during a 30 min test, compared with four
when saline was injected (Parrott et al.,
1986).
Even if it were thought sensible to use
such substances to enhance food intake
under commercial conditions, there are
two limitations: firstly, how are they to be
administered into the brain? Secondly, is it
likely that licences will be granted for their
use in animals whose products are to be
consumed by humans? It is not likely that
central nervous active substances will be
used commercially to enhance voluntary
intake for these reasons and also because, if
the animals are already well fed and
managed so that the rate of production of
meat, milk or eggs is already optimal, then
to stimulate intake would only lead to
more deposition of fat, which is not
required in modern animal production.
While the hypothalamus and sur-
rounding parts of the forebrain are likely
to be the seat of intake control, there are
centres in the hindbrain, such as the
nucleus of the solitary tract, which receive
information from receptors in the visceral
organs such as the stomach and liver. Also
in this area are neurons directly sensitive
to shortage (but not to excess) of energy-
yielding substrates. It is likely, also, that
the hypothalamus itself can sense energy
availability, and it originally was thought
that the sensor for glucose in Mayer’s
‘glucostatic’ hypothesis of intake control
was the ventromedial hypothalamus.
However, it is a vital task of the rest of the
body to protect the CNS from harmful
fluctuations in its environment, including
its nutrient supply, and it is unlikely that
under- or oversupply of nutrients from the
ingestion of food would remain unsensed
by the rest of the body until the CNS itself
was faced with it. As we will see below,
there are numerous mechanisms whereby
the brain is forewarned of events that
might lead to nutrient imbalance in order
that the CNS can take action to prevent a
serious lack of nutrients that might
threaten its own proper functioning.Learning
As stated above, animals developed the
ability to learn to associate the sensory
properties of a food with the metabolic
consequences of eating that food at a very
early stage in evolution; indeed it might be
said that such capability accompanied the
origin of the chemical and visual senses.
We will see later how such learned associa-
tions are used in diet selection.Physiological and Metabolic Aspects 3216050403020100Reinforcements 30 min^10 25 50 100
Dose of NPY (μg)*
**
Fig. 15.2.Increase in number of times pigs press a button for a food reward in 30 min when injected
intracerebroventricularly with increasing doses of neuropeptide Y (NPY) (Parrott et al., 1986).