that they do so by consolidating the memory of the preceding meal.
Footnotes
Conflicts of interest: The authors declare no competing financial interests.
Funding: National Institutes of Health, DK114700; National Institutes of Health, MH104384; National Science Foundation (NSF), IOS1121886; Georgia State University (GSU), 100008545.
This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
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