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【Pharmacology】Antidepressants

Antidepressants

Depression: experience unusually long periods of sadness guilt and decreased interest in activities

  • can occur alone or a part of a larger disorder such as bipolar disorder 
  • people with bipolar disorder experience periods of depression alternating with periods of mania in which person feels abnormally optimistic euphoric and energetic 
  • Treatment: Antidepressant drugs which work by elevating levels of certain neurotransmitters in the brain
    • led to development of monoamine hypothesis

Depression


Content:

1. Monoamine hypothesis
2. Five different classes
3. Serotonergic neuron & Noradrenergic neuron
4. Drug
    a. Selective serotonin reuptake inhibitors (SSRIs)
    b. Serotonin norepinephrine reuptake inhibitors (SNRIs)
    c. Tricyclic antidepressants (TCAs)
    d. Monoamine oxidase inhibitors (MAOIs)
    e. Atypical antidepressants
5. Lithium
6. Reference


1. Monoamine hypothesis

  • states that depression results from deficiency in one or more of the three key monoamines namely serotonin, norepinephrine and dopamine
  • states that this monoamine depletion could also cause the postsynaptic receptors to upregulate, thus leading to depression
  • monoamine hypothesis of gene expression suggests that there might be an abnormal functioning gene that is responsible for causing depression

**hypotheses are overly simplistic and they don't accurately explain everything that we observed in research studies. However they do give us partial explanation as to why antidepressants work.
Monoamine hypothesis

2. Five different classes

  1. Selective serotonin reuptake inhibitors (SSRIs)
  2. Serotonin norepinephrine reuptake inhibitors (SNRIs)
  3. Tricyclic antidepressants (TCAs)
  4. Monoamine oxidase inhibitors (MAOIs)
  5. Atypical antidepressants


3. Serotonergic neuron & Noradrenergic neuron

Presynaptic serotonergic neuron (serotonin producing neuron)
Postsynaptic receptors: serotonin (5-HT receptors)
  • Serotonin is synthesized from an amino acid tryptophan by serotonergic neurons
  • Stored in vesicles awaiting regulated release
  • When these neurotransmitters are released, stimulate the receptors and transported from the synapse back to their neurons (reuptake)
    • serotonin is reabsorbed by serotonin transporter (SERT)
  • Back to the neuron, 
    • partially repackaged into synaptic vesicles 
    • partially broken down into inactive metabolites by an enzyme monoamine oxidase (MAO) 

Presynaptic noradrenergic neuron (norepinephrine producing neuron)
Postsynaptic receptors: beta and alpha-1
  • Norepinephrine is synthesized from an amino acid tyrosine by noradrenergic neurons
  • Stored in vesicles awaiting regulated release
  • When these neurotransmitters are released, stimulate the receptors and transported from the synapse back to their neurons (reuptake)
    • norepinephrine is reabsorbed by norepinephrine transporter (NET)
  • Back to the neuron, 
    • partially repackaged into synaptic vesicles 
    • partially broken down into inactive metabolites by an enzyme monoamine oxidase (MAO) 
Serotonergic neuron & Noradrenergic neuron

4. Drug

a. Selective serotonin reuptake inhibitors (SSRIs)

  • inhibit reuptake of serotonin by blocking serotonin transporter
    • results in increased levels of serotonin, available to bind to postsynaptic receptors
  • Drug:
    • Citalopram 
    • Escitalopram 
    • Fluoxetine 
    • Fluvoxamine 
    • Paroxetine
    • Sertraline
  • Treat: 
    • Depression
    • Generalized anxiety post-traumatic stress disorder
    • Obsessive-compulsive disorder
Selective serotonin reuptake inhibitors (SSRIs)

Why these antidepressants take weeks to produce maximum benefit?

Recently scientists discovered that in people with depression, G-proteins tend to cluster in the patches of brain cell membranes rich in cholesterol, called lipid rafts. 

