Transcript Lecture 35 (Motivation)

BIO 132
Neurophysiology
Lecture 35
Motivation
Lecture Goals:


Understanding the underlying mechanisms
affecting rudimentary motivations (hunger,
thirst, warmth, etc).
Appreciating the common elements behind the
feedback loops controlling hunger, thirst, and
temperature regulation.
Motivation

Motivation – the driving force behind behavior
Get food
Sit in class
Urinate
Listen to music
Sit in class
Current Goal
Behavior
Motivations


The brain area(s) responsible for keeping track
and deciding on what the current behavior
should be is still unknown.
Many motivations arise from internal
homeostatic feedback loops.
Hunger


Hunger: the motivation to eat
Hunger is affected by more than one homeostatic
feedback loop.



Maintenance of blood glucose levels (short-term feeding
behavior)
Maintenance of fat stores (long-term feeding behavior)
Hunger can also be affected by things other than homeostatic
feedback loops such as mood (bored, sad, happy, anxious,
etc).
Long-term Feeding Behavior



Goal of long-term feeding behavior: Maintain
long-term energy stores (fat).
Fat has twice the energy (per weight) as glucose
and doesn’t require excess water storage like
glucose (fat isn’t osmotically active).
The body has a set-point for the amount of fat
it would like stored on the body.
Maintenance of Fat Stores
Experimentally, rats were given food to eat whenever
they wanted (ad libitum), but at two time periods of the
experiment were deprived of food and forced fed.
fasted
force-fed
Body weight (g)

set-point
Time (days)
Energy Balance

Caloric intake = caloric expenditure
Normal weight

Caloric intake > caloric expenditure
Gain weight

Caloric intake < caloric expenditure
Lose weight
Lipostatic Hypothesis


First proposed in 1953, the lipostatic
hypothesis states that the brain monitors fat
levels and maintains them at some fixed setpoint amount.
The lipostatic hypothesis requires that the fat
communicate with the brain in some way.

First suspected was some blood-borne chemincal (a
hormone).
Hormone from Fat

Evidence of a hormone from the fat (1960s):

Parabiosis (the fusing of two animals so that they
share the same blood) of a genetically obese mouse
to a normal mouse caused the obese mouse to
become thin (normal weight).
Obese
Normal
Surgically fused
(share blood)
Hormone from Fat



It was apparent that the blood carried some
signal to the brain from the fat that allowed the
brain to monitor the levels of fat.
The hormone went undiscovered until 1994.
The gene that made genetically obese mice
(ob/ob) was finally isolated and its product
synethesized.

The product of the gene was named leptin
Hormone from Fat - Leptin

Once isolated an synthesized, leptin could be
injected into obese mice (ob/ob) that cannone
make leptin themselves, and the mice would
become thin (normal weight).
Obese
(ob/ob)
Normal
How Does Leptin Work?



It was known since the 1940s that destruction of the
hypothalamus led to abnormal food intake.
Leptin was theorized to have its effect on the
hypothalamus.
It is now known that leptin binds to αMSH and CART
receptors in the arcuate nucleus of the hypthalamus.


αMSH stands for alpha-melanocyte-stimulating hormone.
CART stands for cocaine-and amphetamine-regulated
transcript.
* You do not need to memorize these names, just the abbreviations.
Effects of Leptin on the Arcuate Nucleus


Once leptin binds to receptors in the arcuate nucleus,
activated neurons project to the periventricular and the
lateral zones.
The periventricular zone activates both the sympathetic
NS and neurons projecting to the pituitary gland.


Activated SNS causes in increase in metabolism (burning
calories).
Hypothalamic neurons projecting to the pituitary release
thyroid releasing hormone (TRH) which causes the release of
thyroid stimulating hormone (TSH) from secretory cells in
the anterior pituitary, causing the release of thyroid hormone
from the thyroid gland, increasing metabolism.
Effects of Leptin on the Arcuate Nucleus


Other hypothalamic neurons projecting to the pituitary
release corticotropin releasing hormone (CRH) which causes
the release of adrenocorticotropic hormone (ACTH) from
secretory cells of the pituitary, causing the release of cortisol
from the adrenal gland which increases metabolism.
The lateral zone activates neurons that decrease the
motivation to eat by decreasing hunger and increasing
the feeling of satiety. This decreases caloric intake.
Effects of Leptin
nutrients
Lateral zone
Satiety
Fat
ventrical
inhibit
Periventricular
zone
Hunger
leptin
Feeding behavior
Pituitary
αMSH
CART
TRH
CRH
Arcuate nucleus
TSH
ACTH
Caloric intake
SNS
thyroid hormone
Metabolic rate
cortisol