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When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm

 
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When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm

Scientific American

2009-01-31

What makes harmless little green grasshoppers turn into brown, crop-chomping clouds of swarming locusts? Serotonin, according to a study published this week in Science. Researchers from universities in the UK and Australia found that that neurotransmitter (a chemical compound that sends impulses between nerve cells and affects everything from sleep to aggression in humans) spurs a cascade of Dr. Jekyll-to-Mr. Hyde–like changes in at least one species of grasshopper — the desert locust (Schistocerca gregaria). This species is infamous for wreaking havoc from Africa to Asia.

Knowing what causes this swift metamorphosis may help governments and farmers develop methods to control future locust outbreaks with chemicals that would suppress the offending serotonin.

It took just two to three hours for timid grasshoppers in a lab to morph into gregarious locusts after they were injected with serotonin. Conversely, if they were given serotonin blockers, they stayed solitary even in swarm-inducing conditions.

"These little guys changed from a shy creature that actively avoided making contact with other grasshoppers [into a creature] actively seeking out other insects and joining a gang," says study co-author Malcolm Burrows, a zoology professor at Cambridge University in England. And we're not just talking about a gaggle of grasshoppers: Just last year, a swath of locusts more than three and a half miles (six kilometers) long tore through Australia, devastating crops in its path.

"They eat everything in sight," says Sean Mullen, an assistant professor of evolutionary genetics at Lehigh University in Bethlehem, Pa., about swarming locusts.

When these insects go into swarm mode, they don't just get super social, they also completely change physically, becoming stronger, darker and much more mobile, says study co-author Swidbert Ott, a research fellow at Cambridge. In fact, he says, the before-and-after bugs look so different that, until the 1920s, they were assumed to be two unique species.

In the wild, swarms usually appear after a rainy period followed by a time of drought. After rains, populations of grasshoppers explode, Burrows says, because there is food aplenty. But when the land becomes parched and grass scarce, the populations get pushed into smaller and smaller areas, becoming more packed as desirable pasture diminishes, he says. At a certain point of density, the swarm-inducing serotonin gets triggered and the locusts set off en masse to find greener pastures. After that, few things — other than an end to the food supply or an ocean — can stop them.

Burrows says that locusts can switch out of swarm mode, though it takes days rather than hours. He notes, however, that the about-face rarely happens in the wild, because the offspring of locusts that breed while swarming are born swarmers.

Today, locust invasions are controlled with pesticides that also wipe out other insects, note Burrows and Ott. This new research, however, paves the way for development of a chemical that would specifically inhibit serotonin production in the solitary grasshoppers, says Hojun Song, a postdoctoral researcher at Brigham Young University in Provo, Utah.

But remember, as Kung Fu's Master Po advised his young charge in the 1986 movie, "Do not go in fear, Grasshopper." Of the approximately 8,000 species of grasshoppers, only about 10 of them are likely to morph into swarming locusts, Burrows says. But, Song adds, more research should be conducted to determine whether other types of locusts also get hopped-up on serotonin.
a (OP)
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02/02/2009 09:35 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
..................................................

so all they have to do
is spraying serotonin blockers on crops
and have the side effect of people gaetting scared and weak instead of social and strong

two kills with a single stone

serotonin blockers' research is quite advanced:

[link to www.nature.com]
We describe a new class of drugs that selectively block serotonin M-receptors on peripheral neurones. Because of their high affinity, some of these drugs are the most potent of any pharmacological class yet reported. They have allowed the identification of three M-receptor subtypes, one of which is responsible for mediating the painful effects of serotonin in humans.