When stuck on these rafts, G-proteins lack access to molecule, called cyclic AMP which is necessary to work and transmit signals of serotonin.

However, later on it was discovered that SSRIs also tend to build up in these lipid rafts which resulted in the gradual movement of G-proteins out of the rafts toward regions of membrane where they are able to function better.

Why these antidepressants take weeks to produce maximum benefit?



Side effects
  • Insomnia → increase anxiety and irritability
    • excessive stimulation of serotonin receptors in the brain
  • Erectile dysfunction
    • excessive stimulation of spinal serotonin receptors
  • Nausea, Vomiting, and Diarrhea
    • stimulation of serotonin receptors in the gastrointestinal tract & CNS
  • Headache, Nausea, Vomiting, Agitation and Sleep disturbances
    • abrupt withdrawal of an SSRI → temporary deficiency of synaptic serotonin

b. Serotonin norepinephrine reuptake inhibitors (SNRIs)

  • work by inhibiting reuptake of serotonin via inhibition of serotonin transporter
  • additionally inhibit norepinephrine transporter
  • results in increased levels of both serotonin and norepinephrine, which can then bind to the postsynaptic receptors
  • Drug:
    • Venlafaxine
    • Desvenlafaxine
    • Duloxetine
    • Levomilnacipran
  • Treat:
    • Depression 
    • Anxiety and panic disorders
    • Fibromyalgia as well as other pain caused by neuropathy
      • effective in reducing pain (related to enhanced noradrenergic activity)
Serotonin norepinephrine reuptake inhibitors (SNRIs)

Side effects
  • Similar to SSRIs
  • Increase blood pressure & heart rate
    • additional noradrenergic activity

c. Tricyclic antidepressants (TCAs)

  • was named after their core chemical structure which contains three rings connected together
  • primarily inhibit reuptake of both serotonin and norepinephrine by blocking both of their transporters
  • however different tricyclic agents do this with different level of selectivity
    • eg, Desipramine more selective inhibitors of norepinephrine transporter then serotonin transporter
  • TCAs also block many other receptors
    • alpha receptors 
    • histamine receptors
    • muscarinic receptors
      • responsible for their side effects more than their antidepressant activity
  • Drug:
    • Amitriptyline 
    • Amoxapine 
    • Clomipramine 
    • Desipramine 
    • Doxepin 
    • Imipramine
    • Maprotiline 
    • Nortriptyline 
    • Protriptyline
  • Treat:
    • Depression
    • Amitriptyline and Nortriptyline: migraine prevention & treatment of neuropathic pain
    • Doxepin: Insomnia
Tricyclic antidepressants (TCAs)

Side effects
  • Orthostatic hypotension & Dizziness
    • inhibition of alpha receptors
  • Sedation
    • inhibition of histamine receptors
  • Anticholinergic effects such as blurred vision, dry mouth, constipation and urinary retention
    • inhibition of muscarinic receptors
  • Cardiac conduction abnormalities
    • block cardiac sodium channels and produce effects similar to antiarrhythmic agents such as Quinidine


d. Monoamine oxidase inhibitors (MAOIs)

Monoamine oxidase is a mitochondrial enzyme that degrades monoamines such as serotonin and norepinephrine.
MAO exists in two subtypes: A and B
differently distributed in tissues such as brain, gut, and liver

i. MAO subtype A 
preferentially metabolizes serotonin, but will also metabolize norepinephrine and dopamine
inhibition of MAO subtype A is thought to be responsible for antidepressant effects

ii. MAO subtype B preferentially metabolizes dopamine

MAOIs inhibit the activity of MAO enzymes, preventing breakdown of monoamine neurotransmitters, ultimately increasing their availability

Drug:
  • Isocarboxazid 
  • Phenelzine
  • Tranylcypromine
    • irreversible inhibitors of both MAO subtype A and MAO subtype B
    • effective for treatment of depression
  • Selegiline
    • selective inhibitor of MAO subtype B
    • reducing symptoms of Parkinson's disease (depletion of dopamine) 
Monoamine oxidase inhibitors (MAOIs)

In practice, MAOIs usually a very last choice....

