Food Addiction: The BALANCE OF EXCITATION AND INHIBITION
Food Addiction: The BALANCE OF EXCITATION AND INHIBITION
Normal neural function involves a delicate balance between different
centers and levels of function, mediated by a balance of inhibition and excitation.
The normal brain is never either silent or in uncontrollable seizure
activity. It remains in a dynamic equilibrium of controlled activity, with
trillions of nerve impulses coursing through the brain every second. What
keeps the brain from slipping into chaos, into massive seizures? The answer
is inhibition, working within the high degree of structure of the nervous system.
A carefully orchestrated interplay of inhibition and excitation keeps
the system active and responsive, but not overactive. The powerful role of
inhibition is revealed by the devastating convulsions produced by the drug,
strychnine, which you will remember blocks inhibitory processes.
Think of two "centers" (brain areas with specific functions), such that
center A inhibits center B. What will happen if A IS damaged or destroyed?
There will be less inhibition on B, so B will show increased activity. This is
called a release from inhibition, or disinhibition. Release phenomena are
seen clinically in the increased intensity or frequency of some behavior after
damage to some parts of the brain (Teitelbaum, 1997).
A particularly clear example of release is the Babinski sign, a reflex normally
shown only by infants. When the bottom of the foot is irritated, the
toes fan out. This reflex disappears early in life. The circuits
that mediate it remain intact, however, inhibited by higher centers. Severe
damage to higher motor centers releases this reflex; this is one of the cardinal
signs of damage to the higher parts of the motor system.
PARKINSON'S DISEASE AND HUNTINGTON'S
CHOREA: A BALANCE IN NEUROTRANSMITTERS
The balance of excitation and inhibition is ultimately mediated by control of
neurotransmitters. This is well-illustrated by two disorders of movement: Parkinson's disease and Huntington's chorea. Parkinson's disease is characterized by tremor of the hands, rigidity, and slow movement. It afflicts, in some degree, about 1% percent of the people over fifty in the United States. It is caused by degeneration of specific neurons, which causes a depletion of the neurotransmitter, dopamine, in certain structures in the brain. The symptoms can be effectively relieved (though the disease is not so cured) by administration of the drug l-DOPA, which is converted to dopamine in the brain. Huntington's chorea is an inherited disease,
whose principal symptoms are involuntary movements: either rapid, forcible, and jerky, or smooth and sinuous.
These disorders are often associated with dementia (loss of intellectual abilities). Chorea results from degeneration of a different group of neurons than in Parkinson's disease, with the result that there is increased sensitivity to dopamine in the some cells that show depleted dopamine in Parkinson's disease. In other words, the normal balance of activity in this part of the brain is pushed in opposite directions by the two diseases. Given this opposition, it makes sense that when Parkinson's patients are given too much I-DOPA, that is, if the neurotransmitter depletion is converted into an excess, the symptoms of Huntington's chorea appear (Adams and Victor, 1991; Cote, 1991).
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http://theliberatormethod.com
Normal neural function involves a delicate balance between different
centers and levels of function, mediated by a balance of inhibition and excitation.
The normal brain is never either silent or in uncontrollable seizure
activity. It remains in a dynamic equilibrium of controlled activity, with
trillions of nerve impulses coursing through the brain every second. What
keeps the brain from slipping into chaos, into massive seizures? The answer
is inhibition, working within the high degree of structure of the nervous system.
A carefully orchestrated interplay of inhibition and excitation keeps
the system active and responsive, but not overactive. The powerful role of
inhibition is revealed by the devastating convulsions produced by the drug,
strychnine, which you will remember blocks inhibitory processes.
Think of two "centers" (brain areas with specific functions), such that
center A inhibits center B. What will happen if A IS damaged or destroyed?
There will be less inhibition on B, so B will show increased activity. This is
called a release from inhibition, or disinhibition. Release phenomena are
seen clinically in the increased intensity or frequency of some behavior after
damage to some parts of the brain (Teitelbaum, 1997).
A particularly clear example of release is the Babinski sign, a reflex normally
shown only by infants. When the bottom of the foot is irritated, the
toes fan out. This reflex disappears early in life. The circuits
that mediate it remain intact, however, inhibited by higher centers. Severe
damage to higher motor centers releases this reflex; this is one of the cardinal
signs of damage to the higher parts of the motor system.
PARKINSON'S DISEASE AND HUNTINGTON'S
CHOREA: A BALANCE IN NEUROTRANSMITTERS
The balance of excitation and inhibition is ultimately mediated by control of
neurotransmitters. This is well-illustrated by two disorders of movement: Parkinson's disease and Huntington's chorea. Parkinson's disease is characterized by tremor of the hands, rigidity, and slow movement. It afflicts, in some degree, about 1% percent of the people over fifty in the United States. It is caused by degeneration of specific neurons, which causes a depletion of the neurotransmitter, dopamine, in certain structures in the brain. The symptoms can be effectively relieved (though the disease is not so cured) by administration of the drug l-DOPA, which is converted to dopamine in the brain. Huntington's chorea is an inherited disease,
whose principal symptoms are involuntary movements: either rapid, forcible, and jerky, or smooth and sinuous.
These disorders are often associated with dementia (loss of intellectual abilities). Chorea results from degeneration of a different group of neurons than in Parkinson's disease, with the result that there is increased sensitivity to dopamine in the some cells that show depleted dopamine in Parkinson's disease. In other words, the normal balance of activity in this part of the brain is pushed in opposite directions by the two diseases. Given this opposition, it makes sense that when Parkinson's patients are given too much I-DOPA, that is, if the neurotransmitter depletion is converted into an excess, the symptoms of Huntington's chorea appear (Adams and Victor, 1991; Cote, 1991).
For the Food Addiction Treatment I recommend click this link:
http://theliberatormethod.com