Tricyclic antidepressants

Mechanism of action- Act by inhibition of reuptake of amines (NA. 5-HT)

Pharmacokinetics
Rapidly absorbed
Extensively protein bound
Metabolized in liver
On prolong administration-toxicity

Pharmacological actions
CNS
In normal subjects: Diziness, drowsiness, confusion, difficulty in thinking
In depressed subjects:elevation of mood (2-3 weeks after treatment), sleep patterns
Become normal
CVS
Due to blockade of alpha adrenergic and muscarinic receptors causes
postural hypotension and tachcardia
ANS
Exhibit anticholinergic properties like dryness of mouth, blurred vision, constipation
Urinary retension
Adverse effects
 Drug Interactions

1. TCAs abolish the antihypertensive action of guanethidine and clonidine by

preventing their transport into adrenergic neurones.
2.TCAs potentiate CNS depressants, including alcohol and antihistaminics.
3.Phenytoin, phenylbutazone, aspirin and CPZ can displace TCAs from protein binding sites and \
cause transient overdose symptoms.
 Selective serotonin reuptake inhibitors (SSRI)

Mechanism of action
Advantages
Drug interactions
1. SSRI inhibits CYP2D6 and CYP3A4 and hence elevates the plasma levels of certain drugs like
2. TCAs , warfarin, cisapride etc
2.SSRI+MOI leads ro elevated levels of 5-HT causing sertonin syndrome(hyperthermia, rigidity,
tremors)

MAO inhibitors

Mechanism of action- Act by inhibiting MAO that are involved in metabolism of biogenic amines
Ex:Tranylcypromine(Non selective)
Moclobemide(selective MAO-A)

Drug interactions
MAOIs + Morphine- causes severe respiratory depression
MAOIs+ Sulfonylureas(Tolbutamide)-Hypoglycemic coma
MAOIs+Chloroquine-Increased toxicity