CNS drugs
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Here is a full pharmacology overview of all major CNS drug classes, covering mechanism of action (MOA), clinical uses, adverse effects (ADRs), and key interactions. Based on Katzung's Basic and Clinical Pharmacology, 16th Edition and Bradley and Daroff's Neurology in Clinical Practice.
CNS Drugs - Complete Pharmacology Reference
Principle: Nearly all CNS drugs act on specific receptors that modulate synaptic transmission. Key neurotransmitters involved include GABA, glutamate, dopamine, serotonin, norepinephrine, acetylcholine, and opioid peptides. - Katzung's Basic and Clinical Pharmacology, 16e, p.577
1. SEDATIVES, HYPNOTICS & ANXIOLYTICS
Benzodiazepines
Examples: Diazepam, lorazepam, alprazolam, midazolam, clonazepam, temazepam
| Details | |
|---|---|
| MOA | Positive allosteric modulators of GABA-A receptors - increase frequency of Cl⁻ channel opening (not duration). Bind at a distinct site from GABA. |
| Uses | Anxiety disorders, panic disorder, insomnia, alcohol withdrawal, status epilepticus (IV lorazepam/diazepam), muscle relaxation, procedural sedation |
| ADRs | Sedation, anterograde amnesia, respiratory depression (especially with opioids), tolerance, dependence, withdrawal seizures on abrupt discontinuation |
| Interactions | Additive CNS depression with alcohol, opioids, antipsychotics; CYP3A4 metabolism - inhibitors (ketoconazole, erythromycin) increase levels |
Non-benzodiazepine Hypnotics ("Z-drugs")
Examples: Zolpidem, zaleplon, eszopiclone
| Details | |
|---|---|
| MOA | Selective agonists at BZ1 (ω1) subtype of GABA-A receptor. Preferentially promote sleep over anxiolysis/muscle relaxation |
| Uses | Short-term insomnia |
| ADRs | Sleepwalking/parasomnias, anterograde amnesia, next-day sedation, less dependence than BZDs |
| Interactions | Additive with other CNS depressants; CYP3A4 substrate |
Barbiturates
Examples: Phenobarbital, pentobarbital, thiopental
| Details | |
|---|---|
| MOA | Positive allosteric modulators of GABA-A - increase duration of Cl⁻ channel opening. At high doses, directly activate GABA-A receptor (no GABA required) |
| Uses | Epilepsy (phenobarbital), anesthesia induction (thiopental), refractory status epilepticus |
| ADRs | Respiratory depression (narrow therapeutic index), severe dependence, induction of CYP450 enzymes |
| Interactions | Potent CYP inducers - reduce levels of warfarin, OCP, phenytoin, and many others |
Buspirone
| Details | |
|---|---|
| MOA | Partial agonist at 5-HT1A receptors; no effect on GABA-A |
| Uses | Generalized anxiety disorder (GAD) - requires 2-4 weeks to work; no abuse potential |
| ADRs | Dizziness, nausea, headache; no sedation, no withdrawal |
| Interactions | MAOIs (avoid); CYP3A4 substrate |
2. ANTIDEPRESSANTS
SSRIs (Selective Serotonin Reuptake Inhibitors)
Examples: Fluoxetine, sertraline, paroxetine, escitalopram, citalopram, fluvoxamine
| Details | |
|---|---|
| MOA | Block SERT (serotonin transporter), increasing synaptic 5-HT. Full effect takes 2-4 weeks due to autoreceptor desensitization |
| Uses | MDD, GAD, panic disorder, OCD, PTSD, social anxiety, premenstrual dysphoric disorder, bulimia (fluoxetine) |
| ADRs | GI upset, sexual dysfunction (decreased libido, anorgasmia), insomnia/agitation, weight gain, serotonin syndrome (with MAOIs/other serotonergic agents), QTc prolongation (citalopram) |
| Interactions | MAOIs - contraindicated (risk of serotonin syndrome); fluoxetine/paroxetine are potent CYP2D6 inhibitors (increase TCA, codeine, antipsychotic levels) |
SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors)
Examples: Venlafaxine, duloxetine, desvenlafaxine, levomilnacipran
| Details | |
|---|---|
| MOA | Block both SERT and NET (norepinephrine transporter) |
| Uses | MDD, GAD, neuropathic pain (duloxetine), fibromyalgia (duloxetine), diabetic peripheral neuropathy, stress urinary incontinence (duloxetine) |