MAOIs show not only high incidence of drug-drug interactions, but also drug-food interactions. 
This is because MAO enzymes are present in the gut and play important role in breakdown of monoamines ingested in food.
When inhibited, MAO enzymes can't metabolize tyramine which is contained in foods that have been aged or fermented.
Built-up tyramine is taken up into the synaptic nerve terminals where it acts as a catecholamine releasing agent.
The release of large amount of catecholamines caused by tyramine leads to hypertensive crisis and potentially a stroke.
Hence, patients that are prescribed MAOIs should avoid tyramine-rich foods

e. Atypical antidepressants

includes agents that have actions at several different sites and thus don't exactly fit into the other classes

Drug:
Bupropion 
  • a weak norepinephrine and dopamine reuptake inhibitor
  • Treat:
    • depression
    • reducing nicotine cravings and withdrawal symptoms
Bupropion

Mirtazapine 
  • alpha-2 receptor antagonist
    • By blocking presynaptic alpha-2 receptors, Mirtazapine increases noradrenergic and serotonergic neurotransmission
  • have some postsynaptic serotonin receptor blocking activity & antihistaminic activity 
    • sedating effects
Mirtazapine

Trazodone & Nefazodone 
  • inhibit reuptake of serotonin
  • block postsynaptic serotonin receptors of subtype 2a
    • subtype 2a: bad serotonin receptors activation, contribute to depression
  • Antagonize histaminic H1 and adrenergic alpha-1 receptors
    • sedative effects 
Trazodone & Nefazodone

Vilazodone 
  • serotonin partial agonist reuptake inhibitor
    • it partially stimulates serotonin receptors and it inhibits reuptake of serotonin
Vilazodone

Vortioxetine
  • mechanism of action that is still a little unclear
  • but it is believed to be related to its ability to 
    • inhibit serotonin reuptake 
    • activate and block different subtypes of serotonin receptors involved in mood regulation
Vortioxetine

5. Lithium

  • mood stabilizing drug
  • initially for depression, but currently for bipolar disorders
  • Unfortunately Lithium has a fairly narrow therapeutic index
    • minor changes in dose or its blood levels can lead to toxicity
  • Mechanism of action of Lithium as a mood stabilizer is still not entirely known, but a few mechanisms of action have been proposed one in particular that has been extensively
    • studied states that Lithium inhibits the recycling of neuronal membrane inositol lipids

In the inositol lipid pathway, 
  • G-protein coupled receptors such as serotonin receptors activate phospholipase-C (PLC)
  • cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) to the signaling molecules
    • diacylglycerol (DAG)
    • inositol 1,4,5-trisphosphate (IP3)
  • IP3's action is terminated by conversion to inositol 4,5-bisphosphate (IP2)
  • enzyme inositol phosphatase comes around and dephosphorylates (IP2) to inositol phosphate (IP1)
  • another inositol phosphatase dephosphorylates IP1 to free inositol which is necessary for the regeneration of PIP2 
inositol lipid pathway

More about inositol lipid pathway: 【Covid-19】Causes & mechanisms that promote thromboinflammation in COVID-19 3e. Purinergic signaling

Lithium action
  • inhibits both inositol phosphatase enzymes 
    • thus decreases cellular responses to neurotransmitters that are linked to this second messenger system
  • was found to inhibit glycogen-synthase-kinase-3 (GSK3) mimicking the Wnt protein signaling pathway
    • Wnt proteins: secreted glycoproteins acting as a signaling molecules
    • GSK3: regulates critical processes such as axon remodelling synapse formation plasticity and neurogenesis
  • When they bind to receptors of frizzled family, 
    • they induce certain reactions which ultimately result in inhibition of GSK3
  • Abnormal activation of GSK3
    • associated with several neurological and psychiatric disorders such as bipolar disorder
      • as Lithium inhibits GSK3 directly and non-directly
Lithium action