[link to general-medicine.jwatch.org]
NEW POWERFUL ANTIEMETICS: SEROTONIN-RECEPTOR BLOCKERS
In recent years, several different receptors for serotonin have been discovered and each has been shown to have a particular physiologic role.



serotonin blockers alter behaviour patterns (kill habits)
in this case, alcoholism relapse:
[link to www.a1b2c3.com]
Controlled trials in larger dependent populations are needed before serotonin blockers can provide hope as a possible adjunct for relapse prevention.

serotonin blockers used in surgery for its blood pressure lowering effect (blood pressure lowering = slower body processes = slower thinking)
[link to www.ncbi.nlm.nih.gov]
The most important available specific S2-serotonergic receptor antagonist is ketanserin. If administered during or after cardiac surgery, ketanserin lowers systemic and pulmonary blood pressure, and improves peripheral and pulmonary perfusion without causing reflex tachycardia or an increase in pulmonary shunt fraction.


serotonin blockers are used as antisickness drugs, because they numb down the natural reflex to vomit ( poisons)
[link to www.cancerhelp.org.uk]

Serotonin blockers
Serotonin blockers work very well for some types of sickness. They work best when you have steroids at the same time. There are several drugs in this group, including ondansetron (Zofran) granisetron (Kytril) and tropisetron (Navoban). Palonosetron (Aloxi) also belongs to this group. This drug works for a longer period. You have it as an injection no more than once a week. These drugs block receptors in the gut and brain that send messages to the chemoreceptor trigger zone and the vomiting centre. They are also called 5HT3 blockers.
a (OP)
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02/02/2009 09:39 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
Serotonin: A hormone, also called 5-hydroxytryptamine, in the pineal gland, blood platelets, the digestive tract, and the brain. Serotonin acts both as a chemical messenger that transmits nerve signals between nerve cells and that causes blood vessels to narrow.

Changes in the serotonin levels in the brain can alter the mood. For example, medications that affect the action of serotonin are used to treat depression.
a (OP)
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02/02/2009 10:38 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
serotonin blocker slows down larvae
[link to asgsb.indstate.edu]
THE ROLE OF THE NERVOUS SYSTEM IN MODULATING GRAVITY-DEPENDENT SWIMMING BEHAVIOUR IN THE LARVAE OF MYTILUS EDULIS. J. T. Plummer1, D. L. Jackson2 and R. P. Croll1, 1Dalhousie University and 2Department of Fisheries and Oceans, Halifax, N.S., Canada.

Previous flight studies in which bivalve veliger larvae deviated from their normal helical swimming in a micro-gravity environment prompted our investigation into the possible role of the larval nervous system in controlling this behaviour. Immunocytochemical techniques coupled with pharmacological studies have provided evidence for a direct control of swimming behaviour by the larval nervous system in in bivalve molluscs. Both serotonin- and catecholamine-containing axons innervate the velum, which serves as tthe primary swimming organ in the larvae. In addition, serotonin and its reuptake inhibitor, fluoxetine, appeared to have a cilio-excitatory effect on larvae causing them to swim at a greater velocity. Conversely, the serotonin antagonist, mianserin, had the opposite effect. The catecholamines, dopamine and norepinephrine, appeared to directly decrease ciliary activity. These results were confirmed by treatment with spiperone, an antagonist to catecholamines which increased swimming velocities. The cilio-inhibitory effect of catecholamines caused the animals to not only decrease their swimming speeds, but also to deviate from their normal helical upward swimming pattern. The compilation of these results suggest a specific role of the larval nervous system in mediating patterns in bivalve larval swimming, and are consistent with the hypothesis that the alterations observed in micro-gravity may possibly result from underlying changes in neuronal development.
entropy

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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
It's devil propaganda!
my re-imaging(cover)
of "Piggies" (The Beatles)
and "Lights in the Sky" (Nine Inch Nails)
is available to listen to now. Won't cost you a dime. Click below to hear it.


[link to www.myspace.com]

Over 1 Million plays, Most popular NIN Remix / Re imaging artist on myspace. I keep it separate:

[link to www.myspace.com]

archive:
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[link to www.facebook.com]

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Anonymous Coward (OP)
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02/02/2009 10:42 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
Biogenic amines (Monoamines)

