Brain and Motivational States:Gastric factors, Lipostatic theory, Neural Control of feeding

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Neurological Basis of Behavior (PSY - 610)

Lesson39

Brain and Motivational States

Objectives:

To familiarize the students with the

Brain and motivational states

Homeostasis, include temperature regulation, Cellular and brain controls of Thirst, Reward

systems and addictions, Fear, aggression, attachment

Hunger, Body weight set point (Theories), Obesity, Anorexia Nervosa, thirst, bio-rhythms,

Sleep and awakening.

Pathology related to sleep cycles

Sleep disorders and treatment

Neurophysiology and biorhythms, Sleep and awakening cycles, Dreams, Sleep disorders

Factors that control Food Intake behaviors (continued)

In the last lesson we have discussed the contribution of the oral factors, (palatability etc) and the smell

and sight of food, cognitive and learning influences on what we eat and how we eat. Now we will find

out if the gastric factors (stomach, the alimentary canal, the digestive system), contribute to feeding

behaviors.

Gastric factors:

The gastrointestinal tract is important in digestion and breaking down of food into nutrients needed by

the body. The stomach seems important intuitively because we eat when the stomach is empty and stop

eating only when there is feeling of fullness in stomach. But this is not true!

Let's find out through the evidence from experiments carried out to isolate the stomach factors.

If the feeling of fullness comes from the stomach as a signal to stop eating, what if we preload the

stomach in some way, and the stomach is distended or expanded (remember that the stomach has the

capacity to flex and contract)? The first experiment of balloon preloading of the stomach was carried out

by Cannon and Washburn (1912 cf Pinel 2002), Cannon was the experimenter and Washburn the

subject, he had to swallow the balloon) and reported whenever hunger pangs felt. As he reported the

pangs Cannon measured electrical activity of stomach contractions through a mechanism placed

beforehand. The hunger pangs were found to be correlated to stomach contractions, leading to the view

that stomach was important in hunger control. When there is preloading of the stomach with water or

some other substance, there is decrease in food intake

But this theory was not supported by the following:

1. The stomach is almost always full; it is never completely empty except in long fasting or starvation.

2. When we are full and have eaten enough, if required or asked to eat even on a full stomach we can

add some more good food (think of the Pakistani hospitality!)

3. In human patients when the denervation or removal of stomach takes place and the esophagus is

connected directly to the duodenum they still report pangs of hunger and feelings of being full, and

continued to eat to maintain their body weight, although their meals were smaller. This is similarly true

of animals as well.

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However, Koopmans ( in 1981) carried out an experiment on animals where he attached another

stomach and connected the blood vessels through the additional stomach. In this procedure, the food

was passed from the additional stomach to the real stomach (measured), but blood vessels only passed

through the new stomach--- interestingly the animals stopped eating in response to some signal from the

blood. It appears that there must be some chemicals not found in the food, but which stimulated signals

for stopping of eating.

Keeping this evidence and the fact that one stops eating even before the process of digestion and

absorption of food starts taking place (as this requires time), there appears to be some role for gastric

cues. Feeding ends even before the nutrient-deficiency signals are terminated, therefore there has to be

another signal to terminate feeding, coming from the gastric region.

Smith, Gibbs and Young in their studies (from 1973-1976 onwards) suggest that there may be peptides

(short amino acid chains) i.e. hormones or neurotransmitters which signal the satiety signal. The

ingested food may be triggering the release of hormones into the bloodstream. One of these gut peptides

cholecystokinin (CCK) when injected led to rats eating smaller meals- or inhibit feeding without

causing any illness or pain. Administration of this peptide directly into the brain is not as effective as

injection into the blood stream. However, later studies by Mineka and Snowdon (1978) have shown that

this effect does not last very long--therefore there are other controlling factors for food intake.

Thus we have found out that the oral and gastric are important in feeding but not enough, therefore we

now look at the metabolic, energy and neural controls to see if those are important in the initiation and

termination of feeding signals.

Metabolic Factors:

If Glucose level in the blood decreases it leads to initiation of eating, increases in blood glucose would

lead to cessation of eating. More recently Campfield and Smith (1990) have shown that rats with free

access to food and water were monitored for blood glucose through a catheter. These rats had constant

level of blood glucose at about 2%, but just before eating, the blood glucose levels dropped to about 8%,

indicating that blood glucose levels may be a signal for food intake. This takes us to the now classic

assumption of set points in the body of glucose and of lipids. The set point means that there is an energy

set point which determines how much is eaten and when. This has three basic components: the set point

mechanism (assumption is that these are neuronal receptors), the detector mechanisms (which detect

differences from the set point), and the effector mechanisms which are to bring about a change so that

the set point level is met. Thus, there is a set point for glucose levels, a set point for fat levels, a set point

for weight etc. We will discuss the theories which propose the first two.

Glucostatic Theory proposed by Mayer

This theory suggests that feeding regulatory system is actually keeping the glucose set point in the blood

at a constant level. There are glucostatic set point monitors. Gluco-receptors in the hypothalamus

constantly gauge the level of glucose in the blood. This is a short term mechanism for initiation and

cessation of feeding.