| ADRs | Similar to SSRIs + hypertension (especially venlafaxine at high doses), sweating, discontinuation syndrome (especially venlafaxine - short t½) |
| Interactions | MAOIs; SNRIs have lower CYP inhibition than SSRIs generally |
TCAs (Tricyclic Antidepressants)
Examples: Amitriptyline, imipramine, nortriptyline, clomipramine, doxepin
| Details | |
|---|---|
| MOA | Block SERT and NET; also block muscarinic (M1), histamine (H1), alpha-1 adrenergic receptors, and Na⁺ channels |
| Uses | MDD (often second-line), neuropathic pain, migraine prophylaxis, enuresis (imipramine), OCD (clomipramine), insomnia (low-dose doxepin) |
| ADRs | Anticholinergic: dry mouth, urinary retention, constipation, blurred vision; Antihistamine: sedation, weight gain; Alpha-1 block: orthostatic hypotension; Na⁺ channel block: cardiotoxicity (wide QRS), seizures in overdose - lethal in overdose |
| Interactions | MAOIs (serotonin syndrome); CNS depressants; SSRIs (inhibit CYP2D6, increase TCA levels); antiarrhythmics |
MAOIs (Monoamine Oxidase Inhibitors)
Examples: Phenelzine, tranylcypromine (irreversible); moclobemide (reversible MAO-A selective)
| Details | |
|---|---|
| MOA | Inhibit MAO-A and MAO-B, preventing breakdown of 5-HT, NE, dopamine, tyramine |
| Uses | Atypical depression, treatment-resistant depression, phobia (phenelzine) |
| ADRs | Tyramine hypertensive crisis (aged cheeses, cured meats, red wine - "cheese reaction"); serotonin syndrome; orthostatic hypotension; insomnia |
| Interactions | Tyramine-rich foods; SSRIs/SNRIs/TCAs/meperidine (serotonin syndrome); sympathomimetics; require 14-day washout before switching to/from other antidepressants (5 weeks for fluoxetine) |
Other Antidepressants
| Drug | MOA | Key Feature |
|---|---|---|
| Bupropion | Blocks DAT and NET; no serotonin activity | Smoking cessation, ADHD, no sexual dysfunction; lowers seizure threshold - avoid in eating disorders/epilepsy |
| Mirtazapine | Alpha-2 antagonist + H1 antagonist + 5-HT2/3 antagonist | Weight gain, sedation; good for depression with insomnia/weight loss |
| Trazodone | 5-HT2A antagonist + weak SERT inhibitor | Mainly used for insomnia; priapism (rare) |
| Vortioxetine | SERT inhibitor + 5-HT1A agonist + 5-HT3/7 antagonist | Cognitive benefits in depression |
3. ANTIPSYCHOTICS
First-Generation (Typical) Antipsychotics
Examples: Haloperidol, chlorpromazine, fluphenazine, perphenazine, thioridazine
| Details | |
|---|---|
| MOA | Block D2 dopamine receptors (mesolimbic pathway - antipsychotic effect). Also block D2 in nigrostriatal, tuberoinfundibular, and mesocortical pathways (causing ADRs) |
| Uses | Schizophrenia (positive symptoms), acute agitation, Tourette syndrome (haloperidol), antiemesis (prochlorperazine) |
| ADRs | EPS (extrapyramidal symptoms): Acute dystonia, akathisia, parkinsonism (all from nigrostriatal D2 block); Tardive dyskinesia (irreversible choreoathetoid movements after long-term use); Hyperprolactinemia (tuberoinfundibular block) - amenorrhea, galactorrhea; QTc prolongation (thioridazine); Neuroleptic Malignant Syndrome (NMS) - fever, rigidity, autonomic instability, elevated CK (rare but life-threatening) |
| Interactions | Additive with CNS depressants; anticholinergics can worsen sedation; drugs that prolong QT |
Second-Generation (Atypical) Antipsychotics
Examples: Clozapine, olanzapine, risperidone, quetiapine, aripiprazole, ziprasidone, paliperidone, lurasidone, asenapine, cariprazine, brexpiprazole, lumateperone
| Details | |
|---|---|
| MOA | Vary by drug, but generally D2 + 5-HT2A antagonism (serotonin-dopamine antagonists). Aripiprazole/brexpiprazole/cariprazine are D2 partial agonists ("dopamine system stabilizers"). Clozapine has low D2 affinity but high D4 + many other receptor effects |