The biogenic amines comprise (1) the catecholamines norepinephrine, epinephrine, dopamine, and
(2) serotonin (5-Hydroxytryptamine). They are chemical messengers used by neurons as well as by endocrine
and other cells. A catecholamine is an organic compound that contains a catechol nucleus and an amino group.
The monoamines are synthesized within each neuron from the amino acid tyrosine in the presence of
appropriate enzymes. The sequence of enzymatic steps from tyrosine are dopamine to norepinephrine to
epinephrine. Serotonin is synthesized within the neuron from the amino acid tryptophan.
The monamine transmitters are released into the synaptic cleft. The recovery of the released transmitter
occurs by uptake into the presynaptic ending where it is recycled for future use. Neurons releasing
norepinephrine and epinephrine are adrenergic, those releasing doparnine, dopaminergic, and those releasing
serotonin, sertonergic. The activity of these monoamine transmitters is limited by their reuptake by transporters
into the presynaptic ending, where they are recycled into vesicles for future release.
Monoamines may have different specific effects on the postsynaptic cell depending on the type or subtype of
receptor protein. Several varieties of subtypes of receptors are present for each monoamine. These receptors
have different properties and are differentially distributed in the nervous system with the result that they have a
variety of effects and even opposite responses. Thus, it is not possible to state that a specific neurotransmitter
is either excitatory or inhibitory in its action; it can be both depending on the postsynaptic receptor type.
The three biogenic pathways in the brainstem are (1) the dopaminergic pathways (system) which originate in
the midbrain; (2) the noradrenergic pathways (system) which originate in two nuclear groups called the locus
coeruleus (LC) and lateral tegmental nucleus; and (3) the serotonergic pathways (system) which originate in the
raphe nuclei.
[link to www1.indstate.edu]
Serotonin (5-hydroxytryptamine, 5-HT)


Serotonin is present in the cell bodies of neurons located primarily in the raphe nuclei of the brainstem. It is
also found in mast cells (associated with nociception), platelets, and enterochromaffin cells of the gut. Axons
from the raphe nuclei are distributed diffusely throughout the brain and spinal cord. Neurons of the rostral
(midbrain) raphe nuclei have axons that join the median forebrain bundle and terminate in the diencephalon,
striatum, cerebral cortex, and the ependyma lining the ventricles. Those in the middle nuclei (Pons) have
axons that terminate in the cerebellum and reticular formation, and those from the caudal nuclei (medulla) have
axons that project to the spinal nucleus of the trigeminal nerve and to the gray matter of the spinal cord.
Following its release from mast cells and other damaged cells, serotonin is the agent that activates and
sensitizes the nociceptors of the primary "pain" fibers (A-delta and C fibers). In the nervous system, serotonin
is involved with second messenger systems as a modulator. The projections to the spinal trigminal nucleus and
dorsal hom of the spinal cord act to inhibit the pain fibers, and those to the ventral hom act to activate by
facilitation. In addition, serotonin has roles in a complex of physiologic activities including changes in blood
pressure, body temperatures, the sleep-wake cycle, certain psychological and psychotic states, and responses
to certain drugs.
The drug fluoxetine (Prozac) is widely used to help people cope with a range of behavioral symptoms
including degrees of mild to severe depression, deficiency in the ability to experience pleasure, fear of rejection,
and lack of self confidence. It acts by blocking the serotonin transporter in the axon terminal and the reuptake
of serotonin from the synaptic cleft. The result is an increase in the level and duration of the action of serotonin,
which is translated in a few weeks into the therapeutic effect.
a (OP)
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02/02/2009 10:51 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
It's devil propaganda!
 Quoting: entropy

3. Neurochemistry of sleep.
a. Basic concepts.
1. Noradrenalin (norepinephrine)
2. Serotonin (5HT)
3. Dopamine
a. Parachlorophenyalanine (PCPA) - prevents the neuronal manufacture of serotonin.
b. Alpha-methyl-para-tyrosine (AMPA) -inhibits synthesis of catecholamines NE and DA.
c. 6-hydroxydopamine - suppresses or destroys dopamine producing neurons.


[link to www1.indstate.edu]

a. There are two types of insomnia:
1. One is due to a lack of serotonin with diminished synchronization of the EEG. Such periods of sleeplessness isn’t followed during subsequent secondary rebound states of SWS and PS.

2. The other is due to activation of ascending noradrenergic elements by stimulation of mesencephalic reticular formation noradrenergic cells. This is always followed by SWS and PS rebound that is proportional to duration of insomnia.

