Sunday, February 11, 2007

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Dictionary of Biology Boeck

The new Webster's 2007 Dictionary of Biology

Cambridge

Lexicon EncycloBio site of Science City

site Doctissimo

site state depressif.com

Encyclopaedia Universalis

site CHU Rouen

The site

CNRS

articles of A.. Poacher ( specialist child psychiatrist adolescence)

The brain atlas ed. World

site lecerveaumcgill.ca

The magazine Psycho & Brain

and other books websites and to a lesser extent.

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Guide Glossary Bibliography

A
Amino
a component of protein food.

ACTH (adrenocorticotropic ) : hormone secreted by the pituitary influencing the secretion cortisol.

Adrenaline: A hormone secreted by the adrenal medulla very important in the functioning of the nervous system and the body's response to various attacks (stress).

Amygdala: situated half in the right hemisphere and half in the left is the control center of emotions. If it is destroyed, it deletes any violence, fear, but also any emotional reaction; if it stimulates, the behavior becomes excessive, extremely violent or extremely affectionate sweetness.

Antidepressant: A drug that opposes the depression.

Anxiety: state of mental disorder caused by the feeling of an impending adverse event or dangerous.

Anxiolytic : A drug that reduces anxiety.

Axis catecholaminergic : axis that stimulates the creation of catecholamines (especially norepinephrine).

HPA Axis : axis that stimulates the creation of cortisol by the adrenal cortex .

Axone : constant extension of the neuron cell body.

C
Catecholamines
: substance secreted by adrenal medulla, acting as a neurotransmitter.

Cingulum bundle of nerve fibers that allows communication between the various components of the limbic system .

corticotropin (TSH ) : hormone stimulated by hypoglycemia, trauma, emotions, and physical activity.

Cortisol : Main glucocorticoid hormone secreted by the adrenal cortex glands .

D
Dopamine: a neurotransmitter essential for normal brain activity, the precursor of norepinephrine.

dopaminergic name given to elements involved in the production of dopamine.

E
Enzyme:
Enzymes are proteins present in cells of all living beings. Their function is to facilitate the chemical reactions that occur there naturally. For example, during digestion, are enzymes that accelerate the decomposition and transformation of food

G
gland medulla and adrenal gland
: The adrenal glands are located above each kidney. They secrete hormones that help fight against stress.

Glucocorticoids : main substances secreted by cortex, acting as neurotransmitters.

H
Hormones:
chemical developed by a group of cells or an organ, which exerts a specific action on another tissue or another body.

pituitary gland or pituitary : small gland about the size of a pea in the brain, very important, it secretes growth hormone and other hormones like ' ACTH.

Hypothalamus : main regulatory body of pituitary hormones.

I
Influx nervous
: Series of events for the transmission of excitation in the nervous element.

M
monoamines
: amine which does that a radical. Family composed of catecholamine neurotransmitters and indoleamine (serotonin).

N
nerve: cord that connects a central nervous (eg brain) to an organ or an organic structure and consists of many axons. Pain on the path of a nerve.

Neuron: nerve cell that includes a cell body (with nucleus) and extensions whose axons.

Neurotransmitter or neurotransmitter: a chemical that transmits nerve impulses from one neuron to another across the space between two consecutive neurons (synapses) and by binding to receptors specific situated the postsynaptic neuron .

Norepinephrine: neurotransmitter family catecholamines, a precursor of adrenaline.

noradrenergic : name given to elements involved in the production of norepinephrine.

R
Recapture
: a phenomenon which is for neurons to recover presynaptic neurotransmitters released into the synapse.

S
Serotonin
name given to elements involved in the production of serotonin. serotonergic neurons .

Stress or general adaptation syndrome: report of a body in reacting to an agent of any assault (injury, injection, pain, joy, ...). Refers both to the action of the stressor and the reaction of the body.

Synapse : contact area of two neurons

T
Tryptophan
: amino acid precursor of serotonin.