| Uses | Schizophrenia (positive AND negative symptoms), bipolar disorder (acute mania, maintenance, bipolar depression), augmentation of antidepressants (quetiapine, aripiprazole, olanzapine), treatment-resistant schizophrenia (clozapine) |
| ADRs | Metabolic syndrome (weight gain, hyperglycemia, dyslipidemia - worst with clozapine and olanzapine); less EPS than typicals; Clozapine: agranulocytosis (1%, requires mandatory WBC monitoring), seizures, hypersalivation, myocarditis; Risperidone: most EPS among atypicals, hyperprolactinemia; Quetiapine/Olanzapine: sedation; Ziprasidone: QTc prolongation; Aripiprazole: akathisia, insomnia |
| Interactions | Clozapine + carbamazepine (both lower WBC - avoid); QTc-prolonging drugs; CYP1A2 substrates (clozapine levels fall with smoking cessation - monitor) |
4. MOOD STABILIZERS
| Drug | MOA | Uses | ADRs | Interactions |
|---|---|---|---|---|
| Lithium | Not fully known; inhibits inositol monophosphatase, modulates glycogen synthase kinase-3 (GSK-3); effects on Na⁺ transport | Bipolar disorder (gold standard for mania and maintenance), augmentation of antidepressants, cluster headaches | Narrow therapeutic index (0.6-1.2 mEq/L): Nausea/diarrhea (early), tremor (fine), polyuria/nephrogenic DI, hypothyroidism, acne, psoriasis; Toxicity: coarse tremor, ataxia, confusion, seizures, cardiac arrhythmia | NSAIDs and thiazides (increase lithium levels by reducing renal clearance - dangerous); ACE inhibitors; loop diuretics less problematic |
| Valproate | Blocks Na⁺ channels + increases GABA synthesis/release; blocks T-type Ca²⁺ channels | Bipolar (mania + maintenance), epilepsy, migraine prophylaxis | Hepatotoxicity (idiosyncratic, worst in children <2 years), pancreatitis, thrombocytopenia, weight gain, teratogenic (neural tube defects), hair loss, tremor | Strong CYP inhibitor - increases levels of lamotrigine, phenobarbital, phenytoin; potentiates CNS depressants |
| Lamotrigine | Blocks voltage-gated Na⁺ channels; also inhibits glutamate release | Bipolar (especially depression phase), epilepsy | Steven-Johnson syndrome / toxic epidermal necrolysis (if dose escalated too rapidly); dizziness, diplopia, ataxia | Valproate doubles lamotrigine levels (titrate slowly); carbamazepine/phenytoin halve lamotrigine levels |
| Carbamazepine | Blocks Na⁺ channels | Bipolar (mania), trigeminal neuralgia, epilepsy | Aplastic anemia, agranulocytosis, hyponatremia (SIADH), SJS (especially in HLA-B*1502 carriers), hepatotoxicity, diplopia/ataxia | Potent CYP3A4 inducer - reduces levels of OCP, warfarin, many drugs; auto-induction of its own metabolism |
5. ANTIEPILEPTICS (ANTICONVULSANTS)
By Mechanism:
Sodium Channel Blockers:
- Phenytoin / Fosphenytoin - epilepsy, status epilepticus; zero-order kinetics at therapeutic doses; ADRs: gingival hyperplasia, hirsutism, cerebellar ataxia, nystagmus, folate deficiency (teratogenic), purple glove syndrome (IV); potent CYP inducer
- Carbamazepine - see above
- Valproate - see above
- Lamotrigine - see above
- Oxcarbazepine - similar to carbamazepine but fewer drug interactions, lower SJS risk
- Lacosamide - enhances slow inactivation of Na⁺ channels; fewer interactions
GABA Enhancement:
- Phenobarbital - GABA-A potentiation; first-line neonatal seizures
- Benzodiazepines - status epilepticus (IV lorazepam, diazepam, clonazepam for absence)
- Tiagabine - blocks GABA reuptake (GAT-1 inhibitor)
- Vigabatrin - irreversible GABA transaminase inhibitor; infantile spasms; causes irreversible visual field defects
Glutamate (NMDA/AMPA) Antagonists:
- Perampanel - AMPA receptor antagonist; focal and generalized seizures
T-type Calcium Channel Blockers:
- Ethosuximide - first-line for absence seizures only; ADRs: GI upset, hiccups, blood dyscrasias (rare)
SV2A Ligands:
- Levetiracetam - binds synaptic vesicle protein 2A; broad-spectrum; minimal drug interactions; renally excreted; ADRs: behavioral changes, irritability