3. Both types of insomnia can be reversed to sedation by diminishing the turnover of catecholamines (administer alpha-amino-p-tyrosine).


b. There are two types of hypersomnia:

1. Active hypersomnia with accompanying SWS and PS which is due to the release of serotonin.

2. Prolonged cortical synchrony due to a disturbance of mesencephalic catecholamine producing neurons. There is no true increase of SWS and PS.
a (OP)
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02/02/2009 10:59 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
yet, if serotonin decrease has negative effects, modern medicinal use of this knowledge is barbaric



The most widely used antidepressant drugs fall into three major classes: (1) the monoamine oxidase inhibitors, such as phenelzine (Figure 2A), (2) the tricyclic compounds , such as imipramine, so named for their three-ring molecular structure (Figure 2B), and (3) the serotonin uptake blockers, fluoxetine and trazodone. The monoamine oxidase inhibitors and the tricyclic antidepressants produce remission or marked improvement in about 70% of patients with major depressions. When high doses are given (and blood drug levels are monitored so as to achieve and maintain an adequate therapeutic concentration), the success rate with tricyclic drugs and the specific serotonin uptake inhibitors may reach 85%, almost as effective as electroconvulsive therapy. Patients with bipolar depression occasionally become manic during treatment with either class of antidepressant. Although a few patients begin to improve immediately, there usually is a lag of 1-3 weeks before the symptoms of depression begin to improve, and 4 to 6 weeks are generally required for full response.
[link to www1.indstate.edu]

[link to wandering-minds-on-depression.blogspot.com]
The Dangers of Antidepressants
The Dangers of Prozac, Zoloft, Paxil, Celexa and Luvox
Peter R. Breggin, M.D. in “The Anti-Depressant Fact Book” outlines a number of potentially harmful effects of SSRI antidepressants. The primary harmful effects of taking an SSRI include the following: (1) Potentially permanent brain-damaging effects (2) mania, psychosis, and other extreme mental and behavioral reactions; (3) the paradox of increased depression leading to suicidal tendencies (4) sexual dysfunction and; (5) withdrawal problems when trying to stop taking SSRIs. This article highlights only the potentially permanent brain-damaging effects of taking antidepressants.

How Prozac, Zoloft, Paxil, Celexa and Luvox Work
Selective serotonin reuptake inhibitors (SSRIs) disrupt the serotonin system of the brain and block the removal of serotonin from the synapses. A buildup in the levels of serotonin in the brain leads to an increase in the activation or firing of the serotonin nerve cells and puts them into overdrive. Increasing the levels of serotonin also normalizes the functioning of the norepinephrine and dopamine systems.

The Brain Fights Back
The brain fights back against the effect of increased levels of serotonin, and no one knows the net effect of the overall outcome. The brain senses the abnormal increase of serotonin in the synapses and tries in several ways to reverse it. The cells that produce serotonin begin to shut down and stop releasing serotonin. In addition to shutting down the output of serotonin, the brain also compensates by becoming less sensitive to the effects of serotonin. When the brain senses that Prozac has caused too much serotonin to pool in the synapse, the brain reacts defensively by destroying its own receptors for serotonin. The receptors actually die back and disappear. In some regions of the brain, the dieback may result in significant loses—this is known as down regulation. In the end, drug induced brain changes (brain cell death and abnormal brain cell growth) are likely drastic and may become permanent with the prolonged use of antidepressant medication.
a (OP)
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02/02/2009 11:26 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
Drugs known as antidepressants
CLASS:- "SPECIFIC SEROTONIN RE-UPTAKE INHIBITORS"
(SSRIs or sometimes the "5-HT RE-UPTAKE BLOCKERS")
Drugs available Brand name(s)

Forms available

Tablets

Capsules

Liquid

Injection

Citalopram Cipramil (Seropram in France)


Escitalopram (2) Cipralex


Fluoxetine Prozac


Fluvoxamine Faverin

Paroxetine Seroxat (Deroxat in France)


Sertraline Lustral


Related drugs*;-
Nefazodone (1) Dutonin, now discontinued


Trazodone (1) Molipaxin

(sugar-free)
entropy

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02/02/2009 11:28 AM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
It's devil propaganda!

