BRAIN MECHANISMS

OF HUNGER

DEVIKA RAJAN
1 ST MSC. PSYCHOLOGY
 INTRODUCTION

 Hunger depends on :
-the contents of our stomach & intestine
- availability of glucose to the cells
- body’s fat supplies
- health
- body temperature.
• Appetite depends on more than your need for food.
 ARCUATE NULEUS

 Arcuate nucleus is a collection of neurons in the

hypothalamus of the brain. It contain a substance called
neuropeptide Y ( NPY ) and influence hunger.

hunger motive satiety motive

starvation (damage) excessive eating

 The hunger-sensitive cells receive
excitatory input from the taste
pathway and from axons releasing
the neurotransmitter ghrelin
(GRELL-in).
 GHRELIN

 This odd-looking word takes its name from the fact that it
binds to the same receptors as growth-hormone releasing
hormone (GHRH).
 The stomach releases ghrelin during a period of food
deprivation, where it triggers stomach contractions.
 Ghrelin also acts on the hypothalamus to increase appetite.
 People who produce greater than average amounts of
ghrelin respond more strongly than average to the sight of
food, and they are almost twice as likely as other people to
become obese (Karra et al., 2013).
 Signals of both short-term and long-term satiety provide input to the
satiety-sensitive cells of the arcuate nucleus.
 Distension of the intestines triggers neurons to release the
neurotransmitter CCK, a short-term signal (Fan et al.,2004).
 Blood glucose (a short-term signal) stimulates satiety cells in the
arcuate nucleus (Parton et al., 2007) and leads to increased secretion
of insulin, which also stimulates the satiety cells.
 Body fat (a long-term signal) releases leptin, which stimulates the
satiety neurons and inhibits the hunger neurons (Diéguez, Vazquez,
Romero, López, & Nogueiras, 2011).
 PARAVENTRICULAR NUCLEUS

 Much of the output from the arcuate nucleus goes to the

paraventricular nucleus of the hypothalamus.
 The paraventricular nucleus (PVN) inhibits the lateral
hypothalamus, an area important for eating.
 The inhibitory transmitters here are a combination of GABA
, neuropeptide Y (NPY), and agouti-related peptide
(AgRP). Inhibiting an inhibitor produces net excitation,
and that is how the stimuli for hunger increase eating and
arousal.
 If the inhibition of the paraventricular nucleus is strong
enough, rats eat huge meals.
 Axons from the satiety-sensitive cells of the arcuate
nucleus deliver an excitatory message to the
paraventricular nucleus, releasing melanocortins.
 MELANOCORTIN

 Melanocortin receptors in the paraventricular nucleus are

important for limiting food intake, and anything that
damages these receptors leads to overeating.
 Researchers have attempted to find a safe drug that would
stimulate melanocortin receptors as a weight-reduction
treatment. So far, no acceptable treatment has emerged.
 The amygdala and related areas send two kinds of input to
the lateral hypothalamus.
 One path inhibits eating during illness and mediates
aversion to foods previously associated with illness.
 The other path stimulates eating in response to highly tasty
foods.
 An additional pathway from the paraventricular nucleus leads to
cells in the lateral hypothalamus that release orexin.
 In addition to its role in wakefulness, orexin has two roles in
feeding.
 First, it increases animals’ persistence in seeking food.
 Second, orexin responds to incentives in general.
If orexin receptors are blocked, an animal becomes less active
and less likely to work for reinforcement of any kind. Stimulation
of orexin receptors increases activity and motivation.
 Hypothalamic transmitters of feeding
Hunger signals increase feeding by inhibiting
inhibitory messages to the lateral hypothalamus.
 OTHER CHEMICALS

 One consequence of control by so many chemicals is that the control of

feeding can go wrong in many ways.
 However, when an error occurs in one way, the brain has many other
mechanisms to compensate for it.
 A closely related point is that researchers could develop drugs to
control appetite by working on many routes— leptin, insulin, NPY, and
so forth—but changing any one circuit might be ineffective because of
compensations by the others.
 REFERENCE

J.W. Kalat (1995) Biological Psychology, 5 th Ed. USA

Brooks/code Pub. Co. p (313- 314).
 The lateral hypothalamus

 Output from the paraventricular nucleus acts on the

lateral hypothalamus.
 It indicates somany neuron clusters and passing
axons that it has been compared to a crowded train
station.
 It controls insulin secretion, alters taste
responsiveness and facilitates feeding in other ways.
 The animal with damage in this area refuses Food
and water intake, averting his head as if the food
were distasteful.
 The animal may starve to death unless it force fed,
but if kept alive, it gradually recovers much of its
ability to eat.
 Stimulation of this area increases the drive to eat.
 Many axons containing dopamine pass through the
central hypothalamus, so damage to the lateral
hypothalamus interrupts these fibers.
 To separate the roles of hypothelamic cells from
those of passing fibers experimenters used chemicals
that damages only the cell bodies, or induced lesion
in very young rats, before the dopamine axons
reached the lateral hypothalamus.
 In both cases, damaging the cell bodies without
damaging the passinv dopamine axons produced a
loss of feeding without loss of arousal and activity
Hunger pathways from lateral
hypothalamus
The lateral hypothalamus contributes to feeding in several
ways
 Axons from the lateral hypothalamus to the NTS (nucleus
of the tractus solitarius), part of the taste Pathway, alter
the taste sensation and the salivation Response to the
tastes. When the lateral hypothalamus detects hunger, it
sends messages that make the food Taste better.
 Axons from the lateral hypothalamus extend into several
Parts of the cerebral cortex, facilitating ingestion and
Swallowing and causing cortical cells to increase their
Response to the taste, smell, or sight of food
 The lateral hypothalamus increases the pituitary
gland’s Secretion of hormones that increase insulin
secretion.
 The lateral hypothalamus sends axons to the spinal
cord, controlling autonomic responses such as
digestive Secretions. An animal with damage to the
lateral hypothalamus has trouble digesting foods
 REFERENCE

J. W., kalaT (2015). Biological psychology 12tH Edition

(pageno: 315-316)