HCN Channel Blockers:
- Gabapentin / Pregabalin - bind alpha-2-delta subunit of voltage-gated Ca²⁺ channels (not GABA-ergic despite names); reduce Ca²⁺ influx and neurotransmitter release; uses: epilepsy, neuropathic pain, fibromyalgia (pregabalin), anxiety (pregabalin); ADRs: sedation, dizziness, weight gain, peripheral edema
6. ANTIPARKINSONIAN DRUGS
| Drug/Class | MOA | Uses | Key ADRs |
|---|---|---|---|
| Levodopa + Carbidopa | L-DOPA crosses BBB, converted to dopamine; carbidopa (peripheral DOPA decarboxylase inhibitor) prevents peripheral conversion, reducing nausea and allowing lower doses | Parkinson's disease (most effective) | Dyskinesias, wearing-off, on-off fluctuations, nausea, orthostatic hypotension, psychosis |
| Dopamine agonists (pramipexole, ropinirole, rotigotine) | Direct D2/D3 receptor agonists | Early PD (monotherapy), augment levodopa; restless legs syndrome | Impulse control disorders (gambling, hypersexuality), hallucinations, nausea, orthostatic hypotension, somnolence ("sleep attacks") |
| MAO-B inhibitors (selegiline, rasagiline, safinamide) | Selective MAO-B inhibition reduces dopamine breakdown | Adjunct to levodopa, early PD neuroprotection (debated) | Insomnia (selegiline metabolized to amphetamine), "cheese reaction" much less severe than MAO-A inhibitors |
| COMT inhibitors (entacapone, tolcapone, opicapone) | Inhibit COMT enzyme, preventing conversion of L-DOPA to 3-O-methyldopa; extend levodopa effect | Adjunct to levodopa to reduce wearing-off | Tolcapone: hepatotoxicity (requires LFT monitoring); entacapone: diarrhea, orange discoloration of urine |
| Amantadine | Blocks NMDA glutamate receptors, increases dopamine release | Early PD, levodopa-induced dyskinesias | Livedo reticularis, ankle edema, confusion, hallucinations |
| Anticholinergics (benztropine, trihexyphenidyl) | Block muscarinic receptors; correct dopamine/ACh imbalance | Tremor-dominant PD (less effective for bradykinesia/rigidity), drug-induced EPS | Dry mouth, urinary retention, confusion, hallucinations; avoid in elderly |
7. OPIOID ANALGESICS
Examples: Morphine, codeine, oxycodone, hydrocodone, fentanyl, hydromorphone, methadone, buprenorphine, tramadol, tapentadol
| Details | |
|---|---|
| MOA | Bind mu (µ), kappa (κ), delta (δ) opioid receptors (GPCRs). Activation decreases cAMP, opens K⁺ channels (hyperpolarization), closes Ca²⁺ channels - net effect: decreased neuronal excitability and neurotransmitter release |
| Uses | Moderate-severe pain (acute and chronic), cough suppression (codeine, dextromethorphan), diarrhea (loperamide, diphenoxylate), opioid use disorder (methadone, buprenorphine), dyspnea (morphine in palliative care) |
| ADRs | "3 Rs": Respiratory depression (most dangerous), constipation (tolerance does NOT develop), miosis; also: nausea/vomiting, sedation, euphoria/dysphoria, urinary retention, histamine release (morphine - pruritus, hypotension), SIADH, hyperalgesia (chronic use) |
| Tolerance vs. Dependence | Tolerance develops to analgesia, sedation, euphoria, respiratory depression - but NOT to constipation or miosis |
| Key drugs | Methadone: long t½ (24-36h), used for OUD and chronic pain; risk of QTc prolongation; Buprenorphine: partial µ agonist + kappa antagonist; ceiling effect on respiratory depression; combined with naloxone (Suboxone) for OUD; Tramadol: weak µ agonist + SNRI - lowers seizure threshold; serotonin syndrome risk |
| Reversal | Naloxone (IV/IN/IM) - competitive µ antagonist; short duration (30-90 min) - may need repeated dosing |
| Interactions | CNS depressants (additive respiratory depression - major risk with BZDs); MAOIs + meperidine (serotonin syndrome or opioid toxidrome); CYP3A4/2D6 involvement for many opioids |
8. GENERAL ANESTHETICS
Inhalational
| Drug | MOA | Key Feature |
|---|---|---|