3. Neurochemistry of sleep.
a. Basic concepts.
1. Noradrenalin (norepinephrine)
2. Serotonin (5HT)
3. Dopamine
a. Parachlorophenyalanine (PCPA) - prevents the neuronal manufacture of serotonin.
b. Alpha-methyl-para-tyrosine (AMPA) -inhibits synthesis of catecholamines NE and DA.
c. 6-hydroxydopamine - suppresses or destroys dopamine producing neurons.


[link to www1.indstate.edu]

a. There are two types of insomnia:
1. One is due to a lack of serotonin with diminished synchronization of the EEG. Such periods of sleeplessness isn’t followed during subsequent secondary rebound states of SWS and PS.

2. The other is due to activation of ascending noradrenergic elements by stimulation of mesencephalic reticular formation noradrenergic cells. This is always followed by SWS and PS rebound that is proportional to duration of insomnia.

3. Both types of insomnia can be reversed to sedation by diminishing the turnover of catecholamines (administer alpha-amino-p-tyrosine).


b. There are two types of hypersomnia:

1. Active hypersomnia with accompanying SWS and PS which is due to the release of serotonin.

2. Prolonged cortical synchrony due to a disturbance of mesencephalic catecholamine producing neurons. There is no true increase of SWS and PS.
 Quoting: a 606036

hf
:bblwise:
my re-imaging(cover)
of "Piggies" (The Beatles)
and "Lights in the Sky" (Nine Inch Nails)
is available to listen to now. Won't cost you a dime. Click below to hear it.


[link to www.myspace.com]

Over 1 Million plays, Most popular NIN Remix / Re imaging artist on myspace. I keep it separate:

[link to www.myspace.com]

archive:
[link to www.vampirefreaks.com]

Thanks.
[link to www.facebook.com]

aSBhbSB5b3VyIHNhdmlvcg0KaSBhbSBjb3JydXB0aW9uDQppIGFtIHRoZSB​hbmdlbA0Kb2YgeW91ciBkZXN0cnVjdGlvbg0KaSBhbSBwZXJ2ZXJzaW9uDQpz​ZWNyZXQgZGVzaXJlDQppIGFtIHlvdXIgZnV0dXJlDQpzd2FsbG93ZWQgdXAga​W4gZmlyZQ==
a (OP)
User ID: 606036
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02/02/2009 12:23 PM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm
It's devil propaganda!

3. Neurochemistry of sleep.
a. Basic concepts.
1. Noradrenalin (norepinephrine)
2. Serotonin (5HT)
3. Dopamine
a. Parachlorophenyalanine (PCPA) - prevents the neuronal manufacture of serotonin.
b. Alpha-methyl-para-tyrosine (AMPA) -inhibits synthesis of catecholamines NE and DA.
c. 6-hydroxydopamine - suppresses or destroys dopamine producing neurons.


[link to www1.indstate.edu]

a. There are two types of insomnia:
1. One is due to a lack of serotonin with diminished synchronization of the EEG. Such periods of sleeplessness isn’t followed during subsequent secondary rebound states of SWS and PS.

2. The other is due to activation of ascending noradrenergic elements by stimulation of mesencephalic reticular formation noradrenergic cells. This is always followed by SWS and PS rebound that is proportional to duration of insomnia.

3. Both types of insomnia can be reversed to sedation by diminishing the turnover of catecholamines (administer alpha-amino-p-tyrosine).


b. There are two types of hypersomnia:

1. Active hypersomnia with accompanying SWS and PS which is due to the release of serotonin.

2. Prolonged cortical synchrony due to a disturbance of mesencephalic catecholamine producing neurons. There is no true increase of SWS and PS.

hf
:bblwise:
 Quoting: entropy


grasshoppers:
[link to etc.usf.edu]
[link to www.cirrusimage.com]
[link to chosetec.darkclan.net]
[link to www.geocities.com]
[link to www.astrographics.com]
a (OP)
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02/02/2009 12:33 PM
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Re: When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm

Selective Serotonin Reuptake Inhibitors

History of development

Prior to the SSRIs, most of psychotropic medications were the result of chance observation. Tricyclic antidepressants were discovered by chance. The TCAs were the result of an unsuccessful attempt to improve on the antipsychotic effectiveness of phenothiazines (medication used in the treatment of schizophrenia). Molecular modifications of phenothiazines led to synthesis of imipramine, the first clinically useful tricyclic antidepressant.

