Running Head: TRICYCLIC ANTIDEPRESANTS 1

Tricyclic Antidepressants

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TRICYCLIC ANTIDEPRESANTS 2

Antidepressant drugs help in the reduction of symptoms related to depressive

disorders through the alteration of chemical imbalances of the neurotransmitters in the brain.

The changes in the mood are as a result of chemical imbalance. The neurotransmitters are

located in the vesicles in the nerve cells and communication links between the neurons in our

brain. The tricyclic antidepressants are among the first antidepressants to be created in the

20th century. The TCAs that are used in the clinical practice are amitriptyline, nortriptyline,

imipramine, desipramine, clomipramine, protriptyline, trimipramine and doxepin. These

types of tricyclic antidepressants were the dominating class until the 1990s when the SSRIs

were introduced. The tricyclic antidepressants (TCAs) mechanism to produce the

antidepressant effect is through blocking of the reuptake pumps of norepinephrine (NET) as

well as the selection of serotonin (SERT) with less or no action on the dopamine reuptake

pumps (DAT).

The primary route of TCAs administration is oral. However, some of the TCAs can be

administered through injected intramuscularly. The TCAs are about five drugs in one as it

includes a norepinephrine reuptake inhibitor (NRI), a serotonin reuptake inhibitor and some

contain weak dopamine reuptake inhibitor (DRI). The other two are alpha one adrenergic

antagonist and an anticholinergic-antimuscarinic drug that is unselective muscarinic

acetylcholine M receptors for blockade activity. When the tricyclic antidepressants are taken,

they increase the levels of norepinephrine and serotonin as well as the two neurotransmitters.

The increase of these two neurotransmitters blocks the action of acetylcholine which

is another neurotransmitter. This helps in the restoration of balance in the neurotransmitters in

the brain and result in the alleviation of depression.

TRICYCLIC ANTIDEPRESANTS 3

The tricyclic antidepressants block the reuptake of both the norepinephrine (NE) and

serotonin (5HT). The TCAs are potent inhibitors of the neuronal reuptake of the

norepinephrine as well as serotonin into presynaptic nerve terminals. When at therapeutic

concentrations, these TCAs do not block the dopamine transporters.

The impact of the TCAs cause increased concentrations of monoamines into the

synaptic cleft, which ultimately result in antidepressant effects. TCAs such as desipramine

and Maprotiline is relative selective inhibitors of norepinephrine reuptake that lead to

blocking of receptors. Moreover, tricyclic antidepressants block serotonergic, alpha-

adrenergic, muscarinic and histaminic receptors. The phenomenon is the primary mechanism

at which the action of antidepressants results to changes in the physiological behaviour of

neuro-receptors. Besides, the TCAs are reported to block the alpha one adrenergic,

muscarinic and histaminic receptors. However, the molecules can result in the occurrence of

different side effects in the body.

Conclusively, the tricyclic antidepressants were the most dominant until the 1980s

when the SSRIs were introduced. Different types of TCAs are available for use in the USA.

These drugs cause the antidepressant effect by causing an increase in the level of

norepinephrine and serotonin, block the action of acetylene and two neurotransmitters

resulting in a balance the neurotransmitters in the brain. Consequently, the process results in

the alleviation of depression. They are effective when taken in therapeutic concentrations. If

there is an overdosage, the drug causes several health effects to the patient. The impacts of

these antidepressants are felt after about eight weeks since the time they are administered.

Patients are given the tricyclic antidepressants orally.