Data from: Sequential appetite suppression by oral and visceral feedback to the brainstem

The termination of a meal is controlled by dedicated neural circuits in
the caudal brainstem. A key challenge is
to understand how these circuits transform the sensory
signals generated during feeding into dynamic control of behaviour. The
caudal nucleus of the solitary tract (cNTS) is the first site in the brain
where many meal-related signals are sensed and integrated, but how the
cNTS processes ingestive feedback during behaviour is unknown. Here, we
describe how prolactin-releasing hormone (PRLH) and GCG neurons, two
principal cNTS cell types that promote non-aversive satiety, are regulated
during ingestion. PRLH neurons showed sustained activation by visceral
feedback when nutrients were infused into the stomach, but these sustained
responses were substantially reduced during oral consumption. Instead,
PRLH neurons shifted to a phasic activity pattern that was time-locked to
ingestion and linked to the taste of food. Optogenetic manipulations
revealed that PRLH neurons control the duration of
seconds-timescale feeding bursts, revealing a mechanism by which
orosensory signals feed back to restrain the pace of ingestion.
By contrast, GCG neurons were activated by mechanical feedback from the
gut, tracked the amount of food consumed and promoted satiety that lasted
for tens of minutes. These findings reveal that sequential negative
feedback signals from the mouth and gut engage distinct circuits in the
caudal brainstem, which in turn control elements of feeding behaviour
operating on short and long timescales.