6. Reference

https://youtu.be/T25jvLC6X0w



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 5/5/2025  居銮德教会义诊 - 罗达盛医师 （五）六味地黄丸 一位 68 岁的患者因跌倒后肩痛前来就诊，老师处方柴胡疏肝散合筋骨跌伤丸、六味地黄丸。我一如既往地认为，六味地黄丸是为了顾护患者体质、益肾固本。老师却追问：“除此之外呢？”我一时语塞，百思不得其解。老师笑着点拨：筋骨跌伤丸性属活血化瘀、消肿止痛，药性偏散；而年长患者肝肾渐亏、正气不足，为防其药性太散而伤正，故加六味地黄丸以滋阴潜阳、固护根本，取散中有收、攻中有补之意。 见我对六味地黄丸的理解仍偏狭，老师又举一例启发思考：一位 87 岁肩痛伴肢体麻木的患者，所用方为半夏天麻白术汤合镇肝熄风汤，并配伍六味地黄丸。六味地黄丸虽以滋阴补肾、顾护体质见长，但其中更蕴含“滋水涵木”之意——通过滋养肾阴，濡养肝阴，以平肝潜阳、调和风动，正契合本证肝肾同调的治则。   （六）天麻钩藤饮 VS 镇肝熄风汤 接着，老师提出一个思辨性问题：“这个患者是否可以改用天麻钩藤饮替代镇肝熄风汤？”我尝试分析其异同：天麻钩藤饮主治肝火上扰，方中用栀子、黄芩等清泄肝火，适用于肝火亢盛。而患者并未表现热象故不适宜使用。老师笑笑点头说，也要注意年龄大的患者不宜过于寒凉、攻下之品。而镇肝熄风汤则偏于肝阳上亢、因肾阴亏虚所致，其立法中存在明确的因果关系——肾虚不能制肝，致肝阳上亢、化风动扰。方中怀牛膝归肝肾经，入血分，性善下行，故重用以引血下行，并有补益肝肾之效为君。相比之下，天麻钩藤饮虽也含补肾药，但偏于平补肾气，且未必强调肝火与肾虚之间的因果链条。 此外，两方证候所对应的舌象亦有所区别：镇肝熄风汤适用于阴虚火旺之体，舌质多红、舌面偏干；而天麻钩藤饮则多用于夹湿之象，方中配伍茯神、杜仲、益母草等，具一定祛湿之功。此患者舌润，加之肢体的酸胀不适与痰有密切联系。若一味用镇肝熄风汤，恐不相宜，故原方以镇肝熄风汤为基础，加半夏天麻白术补脾燥湿、化痰熄风，以调和偏颇，契合实情。   （七）五行关系 咳嗽、干咳无痰、喉咙痛一个星期，曾有伤风史，现在已无鼻塞、流涕。舌苔腻，舌两旁有点紫。脉弦细滑。其舌脉提示有肝郁之症。但患者主诉是咳嗽，病位应属肺。故我的思路还是用桑菊饮、桑杏汤等治疗。定睛一看老师开方为柴胡疏肝散、小柴胡汤合白果定喘汤。“有一分恶寒便有一分表证”，其脉也无浮脉，说起外感病已转内。根据五行相生相克...
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【Pharmacology】General and local anesthetics

Anesthesia  A reversible condition induced by anesthetic drugs that cause reduction or complete loss of response to pain or another sensation such as consciousness and muscle movements during surgery or other invasive procedures that can be painful. Two main types of anesthesia: General anesthesia: makes the whole body lose feeling movement and consciousness drugs Local anesthesia: numbs only a specific targeted area of the body drugs   Content: 1. Anesthesia stage 2. Mechanism of action 3. General anesthetics      i. 1st group (Intravenous agents)      ii. 2nd agent (Intravenous & Inhalation agent)      iii. 3rd agent (halogenated volatile anesthetics) 4. Dexmedetomidine 5. Local anesthetics 6. Reference 1. Anesthesia stage Anesthesia performed with general anesthetics occurs in four stages: Stage 1: Induction a period during which the patient goes from state of consciousness to a state of unconsciousness Stage 2: Exc...
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【Pharmacology & 方剂学】Traditional Chinese Medicine (TCM) – Does its contemporary business booming and globalization really reconfirm its medical efficacy & safety?