Tyrosine: amino acid precursor of dopamine, norepinephrine.

V
vasopressin
: hormone secreted by the pituitary gland, which influences the secretion of ACTH .

Gall : body-shaped bag that serves as a reservoir (in this case, synaptic vesicles: tank neurotransmitters)

Z
Zone frontotemporal
: brain area between the forehead and temples.

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Depression in the news

TPE are finished for a long time, even the BAC is over. However, depressive disorders are still the leading cause of mortality and disability in developing countries and industrialized countries.
Reading an article about it made me want to continue to make news on the knowledge of this disease and how to avoid it. I will try to complete this section from time to time.


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Following experiments on mice, researchers have discovered the existence of a protein (VGF) produced in the brain from a gene sensitive to physical activity. This protein would have a direct and powerful antidepressant.
Some patients are unresponsive to conventional treatments such as therapy and antidepressants, it seems worthwhile to develop a new drug based on this protein. But it will take many years before finding such a drug and be put into circulation. Since a depressed person is usually slow on the psychomotor, it seems difficult to propose a physical activity.

By cons, This study shows that there is at least one way to avoid depression: having a regular physical activity.


(summary of article in Science & Vie July 2008).

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Depression in adolescents can be cured completely even if care is long but the only way to avoid it are adaptive strategies that are unconscious, and remove all the factors favorable to this depression remains a purely statistical way to avoid this disease.
There is no way to avoid a voluntary depression because we do not always distinguish the causes and effects of the disease or its point of departure neural or psychological.
We can prevent this disease with ongoing monitoring, which is impossible.
Depression can not be avoided or prevented, but perfectly cured.

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CONCLUSION IV. Drugs and therapies

As we saw earlier, depression has two main axes: one biological and one psychological.

Drugs only address the biological side of depression, which is why that a depression must, be completely healed, combine medication and psychotherapy.
- Versant psychological this side of the disease treated solely with psychotherapy performed by a child psychiatrist or psychiatrist or even a psychologist, that the target (s) involved and the circumstances of occurrence of depression and helps the adolescent to analyze his depression to better cure. Sometimes psychotherapy alone is enough, while the drugs alone may not suffice since , they only treat the symptoms and not causes.
- Versant biological : if one excludes the electro- convulsivothérapie or ECT (formerly ECT), there that one type of drugs that act directly on depression: what are the antidepressants.

Antidepressants have several types of actions on the body. The first antidepressants in 1959, called the WAMI (inhibitors monoamineoxydase ), which as the name implies, inhibit MAO or monoamine oxidase , the enzyme that breaks down neurotransmitters. These molecules, although effective, had many drawbacks: side effects, diet Mandatory Food, which have reduced their usage to almost nothing now. Shortly after the MAOI appeared the Tricyclics that act on serotonin and norepinephrine, these medicines still in use are highly effective but still have many side effects (weight gain, dry mouth ,...). Then came the IRS ( reuptake inhibitors of serotonin ) soon followed by SNRIs ( reuptake inhibitors of serotonin and norepinephrine), which has the advantage that 'they are as effective as the first antidepressant but have much fewer side effects, allowing better compliance requirements.

The onset of action of antidepressants is 10 to 20 days on average: it is from this time that symptoms begin to disappear.
But depression is not cured when all symptoms have disappeared, and we must continue taking medication for several months or longer, to be sure that the cure is achieved.

other hand, it is necessary to take an important precaution at the beginning of treatment: in fact, while the first days treatment the patient remains depressed, the drug restores energy to the patient, is what is called the lifting of psychomotor inhibition, it is this period that suicide risk is stronger because the patient is depressed and has enough force to injure. To counter this adverse effect of antidepressants, it combines them to anxiolytic (or neuroleptics when suicide risk is very high or if the patient has schizophrenia or hallucinations). The anxiolytic , as their name indicates "killed" by lowering anxiety psychomotor ability of patients due to their sedative effect. some anxiolytic herbal have a very high dose (10 to 15 tablets per day).

