In this brief article, we will be talking about the monoamine theory of depression, the monoamine in depression, the background of the monoamine theory of depression, and more information about the monoamine theory fo depression.
What Is Monoamine as a class of neurotransmitter?
Monoamines as a class of neurotransmitters composed of serotonin, norepinephrine, dopamine, and epinephrine.
Antidepressant drugs can contain these kinds of neurotransmitters to increase the flow of monoamine neurotransmitters.
When you have normal levels of serotonin, you will have mood and behaviour regulation, proper sleep, and proper digestion.
Norepinephrine is responsible for keeping you safe due to the activation of the fight or flight response
Dopamine as a monoamine neurotransmitter is responsible for activating movement, pleasure, and motivation in people.
Monoamine oxidases are enzymes that assist the depletion of oxidase of amines in monoamine neurotransmitters.
There are different types of the reaction of biogenic amines that are discovered in the brain and the peripheral tissues can control intracellular activity.
Monoamine oxidase A (MAO-A) is an enzyme which grows monoamines and may be hyperactive in depressed people.
The Monoamine Theory Of Depression
The monoamine theory of depression came from the discovery that the lack of monoamine neurotransmitters can trigger depression.
This kind of therapy is a famous neurophysiological theory that explains this kind of mood disorder.
This also comes from the benefits of serotonin that is used in antidepressant medications.
For instance, the monoamine oxidase inhibitors (MAOI) are agonists of dopamine, norepinephrine, epinephrine, and serotonin.
Due to these kinds of neurotransmitters, antidepressants can affect dominant symptoms of depression.
For instance, people with this kind of mood disorder who has irritable mood should be more at an advantage when they take SSRIs or norepinephrine reuptake inhibitors.
People with depression who have the loss of energy being dominant can take norepinephrine and dopamine enhancing medications.
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Background Of This Theory Of Depression
Antidepressant medications have been found to increase the flow of monoamine neurotransmitters.
These kinds of neurotransmitters are responsible for the treatment of this mood disorder.
This theory has become a famous theory as mentioned before but particularly, in West Europe and USA after fighting off some studies about biometrics.
The monoamine theory of depression has expanded on the pathophysiological assumptions about the actions of antidepressant medications.
These monoamine neurotransmitters include adaptive changes in receptors and can explain that gradual clinical response is present after the antidepressant intervention.
The monoamine theory of depression might have its benefits but this theory has yet to explain about its mechanisms toward panic disorder, OCD, or bulimia and the inability to explain about the serotonergic and noradrenergic transmissions that are not effective in treating depression.
Antidepressant Drugs That Sparked This Theory
Monoamine oxidase inhibitors (MAOIs) are the first type of antidepressant medications used to treat depression.
These kinds of medications are effective against this kind of mood disorder but these are also very dangerous due to the side effects that can be aroused by these medications.
If you are taking one of these MAOIs, you should take some diet restrictions and not take other psychotropic medications.
These kinds of medications are only prescribed to patients with depression who have no hope in responding to other remedies.
MAOIs increase the flow of monoamine neurotransmitters, as mentioned above, are serotonin, norepinephrine, epinephrine, and dopamine.
These kinds of medications make biological changes occur to minimize the symptoms of this mood disorder.
The FDA has authorized the following MAOIs to treat people with depression:
- Isocarboxazid (Marplan)
- Phenelzine (Nardil)
- Selegiline (Emsam)
- Tranylcypromine (Parnate)
You can learn more about these kinds of monoamine oxidase inhibitors by buying this book on this website.
Isocarboxazid is a form of MAOIs that is used to minimize the occurrence of depressive symptoms.
This medication can reduce monoamine oxidase which leads to the increase of the flow of amine neurotransmitters.
The first dose of this medication is typically in single or divided doses.
The dosage of this medication can be increased slowly in the following 4 weeks.
This monoamine medication is prevented in patients with agitation.
There are side effects of this medication which are the tendency to have postural hypotension and hypertensive responses.
People who take this monoamine medication will get withdrawal symptoms if they stop this medication for 5 days.
Since you have gone through withdrawal, you will be having the minimal dosage of this medication over 4 weeks or longer.
Another MAOI is the phenelzine which can minimize depressive symptoms as well.
This monoamine medication can treat this mood disorder by creating equilibrium in neurotransmitters.
This monoamine medication can help in enhancing your mood to promote emotional wellbeing.
This medication is like Isocarboxacid where it’s used typically to patients who haven’t gotten well from different kinds of treatments.
You need to take this monoamine medication orally for 1 to 3 times daily for possible effects.
This medication can be taken orally together with food or without food.
The doctor will typically prescribe you with the starting lower dosage of this monoamine medication to reduce the possibility of side effects.
You can learn more about this monoamine oxidase inhibitor medication and its effects by buying this book on this website.
Selegiline is an enzyme blocker or inhibitor as an MAOI that lowers the speed of neurotransmitters in the brain.
This monoamine medication is effective against the fatigue or exhaustion symptom in depressed patients.
You will be taking this monoamine medication at a lower dosage for 2 to 3 days.
This medication can take several weeks to see the benefits of depressed patients.
You shouldn’t block yourself from taking this monoamine medication as the doctor prescribed.
You might get anxious about not seeing the immediate advantages which you can minimize by going to your doctor.
Tranylcypromine is another medication in MAOI that can create an equilibrium of neurotransmitters in the brain.
Like phenelzine, this monoamine medication can enhance mood from depression.
This monoamine medication is also used when other treatments have failed to create healing in depression.
This medication must be taken orally in divided doses as prescribed by the doctor.
Once your depressive symptoms are minimal, you will be given a lower dosage of this monoamine medication.