| Halothane, isoflurane, sevoflurane, desflurane | Exact mechanism unclear; modulate GABA-A, NMDA, glycine receptors; may dissolve in lipid bilayers | MAC (minimum alveolar concentration) = measure of potency; high lipid solubility = high potency but slower onset/offset |
| Nitrous oxide (N₂O) | NMDA receptor antagonist | Analgesic; inactivates vitamin B12 (methionine synthase); avoid in pneumothorax |
IV Induction Agents
| Drug | MOA | Key Feature |
|---|---|---|
| Propofol | GABA-A potentiation | Rapid onset/offset; antiemetic; "propofol infusion syndrome" in prolonged high-dose use; causes pain on injection |
| Ketamine | NMDA receptor antagonist (dissociative anesthetic) | Preserves airway reflexes and cardiovascular function; bronchodilator; causes dissociation, emergence reactions, increased ICP; used in trauma/hypotensive patients |
| Etomidate | GABA-A potentiation | Minimal cardiovascular effects; adrenal suppression (single dose reduces cortisol for 12-24h) |
| Dexmedetomidine | Alpha-2 agonist | Sedation without respiratory depression; used for ICU sedation; causes bradycardia and hypotension |
9. LOCAL ANESTHETICS
Examples: Lidocaine, bupivacaine, ropivacaine, procaine, benzocaine, prilocaine
| Details | |
|---|---|
| MOA | Block voltage-gated Na⁺ channels (from inside - must cross membrane in unionized form). Block preferentially affects rapidly-firing neurons. Order of block: small myelinated > small unmyelinated > large myelinated (pain and temperature first, then autonomic, then touch/pressure, then motor last) |
| Uses | Local/regional anesthesia, epidural, spinal, topical, nerve blocks; lidocaine also used for ventricular arrhythmias |
| ADRs | CNS: perioral tingling, tinnitus, seizures, then CNS depression; Cardiac: bradycardia, heart block, ventricular fibrillation (bupivacaine most cardiotoxic) |
| Interactions | Epinephrine added to prolong duration and reduce systemic absorption (except digits, penis, nose - risk of ischemia); methemoglobinemia (benzocaine, prilocaine) |
10. CNS STIMULANTS
| Drug | MOA | Uses | Key ADRs |
|---|---|---|---|
| Amphetamine / Dextroamphetamine | Reverses DAT and NET (releases dopamine and NE into synapse); also inhibits MAO | ADHD, narcolepsy | Insomnia, anorexia, hypertension, tachycardia, growth suppression in children, psychosis (high dose), dependence |
| Methylphenidate | Blocks DAT and NET (reuptake inhibition) | ADHD, narcolepsy | Similar to amphetamines but milder; Tourette syndrome exacerbation |
| Modafinil / Armodafinil | Promotes wakefulness; unclear MOA (possibly weak DAT inhibition + orexin activation) | Narcolepsy, shift-work sleep disorder, obstructive sleep apnea (adjunct) | Headache, nausea, minimal abuse potential; CYP3A4 inducer |
| Caffeine | Adenosine receptor antagonist | Headache (analgesic adjuvant), apnea of prematurity (neonates) | Tachycardia, anxiety, insomnia, dependence |
| Cocaine | Blocks DAT, NET, SERT; also Na⁺ channel blocker | Local anesthetic for ENT procedures (only LA with vasoconstrictive properties) | Severe cardiovascular toxicity (MI, stroke), psychosis, dependence |
11. DRUGS FOR ALZHEIMER'S DISEASE
| Drug | MOA | Uses | Key ADRs |
|---|---|---|---|
| Donepezil, rivastigmine, galantamine | Acetylcholinesterase inhibitors - increase ACh in hippocampus/cortex | Mild-moderate and severe (donepezil) AD | GI upset, bradycardia, vivid dreams, syncope |
| Memantine | NMDA receptor antagonist (low-affinity, uncompetitive) - blocks excitotoxic glutamate activity | Moderate-severe AD (can be combined with AChEI) | Dizziness, headache, constipation, confusion |
| Lecanemab, Donanemab | Anti-amyloid monoclonal antibodies; clear amyloid plaques | Early AD (FDA-approved 2023) | ARIA (amyloid-related imaging abnormalities - microhemorrhages/edema); requires MRI monitoring |
12. DRUGS FOR MIGRAINE
| Class | Drug | MOA | Notes |
|---|---|---|---|