Traditional Chinese Medicine (TCM) – Does its contemporary business booming and globalization really reconfirm its medical efficacy & safety? 笔记 1. Introduction 有几个国家同意中医 Promoting the globalization of TCM, Traditional Chinese medicine has been spread to 183 countries and regions around the world.  According to the World Health Organization,  103 member states have given approvalto the practice of acupuncture and moxibustion 29 have enacted special statutes on traditional medicine 18 have included acupuncture and moxibustion treatment in their medical insurance provisions  2. What's in the TCM bottle? The philosophy behind Chinese medicine is a melding of tenets from Buddhism, Confucianism, and the combined religious and philosophical ideas of Taoism.  TCM is based on the concept that illness occurs when a person's “internal Qi” falls out of balance.  Qi: the word the Chinese use to describe the un-measurable energies that theoretically permeate ev...
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【TCM & Western Medicine】阿片类药物（Opioids）& 中药

阿片类药物（Opioids） 是治疗中重度疼痛的首选药物。 其不良反应主要包括： 便秘 恶心呕吐 瘙痒 头晕 尿潴留 嗜睡 谵妄 认知障碍 呼吸抑制 Related link:  【Pharmacology】OPIOIDS 内容： 1. 癌性疼痛 2. 便秘 3. 阿片类成瘾慢性稽延症状 4. 参考文献 1. 癌性疼痛 是晚期恶性肿瘤最常见症状之一 被列为“第五生命体征” 生命四大体征：呼吸、体温、脉搏、血压 癌痛治疗的药物： 非甾体类抗炎药物 (Non-Steroidal Anti-Inflammatory Drug) 阿片类药物 (Opioids) 中医 癌性疼痛属“痛证”范畴 病因：正气亏虚、邪毒内侵 病机：“毒、瘀”壅塞经络 治疗：行气活血、化瘀解毒功效的中药组方外敷联合西药治疗 好处： 增强止痛效果 缩短止痛起效时间 延长镇痛时间从而减少爆发痛次数 提高患者的生活质量 一定的抗肿瘤作用 中药方： “双黄散结散” 全方具有清热解毒、散结止痛的作用。 君： a. 大黄 (Rhubarb) 苦寒泻热：荡涤胸腹之邪热 b. 黄柏 (Phellodendron amurense Rupr) 苦寒泻热：清下焦热 & 大黄：清热解毒散结 臣： a. 苦参 (Sophora flavescens) b. 蒲公英 (Dandelion Herb) 加强清热解毒之功 c. 三棱 (rhizoma sparganii) d. 莪术 (Curcuma) 破血逐瘀 佐使： a. 乳香 (frankincense) 行气舒筋 b. 没药 (Myrrh) 行气化瘀 & 乳香：活血定痛 c. 冰片 (Borneol) 通窍散火、消肿止痛 **现代研究亦表明，大黄、黄柏、冰片、乳香、没药、三棱、莪术、蒲公英等药物均有有很好的抑制肿瘤、止痛等作用。 另外一方： 川芎、白芷、姜黄、乳香、没药、肿节风、山慈姑、蚤休、麻黄、白芥子、王不留行 11味中药精细加工成粉并与凡士林调和而成膏状 功能：扶正气、消肿痛、活血化瘀，调畅经脉，透皮达里，引诸药直达病所。 好处： 避免了异体蛋白过敏现象 因其主要成分为植物 避免药物通过肝脏时的首过效应 其中药有效成分透过皮肤屏障，直接进入人体循环，无胃肠降解和胃肠刺激作用 治疗疼痛效果明显、持续时间长 无不良反...
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