In summary, there are constraints or rules to be observed in drug treatment: "It is a treatment course of 6 to 12 months at least for a single depressive episode. -A minimum dose needed for treatment to be effective. He must never stop treatment suddenly, abrupt constituting a risk of depressive relapse. The most effective way to treat depression remains an alliance psychotherapy and medication. There is no specific antidepressants for adolescents: indeed, it is the same as for adults, but some are banned prescription for minors in France. The major antidepressants.

Listing two molecules used as an antidepressant.

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III. Physiology 3. Stress

3. Assumptions involving stress

You can not separate the effect of depression and anxiety * since we have already seen that the depression is often consequence of stressful event. We will show that * Stress can directly affect depression. . For this, we must regain "stress system" :
stress activates two systems, one * noradrenergic (NA) or axis catecholaminergic * which releases noradrenaline through the adrenal medulla glands *, and the other, * or corticotropic axis HHS ( hypothalamic-pituitary-adrenal ) which releases cortisol *.

Involvement noradrenaline in disorders unipolar and bipolar

A hypothesis proposed in 1960 that depression was caused by a deficiency of norepinephrine. The cell bodies of noradrenergic neurons have implications to many brain regions including the limbic system involved in regulating emotions.
While mania, it would correspond to an overabundance of that neurotransmitter. Indeed, flooded noradrenaline, neurons produce a protein that excites them and disturbs their functioning.
This assumption is always recognized that some people's mood is not affected by such fluctuations.

Moreover, the decrease in the amount of serotonin allow a decrease of noradrenaline.

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III. Physiology 3. Stress

Hypothesis on the involvement of cortisol in the decrease of serotonin

is the hypothalamus * which reacts primarily in response to stress by secreting hormones (corticotropin * or TSH and vasopressin *) which then activate the secretion of ACTH * (adrenocorticotropic hormone ) by the pituitary *. The active ACTH in turn adrenocortical glands * that synthesize and secrete cortisol . The cortisol then activates a release of energy that can cope with stress.

After the alert, the cortisol binds to receptors in the pituitary and the hypothalamus slowing the release of corticotropin and vasopressin, thus decreasing the production of cortisol.


But depressed patients, it seems that it there is a decrease of cortisol receptors in the pituitary and hypothalamus . The cortisol no longer has the role of inhibitor and the individual remains on alert.

accumulation resulting cortisol has toxic effects on cortisol degrades too much of neurons, and inhibits the production of new (or memory and learning among others are the creation of new neurons and new paths nervous ) , and also decreases the concentration of L.tryptophane * Required for the production of serotonin.

Review

The biological impact of neurotransmitters such as norepinephrine or dopamine is still unclear at the understanding of depressive syndromes or schizophrenia, although there is a relationship between norepinephrine and psychomotor activity on the one hand, and between serotonin and anxiety on the other. Significant changes in the amount of norepinephrine were also observed in some depressions. However, today the sole interest of the biological exploration could be the orientation of antidepressants polarity noradrenergic (norepinephrine very disturbed) or to serotonergic antidepressants polarity (normal levels of norepinephrine).


Conclusion

The brain function, mood and behavior are likely to have a link. Stress, in particular, has a significant role in depression, either through the HPA axis or axis catecholaminergic . But research in this area are still ongoing, and can not yet identify all the causes and not all the physiological effects of depression since we said earlier that more than half of the depressions are due largely stress, but not all. Again we do not know if these observations of depressed individuals are due to their mood or whether these are chemical imbalances that lead to these moods.
However, many drugs act on these characteristics, close clinical supervision.

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system stress HPA Axis _



Or Chronic Stress
= excess cortisol
And Depression =
depressed mood + psychomotor retardation

Hence the following hypothesis:
Chronic Stress -> Depression


* Cortisol is a glucocorticoid.