Older chance-discovery drugs have many clinical effects either because they affect a site of action with broad implications for organ function or because they affect multiple site of actions. Chance-discovery drugs typically will produce a number of undesired, as well as desired, effects and will have a narrower therapeutic index in comparison with a drug that was rationally developed to affect only the site of action necessary to produce the desired response.

The SSRIs were developed in response to the need for better tolerated, safer antidepressants than the TCAs, but no less effective for the symptoms of depression. The first SSRI, fluoxetine (Prozac) was released in 1987. Each of the SSRIs was the product of a development strategy in which the goal was to produce a drug capable of inhibiting the reuptake of serotonin, but without affecting the various other neuroreceptors (ie, histamine, acetylcholine, and alpha1-adrenergic receptors), affected by the TCAs.

The development of the SSRIs, with their selective mode of action, has resulted in a class of antidepressant drugs possessing an improved side-effect profile, while retaining good clinical efficacy.

The fact that SSRIs were designed to avoid affecting other neuroreceptors explains many of the pharmacological differences between the SSRIs and the TCAs and explains the similarities among the SSRIs.

Mechanism of action

The brain communicates with itself through the use of special chemicals called neurotransmitters such as serotonin, norepinephrine, and dopamine. There is correlation between the amount of these chemicals in the brain and a person's mood. Low levels of serotonin and norepinephrine have not been proven to cause depression but it widely believed that elevation of these chemicals is associated with improvement in mood in depressed people. Both SSRIs and TCAs work by prolonging the effects of neurotransmitters, but have different mechanism of action.

Tricyclic antidepressants work by raising the levels of neurotransmitters serotonin and norepinephrine in the brain by slowing the rate of reuptake (reabsorption) by nerve cells. TCAs act as strong inhibitors in the reuptake of both norepinephrine and serotonin. Unfortunately, the TCAs also block histaminic, cholinergic, and alpha1-adrenergic receptor sites, and this lack of selectivity is what accounts for the unwanted side effects such as weight gain, dry mouth, constipation, drowsiness, and dizziness.

Unlike TCAs antidepressants, SSRIs are highly selective: they act as weak inhibitors in the reuptake of non-serotonergic neurotransmitters such as norepinephrine, but act as strong inhibitors in the reuptake of serotonin. Because of this selectivity, there are less side effects associated with SSRIs than with TCAs and their side effects are due to actions at other serotonin receptors in the central nervous system and the gut wall.

Unlike TCAs, SSRIs have variances in molecular structures. Tricyclic antidepressants (amitriptyline, amoxapine, clomipramine, dosulepin, doxepin, imipramine, lofepramine, nortriptyline, and trimipramine) are structurally similar. Selective serotonin reuptake inhibitors (citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline) are structurally diverse but share a common mechanism of action.

Efficacy

Both TCAs and SSRIs are effective medications for the treatment of depression. There is no clinically significant difference in effectiveness between SSRIs and TCAs. Generally, about two thirds of people with depression who take any one type of antidepressant will find that it improves the way they feel.

Overall efficacy between the two classes is comparable. The conclusion that TCAs and SSRIs have comparable antidepressant efficacy is based on the fact that they both produce overall response rates of about 60%. Both the SSRIs and the TCAs produce a 20% higher response rate than placebo 10, 11.

Tricyclic antidepressants and selective serotonin reuptake inhibitors are equally effective in the treatment of moderate depressive disorders 14. No significant differences exist in efficacy between selective serotonin reuptake inhibitors and tricyclics in patients in primary care 36.

Although the SSRIs have become the most commonly prescribed drugs for depression, there are clinical situations in which TCAs may be more appropriate:

* Depressed in-patients. SSRIs are not proven to be as effective as TCAs in in-patients and against amitriptyline 11. Several studies have shown that some TCAs may be more effective than SSRIs in depressed in-patients, with the strongest evidence for amitriptyline 3, 40. It may be explained that TCAs have a dual action in inhibiting both 5-HT and noradrenaline reuptake.
* Severe depression. There are indicators the TCAs are more efficacious for severe depression. They have an important place as the first-line treatment for patients with severe (melancholic/endogenous) depression 34.

