Enumerate Therapeutic uses & Side-effects of the following a) Fluoxetine (5 t Clomiphene citrate Interferon 2 =I0 Mark) avlet I9Metronidazole C. Sreptomycin

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Therapeutic Uses and Side Effects of Five Drugs

a) Fluoxetine

Class: Selective Serotonin Reuptake Inhibitor (SSRI) Mechanism: Potent, selective inhibitor of the serotonin transporter (SERT), blocking reuptake of 5-HT. Has minimal affinity for muscarinic (ACh), alpha-1 adrenergic (α1), and histamine (H1) receptors.

Therapeutic Uses

Indication	Notes
Major Depressive Disorder (MDD)	First-line SSRI; effective in adults and adolescents
Obsessive-Compulsive Disorder (OCD)	FDA-approved
Bulimia Nervosa (BN)	60 mg/day shown effective in multiple RCTs; reduces binge/purge episodes
Panic Disorder	Approved indication
Premenstrual Dysphoric Disorder (PMDD)	Approved as Sarafem
Bipolar Depression	Used in combination (e.g., with olanzapine - "Symbyax")
Binge Eating Disorder (BED)	Off-label use
Anxiety Disorders	Generalised anxiety, social phobia

Side Effects

System	Effects
GI	Nausea, diarrhea, dry mouth, anorexia (most common early effects)
CNS/Neurological	Headache, insomnia, nervousness, tremor, dizziness
Sexual	Decreased libido, anorgasmia, ejaculatory delay (common and dose-dependent)
Cardiovascular	QTc prolongation (mild), hypertension
Metabolic	Weight loss initially; weight gain with long-term use
Serious	Serotonin syndrome (with MAOIs or serotonergic drugs), suicidality risk in adolescents (black box warning), hyponatremia (SIADH), bleeding risk (inhibits platelet serotonin)
Discontinuation	Long half-life (48-72 h parent; 180 h for active metabolite norfluoxetine) means less discontinuation syndrome vs other SSRIs

Katzung's Basic and Clinical Pharmacology, 16th Ed.
Kaplan & Sadock's Comprehensive Textbook of Psychiatry

b) Clomiphene Citrate

Class: Selective Estrogen Receptor Modulator (SERM) - triphenylethylene derivative Mechanism: Acts as an estrogen antagonist at the hypothalamus - blocks estrogen negative feedback - increases GnRH pulsatility - raises FSH/LH - induces ovulation. The two isomers: enclomiphene (trans) = potent antagonist; zuclomiphene (cis) = weak agonist.

Therapeutic Uses

Indication	Notes
Ovulation Induction	Primary use - anovulatory infertility (PCOS, hypothalamic-pituitary dysfunction, dysfunctional uterine bleeding)
Polycystic Ovary Syndrome (PCOS)	First-line agent for ovulation induction (though letrozole now preferred by many guidelines)
Amenorrhoea with anovulation	Induction of ovulatory cycles
Male hypogonadism / oligospermia	Off-label use - increases testosterone production
Luteal phase defect	Augments LH surge and progesterone production

Side Effects

Category	Effects
Vasomotor	Hot flushes/flashes (most common)
Ovarian	Ovarian enlargement, ovarian hyperstimulation syndrome (OHSS) - though milder than with gonadotropins
Visual	Blurred vision, scotomas, photophobia (indication to STOP treatment promptly)
Multiple Pregnancy	~8% rate, majority twins
Anti-estrogenic effects	Cervical mucus thickening (reduces sperm penetration), thin endometrium
GI	Nausea, bloating, abdominal discomfort
Mood	Mood swings, depression, irritability
Rare	Alopecia

Goodman & Gilman's Pharmacological Basis of Therapeutics, 14th Ed.
Berek & Novak's Gynecology

c) Interferons

Classes: IFN-α (alfa), IFN-β (beta), IFN-γ (gamma) Mechanism: Bind cell-surface receptors → induce host cell enzymes that inhibit viral RNA translation → degradation of viral mRNA and tRNA. Also have immunomodulatory and antiproliferative effects.

Therapeutic Uses

Interferon Type	Approved Indications
IFN-α (Peginterferon alfa-2a/2b)	Chronic Hepatitis B (preferred agent), Chronic Hepatitis C (in combination, though largely superseded by DAAs), Hairy cell leukaemia, Chronic myelogenous leukaemia (CML), Kaposi sarcoma, Condylomata acuminata (genital warts - HPV)
IFN-β (beta-1a, beta-1b)	Relapsing-remitting Multiple Sclerosis (reduces relapse rate)
IFN-γ	Chronic Granulomatous Disease (CGD) - reduces infection frequency

Side Effects

System	Effects
Flu-like symptoms	Fever, chills, myalgias, arthralgias, fatigue (very common, especially early in therapy)
GI	Nausea, vomiting, diarrhea, anorexia
Haematological	Bone marrow suppression: neutropaenia, thrombocytopaenia, anaemia (principal dose-limiting toxicity)
Neurological/Psychiatric	Fatigue, somnolence, behavioural disturbances, depression (common and potentially severe)
Endocrine	Autoimmune thyroiditis, hypothyroidism/hyperthyroidism
Cardiovascular	Rarely - cardiomyopathy, heart failure
Metabolic	Severe weight loss
Injection site	Local reactions (induration, erythema)

Lippincott Illustrated Reviews: Pharmacology
Goodman & Gilman's Pharmacological Basis of Therapeutics

d) Metronidazole

Class: 5-Nitroimidazole Mechanism: Prodrug - requires reductive activation of its nitro group by anaerobic/microaerophilic organisms. The activated nitro radical anion causes radical-mediated DNA strand breaks → cell death. Active only in low-oxygen environments.