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Prozac and Effexor

Example of two molecules used as active agent in antidepressants.

Prozac Effexor

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III. Physiology of depression

Introduction

As noted previously A large number of factors can cause depression , including environmental factors. We also saw the features that can diagnose whether a state is not really depressed or . From a biological standpoint, we do not know exactly what is the cause or effect, but we can speculate based on the observations of researchers.

It is observed that in depressed quantities of certain neurotransmitters * are very small compared to the average. A neurotransmitter can transmit nerve impulses through the neurons *. Several neurotransmitters are involved in depression, particularly serotonin *, noradrenaline and dopamine * *.

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III. Physiology 1. The synapse

1. Neurotransmitters into the synapse.

* In a synapse, two neurons are in contact, the presynaptic one (before the synapse) and one postsynaptic (post-synapse). * In the axon of the first are, among others, vesicles containing neurotransmitters *. * When a nerve impulse reaches the presynaptic axon opens vesicles in the synapse, which releases neurotransmitters.

neurotransmitter molecules then follow three paths:

-or they bind to postsynaptic receptors and allow the passage of nerve impulses,

-either they are recaptured by the presynaptic neuron * that store again in vesicles,

-or they are degraded in the synapse by specific enzymes *.

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III. Physiology 1. The synapse

In depressed people, the small amount neurotransmitters problematic. On the one hand, there will not be enough to bind to neurotransmitter receptors in the postsynaptic neuron that is to say that the nerve impulse is not transmitted, but more importantly, we observe that, for the sake of economy, the presynaptic neuron will recapture neurotransmitters too quickly, leaving no nerve impulses move properly.

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III. Physiology 2. The neurotransmitter

2. Presentation of neurotransmitters

The * monoamine neurotransmitters are a class of very important, especially in depression. There are two subclasses:
* -catecholamines: dopamine, noradrenaline, adrenaline *
-serotonin or 5HT (for 5-hydroxytryptamine)
In neurons by which pass these neurotransmitters, there is an enzyme, monoamine oxidase (MAO) which degrades naturally monoamines.
(see treatment).

Presentation of catecholamines

Dopamine

Dopamine is a neurotransmitter synthesized from tyrosine *. * The brain dopaminergic systems are closely associated with alertness, pleasure-seeking and active avoidance of punishment (flight or fight).

In humans, the decreased activity of dopamine neurons in some brain region results in decreased reflexes. There is a dopaminergic activity low decrease in motor activity and initiative, decreased motivation.

In summary, dopamine creates a fertile ground in search of pleasure or excitement, the alert status, sexual desire. Conversely, when the synthesis or release of dopamine is impaired, one can see a motivation or depression.

Norepinephrine

Norepinephrine is synthesized from tyrosine as for dopamine.
Norepinephrine stimulates the release of fat storage, and controls the release of hormones that regulate fertility *, libido, appetite and metabolism. Norepinephrine also modulates attention and learning.

In conclusion, norepinephrine appears to create a breeding ground for enlightenment, learning, sociability, sensitivity to signals emotional, sexual desire. Conversely, when the synthesis or release of noradrenaline is impaired, may appear withdrawal, detachment, lack of motivation, depression, decreased libido.


Presentation of serotonin

Serotonin is involved in several physiological functions such as sleep, aggression, eating behavior, sexual and in depression. This is the main neurotransmitter involved in depression since we have already seen that depression was often characterized by disturbances of these functions.

Serotonin is manufactured in serotonergic neurons *. Decreased activity of these neurons is associated with various forms of depression, particularly those whose suicidal thoughts persist until the transition is assumed to act so its involvement in the pulses.

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II.Causes adaptive strategies and effects 1. b. genetic predispositions

b. Genetic predispositions

depression is triggered by major life events like loss of reference or a loved one. However, some forms of genes alter the chances of developing the disease is genetic predisposition.