Remission rate. Remission rate for TCAs (44.1%) is higher than for SSRIs (37.7%) 12.

Adverse effects

SSRIs affect fewer sites of action than TCAs, and as a result cause fewer types of adverse effects. The SSRIs have a better overall tolerability profile than the TCAs in both acute and long-term treatment of major depression 33. SSRIs induce significantly less anticholinergic, antihistaminergic and cardiotoxic side-effects than TCAs 5.

Cardiovascular effects. Tricyclic antidepressants have significantly higher rate of serious cardiovascular side effects 18. Selective serotonin reuptake inhibitors as a class are less likely to affect cardiovascular parameters.

Through a combination of anticholinergic activity, direct myocardial depressant activity and an effect on the adrenergic neuron, TCAs can cause a combination of arrhythmias (disturbances in cardiac rhythm or conduction), blood pressure abnormalities (orthostatic hypotension) and congestive heart failure 31. The major side effects in therapeutic dosage include heart rate increase, postural hypotension and slight prolongation of the intraventricular conduction time and QT interval. 39

SSRIs also appear to affect the cardiovascular system
13, 32.

Anticholinergic effects (dry mouth, blurred vision, drowsiness, constipation, and difficulty in urination). Dry mouth is a most common TCAs' side effect 37. Tricyclic antidepressants produce a greater incidence of dry mouth, drowsiness, constipation and fatigue than SSRIs 4, 38.

Weight gain / appetite increasing effects. Both SSRIs and TCAs can cause unwanted weight gain. However, there is some evidence that tricyclic antidepressants may be more likely to cause weight gain and increased appetite than the selective serotonin reuptake inhibitors 41, 42.

Sexual effects. Sexual dysfunction such as decreased sexual desire, erectile difficulties and delayed ejaculation has been reported with all classes of antidepressants. Sexual dysfunction is one of the most frequent and persistent SSRI adverse effect. These drugs are more likely to cause sexual dysfunction than the TCAs 4, 23.

Central Nervous System effects (headache, dizziness, agitation, insomnia and tremor). In contrast to the tricyclic antidepressants, SSRIs are more likely to cause headache, agitation, insomnia and tremor 42.

Nausea. Nausea occurs more frequently with SSRIs. It is the most common adverse event reported during treatment with SSRIs 37, 38.

Gastro-intestinal effects. Compared to TCAs, SSRIs have higher incidence of gastro-intestinal side effects 23, 42.

With many tricyclics, the most troublesome effect with ongoing use is sedation. They are often administered at bedtime so that this effect is bearable, but it may persist into the following day.

Interactions

Alcohol. TCAs are associated with the dangers of drinking alcohol while taking antidepressant. TCAs cause serious potentiation of the central nervous system (CNS) depressant effects of alcohol and other CNS depressants such as benzodiazepines. Such potentiation occurs when TCAs and alcohol are taken together due to the antihistaminic effects of TCAs. Since SSRIs have been designed to avoid blocking the histamine receptor, they do not pharmacodynamically potentiate the effect of alcohol or other CNS depressants.

Drug-drug interactions. Since TCAs block alpha1-adrenergic receptors they can reverse the antihypertensive effect of guanethidine and clonidine. Orthostatic hypotension may be increased with diuretics and hydralazine. Myocardial depression may occur with lidocaine, phenytoin or propranolol. Dangerous additive effects may result from concomitant use of a tricyclic antidepressant and either quinidine or procainamide 30. SSRIs are designed to avoid blocking the alpha1-adrenergic receptor, so they do not potentiate the effects of concomitantly prescribed antihypertensive medications, in contrast to TCAs.

Serotonin syndrome. The selective pharmacology of the SSRIs results in a lower potential for pharmacodynamic drug interactions relative to other antidepressants. However, the SSRIs have been implicated in the development of the serotonin syndrome - a potentially life-threatening complication of treatment with psychotropic drugs 35.

The serotonin syndrome is an adverse drug interaction characterized by the triad of altered mental status, autonomic dysfunction, and neuromuscular abnormalities.

SSRIs are more likely to cause serotonin toxicity than TCAs.

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