| Acute (triptans) | Sumatriptan, rizatriptan, eletriptan | 5-HT1B/1D agonists - vasoconstriction + inhibit trigeminal nerve firing | Contraindicated in ischemic heart disease, uncontrolled hypertension, basilar/hemiplegic migraine |
| Acute (CGRP antagonists) | Ubrogepant, rimegepant | CGRP receptor antagonists | Can use in cardiovascular contraindications to triptans |
| Prophylaxis | Propranolol, amitriptyline, valproate, topiramate | Various | First-line preventive agents |
| mAbs (CGRP prophylaxis) | Erenumab, fremanezumab, galcanezumab | Anti-CGRP or anti-CGRP receptor mAbs (monthly/quarterly injection) | Highly effective prevention; minimal systemic ADRs |
| Acute (ditans) | Lasmiditan | 5-HT1F agonist - no vasoconstriction | Safe in cardiovascular disease; causes dizziness, can't drive for 8h |
Quick Reference: Key Drug-Drug Interactions to Remember
| Combination | Risk |
|---|---|
| MAOI + SSRI/SNRI/TCA/tramadol/meperidine | Serotonin syndrome (fatal) - 14-day washout required |
| MAOI + tyramine foods | Hypertensive crisis |
| Opioids + benzodiazepines | Respiratory depression / overdose death |
| TCAs + MAOIs | Serotonin syndrome + adrenergic crisis |
| Lithium + NSAIDs/thiazides | Lithium toxicity |
| Valproate + lamotrigine | Lamotrigine toxicity (SJS risk) |
| Clozapine + carbamazepine | Severe neutropenia |
| Phenytoin/carbamazepine/phenobarbital + OCP/warfarin | Reduced contraceptive/anticoagulant efficacy |
Summary Classification Table
| Class | Primary Neurotransmitter Target | Key Receptor |
|---|---|---|
| Benzodiazepines | GABA | GABA-A (increase Cl⁻ frequency) |
| Barbiturates | GABA | GABA-A (increase Cl⁻ duration) |
| SSRIs/SNRIs | Serotonin (± NE) | SERT/NET reuptake inhibition |
| TCAs | Serotonin + NE | SERT, NET, M1, H1, α1 |
| MAOIs | DA, 5-HT, NE | MAO-A/B inhibition |
| Typical antipsychotics | Dopamine | D2 antagonist |
| Atypical antipsychotics | DA + 5-HT | D2 + 5-HT2A antagonist |
| Opioids | Endogenous opioids | µ, κ, δ (GPCR) |
| Levodopa | Dopamine | Dopamine precursor |
| Ethosuximide | Ca²⁺ | T-type Ca²⁺ block |
| Phenytoin | Na⁺ | Voltage-gated Na⁺ block |
| Levetiracetam | SV2A | Synaptic vesicle protein |
| AChEIs | ACh | Cholinesterase inhibition |
| Memantine | Glutamate | NMDA antagonist |
| Stimulants | DA, NE | DAT/NET |
Sources: Katzung's Basic and Clinical Pharmacology 16e; Bradley and Daroff's Neurology in Clinical Practice; Plum and Posner's Stupor and Coma; The Maudsley Prescribing Guidelines in Psychiatry 15e
Nearly all CNS drugs act on specific receptors that modulate synaptic transmission. Key neurotransmitters involved include GABA, glutamate, dopamine, serotonin, norepinephrine, acetylcholine, and opioid peptides. - Generate a image Visual of this topic
Generating Image
A detailed medical education diagram titled "CNS Drug Targets & Neurotransmitters" showing a synaptic cleft between a presynaptic neuron and postsynaptic neuron. The diagram illustrates 7 key neurotransmitter systems with color-coded pathways: GABA (blue) with GABA-A receptor showing benzodiazepines and barbiturates binding sites, Glutamate (red) with NMDA and AMPA receptors showing memantine and ketamine blocking, Dopamine (yellow) with D2 receptors showing antipsychotics blocking and levodopa pathway, Serotonin (purple) with SERT transporter showing SSRIs and 5-HT receptors with triptans, Norepinephrine (orange) with NET transporter showing SNRIs and TCAs, Acetylcholine (green) with muscarinic receptors showing AChEI drugs like donepezil, Opioid peptides (pink) with mu/kappa/delta receptors showing opioid drugs and naloxone. Each neurotransmitter and its corresponding drug class labeled clearly. Clean professional medical illustration style with a dark navy background, bright colors, anatomical accuracy, neuron cell body visible with dendrites and axon terminals, vesicles releasing neurotransmitters into synapse
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