For example, people whose relatives have suffered from depression are 15 % Risk of developing such a while for people whose relatives are not depressed risks are only 2-3%. In addition, children born to parents with a history of depression but adopted by parents who do not suffer from the disease may still make a depression in 15% of cases. So identical twins with exactly the same genes, the probabilities for the twins to live a depression if the other has experienced a rise of 70%.

Yet research in this area are still ongoing and there are only hypothetical.

Thus the mutation gene involved in the transport of serotonin increases the risk of depression. Indeed there are two forms of the gene encoding serotonin: a long form (5 - HTT ) and short allele (5 - HTTLPR ). It was shown that carriers of the short form of the gene most frequently suffer from depression. More in individuals carrying the allele short, subject to anxiety-producing situations the activities of the amygdala and * the cingulum * are disconnected. Instead, their activities are correlated in carriers of the long version. The amygdala, the center of emotions and primitive area of the brain, generate a feeling of anxiety in response to external stimuli, while the cingulum , outer area of the brain, frontotemporal *, would temper this feeling by controlling the activity of the amygdala. The lack of moderation of the amygdala allows runaway activity of the latter, and therefore arouses feelings of fear uncontrolled sources in the long depression. There is no gene for depression or other psychiatric illness. They convey vulnerability to depression.

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II.Causes symptoms and effects 1. c.

c. Adaptive strategies

adaptive strategies are a set of strategies antidepressant form of defense mechanisms which inefficiency lead to a depression. We consider four important:

The narcissistic withdrawal : it is a period or young person trying to get used to his body changing. He tries to resume contact and body control.

regression : Here, adolescence is a period of denial of sexuality and regression oral (eating more or less, smoking, snacking).

The hyperactivity : it will allow the boy does not or no longer think of the different transformations that occur.
The group identification: a period, the adolescent identifies with his peers in the way of dressing, walking, talking.

Several adaptive strategies can may only appear in the same individual. Indeed, adolescents may attempt to identify with a group, smoking (regression), or by copying their dress while trying to regain control of his body ( piercings, hair dyeing ...)

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II. Causes and effects 2.

2. Types and symptoms of depression


Depression is manifested by behavior problems that extend over more than two weeks. These are different from the crisis of adolescence.

Adolescents often become irritable with his parents and his entourage. It can be aggressive, impulsive and has a negative behavior and / or opposition as refusal to attend school.
He loses interest in his leisure activities with friends and bored, he withdraws into himself.
Depression of teenager may be expressed by disinvestment school, frequent absences in court.
Furthermore there may be attempts to run away, concerns morbid risk behavior or suicidal ideation. Moreover
symptoms can be physical: it can lose weight (anorexia) or take (bulimia), complaining of frequent pain (headache, upset stomach ...), become hyperactive or rather inactive and no longer respond to anything. It is also prone to insomnia or hypersomnia nearly every day.

• These symptoms are not accounted for by bereavement, that is to say, after the death of a loved one, the symptoms persist for more than two months.

There unipolar depression and bipolar depression can be distinguished only at relapse. Indeed, throughout his life the subject does unipolar relapse on a slope so that a subject bipolar depressive relapse over a depression or manic episodes or hypomanic. The mania is characterized by a clearly identifiable period of at least a week in which the adolescent is expansive, elated or irritable. During one of these episodes, the individual may start to fidget, talk a lot, sleep less, have an inflation of self-esteem. In addition, the adolescent may feel a leak of his ideas that go too fast, too can get involved in enjoyable activities, but potentially harmful as purchases or sexual disinhibition.

We talk about manic episode when these disorders are accompanied marked disruption of the functioning or requires hospitalization or is accompanied by psychotic features like delusions. A hypomanic episode does not require hospitalization, has no delusions and the operation is not as disturbed.