If the glucose levels in the blood fall then the glucose from pancreas is released in blood stream leads to

an increase in eating, glucogen injection lead to decreased eating and reduced stomach contractions.

Further, Insulin injections lead to marked hypoglycemia (reduced glucose levels in the blood).This lead

to increased eating as insulin increases the entrance of blood glucose into the cells. In an experiment,

this injection was followed by

a) Glucose injection

b) Fructose or mannose (types of sugars: fructose cannot cross blood brain barrier but can be utilized by

the liver, mannose can be used by both brain and liver) or ketone bodies (fuel used by the brain not the

liver). All animals given some nutrient after the insulin injections showed a drop in feeding, indicating

that it is not the brain signals but some controls of the periphery which monitor feeding.

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Lipostatic theory:

Lipostatic theory states that there is a body set point for lipids and any deviation decrease in the body

stores of fats would lead to initiation of feeding. This is long term mechanism body weight maintenance

(Remember in cases of starvation, stored body fats are broken down for providing glucose).

The difficulties with the set point theories are:

a) That these are not consistent with the evolutionary perspective--- when man didn't know if he would

be able to eat next--(if hunt successful only then food would be available right?), how is possible to

have a set point sending out signals to regulate food.

b) Hunger and feeding are not just following glucose patterns, people around the world have culturally

varied food patterns. How can this be explained in glucostatic or lipostatic theory.

Neural Control of feeding:

Research into the neural controls of hunger has been ongoing since the 1940's. There are two brain

areas the Ventromedial Hypothalamus (VMH) and the Lateral Hypothalamus (LH) which have become

more important from the 1940's- 1980's

Hypothalamus is important in eating and drinking. We know hypothalamus is important in motivational

and survival behaviors. If there would be no hypothalamus there would be no feeding, and no drinking

controls. There is specialization within hypothalamus where each region works in coordination with the

bodily needs, and other regions

Ventromedial hypothalamic damaged rats become obese rats. This was first demonstrated by

Anand and Brobeck in 1943! VMH lesions to hyperphagia (overeating), and LH lesions lead to

aphagia (no eating).These have been shown to be the same effect in rats, dogs and monkey--also

humans. The following are the similarities in VMH rats and human.

1. Food Nutritive Content Challenge: If the nutritive content in food is decreased then the normal

would increase food intake to compensate but VMH are finicky eaters. The VMH cannot respond to

these challenges

2. Palatability is important for VMH rats and humans. If we increase the palatability, it leads to

increased eating in VMH animals and human, whereas normals stop eating in response to body's signals

(The VMH become obese as a consequence)

3. Work for food: if effort is involved to work for food, the VMH damaged rats and fat humans would

do minimal work for food. In an experiment, normals and VMH animals and fat humans were given

peeled and unpeeled almonds. Fat humans and the VMH rats ate more unpeeled whereas the normals ate

about 50% of the peeled and unpeeled almonds.

There is a hypothesis that VMH may be the satiety control this areas controls the signals for stopping of

feeding- which is why if VMH is damaged the inhibition is gone, and the animals continue eating!

LH damaged animals are starving rats. These animals are aphagic (do not eat), adipsic (do not drink

water) if they are not tube fed they die. Recovery is slow and takes place in phases. These animals can

recover eating but not drinking. Eventually they start drinking condensed milk but no water. Their

recovery reaches almost normal levels of eating, but these animals cannot respond to challenges. The

LH animals also cannot eat to compensate for initial weight loss. These animals cannot fully recover

their normal weight. It is said that the LH is the center for initiation of eating which is why lesions lead

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to the starvation like state (no LH no signals to eat). However it is difficult to interpret as many NTs

passing through it, NE DA may also be involved.

It is Possible that this damage causes motivational deficit/inertia that animals don't want to eat or drink.

This is supported by the fact that there is no spontaneous activity of these animals. Further there is

sensory neglect (lack of response to visual. Tactile and other stimulus.

Other factors such as Neurotransmitters and hormones have also been found to be important:

The role of Norepinephrine has been highlighted by studies by Liebowitz and her colleagues

especially in the area of LH as stimulation of NE rich neurons leads to initiation of eating.

More recently role of gut peptides have also emerged as important, in the initiation and controlling

feeding.

We have already studied that there is a large amount of serotonin in the gut. There appears to be role

for the chemical in the signals for feeding.

References:

1. Carlson N.R. (2005) Foundations of Physiological Psychology Allyn and Bacon, Boston

2. Pinel, John P.J. (2003) Biopsychology (5th edition) Allyn and Bacon Singapore

3. Bloom F, Nelson and Lazerson (2001), Behavioral Neuroscience: Brain, Mind and Behaviors (3rd

edition) Worth Publishers New York

4. Bridgeman, B (1988) The Biology of Behaviour and Mind. John Wiley and Sons New York

5. Brown,T.S. and Wallace.(1980) P.M Physiological Psychology

Academic Press New York

6. Mogensen, G.J (1977) The Neurobiology of Behavior. LawrenceErlbaum Associates

Note: References 5, 6 more closely followed in addition to the references cited in text.

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