You can learn more about this monoamine oxidase inhibitor by buying this book on this website.
Other Theories Of Depression
Like other psychological disorders, the monoamine theory of depression is only one theory to explain the complexity of this mood disorder.
These kinds of theories have served to find possible reasons for this mood disorder to help improve treatments for these affected people.
There are theories of depression aside from the monoamine theory of depression that is biological and social.
The insights of either of the following theories of this mood disorder have made the understanding of this mood disorder clear and know how to deal with people with this mood disorder.
These kinds of theories of depression are based on experimental trials of people with this kind of mood disorder and successful interventions from case studies.
The following are other theories of this mood disorder aside from the monoamine theory of depression :
- The autoreceptor subsensitivity theory
- Circadian Rhythm Theory of Depression
You can learn one theory of depression that you may have heard about in some psychological literature by buying this book on this website.
The Autoreceptor Subsensitivity Theory
The autoreceptor subsensitivity theory is a theory of depression that focuses on neural compensation and subsensitivity as affecting this mood disorder to occur in people.
These autoreceptors are situated in presynaptic or axonal membranes.
These autoreceptors are sensitive to the number of neurotransmitters in intercellular fluid and inhibitory impact on neurotransmitter creation and release.
Monoamine agonists can stimulate these autoreceptors to minimize the flow of monoamine neurotransmitters.
Autoreceptors can become subsensitive in the next 2 to 3 weeks which can maintain stimulation and stop sending inhibitory signals which create psychological effects.
These autoreceptors are found in the neurotransmitters called serotonin and norepinephrine or noradrenaline.
These neurotransmitters need to be sent to these autoreceptors to manage depressive symptoms.
These autoreceptors can be influenced by the effects of MAOIs which may have different effects on the affected patient.
Circadian Rhythm Theory Of Depression
Abnormal sleep patterns have been attributed to depression since some patients with sleep deprivation have been treated effectively with interventions for this mood disorder.
Antidepressant medications have been found to affect the sleep patterns of people with this mood disorder which is either to make them sleep better or not.
In other words, people with depression are more likely to have sleep interruptions at night.
Some studies have shown that people with sleep deprivation and this mood disorder were found after a short nap to return to their depressive states.
This evidence has given some researchers the assumption that a depressogenic substance may be involved and can affect the person when he or she is awake.
Some have theorized that people with depression have this perception that they will experience this mood disorder in the morning which can indicate that the symptom of the hopelessness of getting rid of this mood disorder is strong.
In other words, sleep patterns can affect the reinforcement of depressive symptoms.
This is why these affected patients should be taking a healthy sleep routine to minimize their prolonged distress.
Limitations Of The Monoamine Theory Of Depression
The core limitation of the monoamine theory of depression is the therapeutic delay between the effects of monoamine medications and the psychological interventions that can affect depressed patients.
Some researchers would state that this is the common issue since the sending of serotonin signals may take too much time to flow to create mood regulation.
The therapeutic impact of antidepressant medications is believed to arise from autoreceptor desensitization over a period of time, gradually increasing firing of serotonergic neurons.
This kind of explanation hasn’t motivated to make new psychotropic medications.
There are many elevating developments made but it seems that it takes a lot of time to understand and apply to create psychotropic medications that don’t impact monoamine neurotransmitters.
In recent times, it may be better to wait out this improvement from the existing studies for this medication.
This kind of situation is not helpless for now since there is still the possibility of developing medications for monoamine reuptake inhibitors.
The therapeutic delay has inspired other researchers to seek possible treatments for depression for now and wait for other studies that can make sense about medications that can’t affect monoamine neurotransmitters to avoid adverse side effects.
In this brief article, we have talked about the monoamine theory of depression, the monoamine in depression, the background of the monoamine theory of depression, and more information about the monoamine theory fo depression.
If you have any questions about the monoamine theory of depression, please let us know and the team will gladly answer your questions.
FAQs: monoamine theory of depression
How does reserpine cause depression?
Reserpine causes depression by depletion of these monoamine neurotransmitters that trigger or contribute to the onset of depression in vulnerable individuals.
This is considered in the monoamine theory of depression that explains this brain phenomenon.
What are the side effects of reserpine?
The side effects of reserpine are nausea, vomiting, diarrhoea, lack or loss of appetite, breast tenderness or swelling, headache, dizziness, drowsiness, itching or rash, weight gain, stuffy nose, nosebleeds, impotence, and decreased interest or motivation in sex.
Why reserpine is not used clinically?
Reserpine is not used clinically because of its side effects that are concentrated in the central nervous system.
Also, the availability or accessibility of much better tolerated and more potent antihypertensive medications.
Reserpine continues to be available or accessible in generic forms as tablets of 0.1 and 0.25 mg which can be taken orally.
What is the mechanism of action of reserpine?
The mechanism of action of reserpine is through inhibition of the ATP/Mg2+ pump responsible for the sequencing and quenching of neurotransmitters into storage vesicles situated in the presynaptic neuron.
Is tetrabenazine an antipsychotic?
Yes, tetrabenazine is an antipsychotic medication in psychotropic medications.
It is a monoamine depletion and used as symptomatic intervention of chorea related to Huntington’s disease. This is now used primarily in the symptomatic intervention of different hyperkinetic disorders.
Mayo Clinic. Monoamine oxidase inhibitors (MAOIs).
MST. Theories of Depression
NCBI. Monoamine Hypotheses of Mood Disorders.
OpenLearn. The monoamine hypothesis of mood disorders.
ResearchGate. Monoamine Theories of Depression: Historical Impact on Biomedical Research.
Wikipedia. Biology of depression.