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II. Causes and effects 1. a. environmental factors

1.The causes

a. Environmental Factors

Adolescence is a period characterized by ambivalence; it is really a child but not yet an adult, he wants contradictory things. It grows, it is puberty, he is survived by his child's body and its relationship with its parents. In addition he built his identity and is therefore a delicate and sensitive period.

is believed that many depressions are related to stressful situations. Stress is a physiological reaction against an unexpected change that requires adaptation. It is caused by one or more stressors. In the case of a teenager, stress can come from school, poor relationships with family, friends or lovers. More changes as an environmental move, parental divorce, changing schools affect the quality of life of adolescents. It also notes that the military, or religious schools such as strict dance schools ("the little rats of the Opera") or prisons the rate of depression is higher than elsewhere .


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Depression is an illness which corresponds to a specific clinical picture, and it is time to differentiate normal passenger suffered depression in adolescence are caused by changes experienced during this period of life as For example, puberty. In addition to physical changes in addition to mental imbalances, where the teenager is torn between children and adults, these mental disorders are managed and contained through adaptation strategies that parents fall into depression and preserve many consequences as dangerous as varied as depression which causes which are sometimes responsible for this disease.

CONTINUED

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I. INTRODUCTION consequences

Depression in adolescents according to different sources shows that the statistical consequences of this disease are numerous and dangerous.

a) Depression is not the only cause of suicide, regardless of the age concerned, but suicide is one of the most serious consequences of this disease, so for several years, a prevention policy Suicide has been established and has begun to show positive results. But with 750 deaths per year, suicide is behind the accidents, the second leading cause of death among 15-25 year olds. A study by the INSERM , girls are 3 times more likely to attempt suicide than boys during adolescence. There are about one death for every 80 attempts.
boys, mortality is twice as large: they choose, in most cases, means more violent radicals, such as hanging or firearms. Girls prefer drug poisoning or phlebotomy (they intersect the veins).
After a first attempt, it is estimated that between 30 and 50% of youth who have attempted suicide reoffend.
is why suicide prevention should be strengthened.

b) Number of adolescent depression see their tuition drop from jusqu'al'échec school.

c) Teens depression are often aggressive. This aggression can result in several forms. They can be aggressive towards others, their friends, their families and sometimes cause a loss of social life that may in some rare cases be total. Or they may be aggressive towards themselves is to say, have behaviors autoagressifs such as scars, burns, bruises (in voluntary bumping against the walls, for example) or phlebotomy.

d) One of the most serious hazards and unfortunately one of the most common among adolescent depression is a drop in the addiction to a product: tobacco, hard or soft drugs, alcohol, drugs. One can also observe teenagers who get stuck in an activity that becomes like a drug: sports, television, internet, reading (very few video games, contrary to that we think). According to the INSERM, the addiction a teenager out of two is due to depression or a depressive state maintained by this addiction precisely. Similarly, a addiction can lead depression.

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Click on the titles to access the articles.

INTRODUCTION


I. Consequences


II. Causes and Effects

1. Causes
-environmental factors
-genetic predispositions
-adaptive strategies

2. Types and symptoms of depression


III. Physiology

1. Neurotransmitters into the synapse:
-in a healthy individual
-in a depressed individual

2. Presentation of neurotransmitters

3. Hypotheses about the involvement of stress-
involvement of noradrenaline
-involvement of cortisol
-balance


IV. Treatment: drugs and therapies


psychological side-slope-biological


CONCLUSION


Depression in the news


* GLOSSARY

- Bibliography


Friday, February 2, 2007

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Welcome on this blog.

We are three students studying science, and we chose as the theme for our TPE "Adolescent Depression".
We wondered about this, if possible, during the period of adolescence, to avoid having a depression?

We invite you, if you wish to leave Comment out your opinions, or your testimony:
Have you had depression?
you feel depressed?
Are you depressed?
Did you manage to avoid depression? How?

We chose the blog as a medium because it is easy to access and that depression is a subject that affects everyone. As teens ourselves, we have reduced the subject to this age.
Your comments and testimonials are welcome.

Access to the summary.