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

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Neurological Basis of Behavior (PSY - 610)
VU
Lesson39
Brain and Motivational States
Objectives:
To familiarize the students with the
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Brain and motivational states
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Homeostasis, include temperature regulation, Cellular and brain controls of Thirst, Reward
systems and addictions, Fear, aggression, attachment
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Hunger, Body weight set point (Theories), Obesity, Anorexia Nervosa, thirst, bio-rhythms,
Sleep and awakening.
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Pathology related to sleep cycles
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Sleep disorders and treatment
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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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Neurological Basis of Behavior (PSY - 610)
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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
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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.
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More recently role of gut peptides have also emerged as important, in the initiation and controlling
feeding.
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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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Table of Contents:
  1. INTRODUCTION:Descriptive, Experimental and/ or Natural Studies
  2. BRIEF HISTORICAL REVIEW:Roots of Behavioural Neurosciences
  3. SUB-SPECIALIZATIONS WITHIN THE BEHAVIORAL NEUROSCIENCES
  4. RESEARCH IN BEHAVIOURAL NEUROSCIENCES:Animal Subjects, Experimental Method
  5. EVOLUTIONARY AND GENETIC BASIS OF BEHAVIOUR:Species specific
  6. EVOLUTIONARY AND GENETIC BASIS OF BEHAVIOUR:Decent With Modification
  7. EVOLUTIONARY AND GENETIC BASIS OF BEHAVIOUR:Stereoscopic vision
  8. GENES AND EXPERIENCE:Fixed Pattern, Proteins, Genotype, Phenotypic
  9. GENES AND EXPERIENCE:Mendelian Genetics, DNA, Sex Influenced Traits
  10. GENES AND EXPERIENCE:Genetic Basis of behavior, In breeding
  11. GENES AND EXPERIENCE:Hybrid vigor, Chromosomal Abnormalities
  12. GENES AND EXPERIENCE:Behavioral Characteristics, Alcoholism
  13. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION
  14. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION:Activating brain
  15. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION:Macro electrodes
  16. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION:Water Mazes.
  17. DEVELOPMENT OF THE NERVOUS SYSTEM:Operation Head Start
  18. DEVELOPMENT OF THE NERVOUS SYSTEM:Teratology studies, Aristotle
  19. DEVELOPMENT OF THE NERVOUS SYSTEM:Stages of development, Neurulation
  20. DEVELOPMENT OF THE NERVOUS SYSTEM:Cell competition, Synaptic Rearrangement
  21. DEVELOPMENT OF THE NERVOUS SYSTEM:The issues still remain
  22. DEVELOPMENT OF THE NERVOUS SYSTEM:Post natal
  23. DEVELOPMENT OF THE NERVOUS SYSTEM:Oxygen level
  24. Basic Neuroanatomy:Brain and spinal cord, Glial cells, Oligodendrocytes
  25. Basic Neuroanatomy:Neuron Structure, Cell Soma, Cytoplasm, Nucleolus
  26. Basic Neuroanatomy:Control of molecules, Electrical charges, Proximal-distal
  27. Basic Neuroanatomy:Telencephalon, Mesencephalon. Myelencephalon
  28. Basic Neuroanatomy:Tegmentum, Substantia Nigra, MID BRAIN areas
  29. Basic Neuroanatomy:Diencephalon, Hypothalmus, Telencephalon, Frontal Lobe
  30. Basic Neurochemistry:Neurochemicals, Neuromodulator, Synaptic cleft
  31. Basic Neurochemistry:Changes in ionic gates, The direct method, Methods of Locating NT
  32. Basic Neurochemistry:Major Neurotransmitters, Mesolimbic, Metabolic degradation
  33. Basic Neurochemistry:Norepinephrine/ Noradrenaline, NA synthesis, Noadrenergic Pathways
  34. Basic Neurochemistry:NA and Feeding, NE and self stimulation: ICS
  35. Basic Neurochemistry:5HT and Behaviors, Serotonin and sleep, Other behaviours
  36. Basic Neurochemistry:ACH and Behaviors, Arousal, Drinking, Sham rage and attack
  37. Brain and Motivational States:Homeostasis, Temperature Regulation, Ectotherms
  38. Brain and Motivational States:Biological Rhythms, Circadian rhythms, Hunger/Feeding
  39. Brain and Motivational States:Gastric factors, Lipostatic theory, Neural Control of feeding
  40. Brain and Motivational States:Resting metabolic state, Individual differences
  41. Brain and Motivational States:Sleep and Dreams, Characteristics of sleep
  42. Higher Order Brain functions:Brain correlates, Language, Speech Comprehension
  43. Higher Order Brain functions:Aphasia and Dyslexia, Aphasias related to speech
  44. Higher Order Brain Functions:Principle of Mass Action, Long-term memory
  45. Higher Order Brain Functions:Brain correlates, Handedness, Frontal lobe