Therapeutic Uses

Category	Specific Uses
Protozoal infections	Trichomoniasis (2 g single oral dose), Amoebiasis (intestinal + amoebic liver abscess - drug of choice), Giardiasis
Anaerobic bacterial infections	Bacteroides fragilis, Clostridium spp., anaerobic gram-negative bacilli - intra-abdominal sepsis, pelvic inflammatory disease
Clostridium difficile (CDI)	Historically first-line for mild CDI (now superseded by vancomycin in severe disease)
H. pylori eradication	Component of triple/quadruple therapy (e.g., PPI + amoxicillin + metronidazole ± bismuth)
Surgical prophylaxis	Pre-operative bowel preparation
Bacterial vaginosis	Oral or topical
Dental infections	Anaerobic oral flora

Side Effects

System	Effects
GI	Nausea, vomiting, metallic taste (very characteristic), dry mouth, anorexia, abdominal cramps
CNS	Headache, dizziness, vertigo, rarely encephalopathy, convulsions, ataxia, incoordination
Peripheral nervous system	Peripheral neuropathy, paraesthesia, numbness (with prolonged use - warrants discontinuation)
Urinary	Dysuria, cystitis, darkening of urine
Skin	Urticaria, flushing, pruritus; rare Stevens-Johnson syndrome
Disulfiram-like reaction	Flushing, vomiting, headache if alcohol is consumed during or within 3 days of therapy
Drug interactions	Potentiates warfarin (prolongs PT), interacts with disulfiram (psychosis), may precipitate lithium toxicity, CNS toxicity in CNS disease
Pregnancy	Avoid in 1st trimester

Goodman & Gilman's Pharmacological Basis of Therapeutics, 14th Ed.
Katzung's Basic and Clinical Pharmacology, 16th Ed.

e) Streptomycin

Class: Aminoglycoside antibiotic (first aminoglycoside - isolated from Streptomyces griseus) Mechanism: Binds irreversibly to the 30S ribosomal subunit (P12 protein) → misreading of mRNA → faulty protein synthesis → bactericidal. Active against extracellular, rapidly dividing bacilli.

Therapeutic Uses

Category	Specific Uses
Tuberculosis (TB)	Second-line agent; used in drug-resistant TB (MDR-TB) or when first-line agents cannot be used. Effective against rapidly multiplying extracellular bacilli; ineffective against persisters. Given IM/IV, 15 mg/kg/day (max 1 g/day), always in combination.
Plague	(Yersinia pestis) - drug of choice, 1 g twice daily IM + oral tetracycline
Tularemia	(Francisella tularensis) - drug of choice, 1-2 g/day IM for 10-14 days
Brucellosis	In combination with doxycycline
Endocarditis	Penicillin + streptomycin for enterococcal endocarditis; streptomycin used for gentamicin-resistant enterococcal strains
Viridans streptococcal endocarditis	2-week penicillin + streptomycin regimen

Side Effects

System	Effects
Vestibulotoxicity	The most serious toxicity - vertigo, nystagmus, loss of balance (targets vestibular apparatus preferentially over auditory); frequency proportional to patient age and blood levels
Ototoxicity	Auditory damage (deafness) - less common than vestibular damage with streptomycin; kanamycin and neomycin more cochleotoxic
Nephrotoxicity	Tubular damage - less common with streptomycin than gentamicin/tobramycin
Neuromuscular blockade	Rare - inhibits acetylcholine release and blocks nicotinic receptors; risk at high doses
Hypersensitivity	Fever, skin rashes, urticaria - more frequent with prolonged courses (e.g., TB treatment)
Injection site	Pain at IM injection site
Foetal risk	Ototoxicity reported in neonates of mothers treated with streptomycin during pregnancy (causes fetal harm)

Katzung's Basic and Clinical Pharmacology, 16th Ed.
Jawetz, Melnick & Adelberg's Medical Microbiology, 28th Ed.
Park's Textbook of Preventive and Social Medicine

Quick Summary Table

Drug	Main Use(s)	Key/Characteristic Side Effect
Fluoxetine	Depression, OCD, Bulimia, Panic disorder	Sexual dysfunction, serotonin syndrome, long t½
Clomiphene citrate	Anovulatory infertility, PCOS	Hot flushes, visual disturbances, multiple pregnancy
Interferon	Hepatitis B/C, CML, MS, CGD	Flu-like symptoms, depression, bone marrow suppression
Metronidazole	Trichomoniasis, Amebiasis, Anaerobic infections	Metallic taste, peripheral neuropathy, disulfiram-like reaction with alcohol
Streptomycin	TB (2nd line), Plague, Tularemia, Endocarditis	Vestibulotoxicity (vertigo/ataxia), ototoxicity, nephrotoxicity

Mechanism of action, uses & side-effects ofValproic acid.

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Valproic Acid (Valproate / Sodium Valproate)

Chemical nature: n-Dipropylacetic acid - a short-chain branched fatty acid. The active form at body pH is the valproate ion. Formulations include valproic acid capsules/syrup, sodium valproate, and divalproex sodium (a coordination complex of equal parts valproic acid + sodium valproate).

I. Mechanism of Action

Valproic acid has broad-spectrum antiseizure activity and its exact mechanism is not fully established. It acts via at least three complementary pathways:

1. Blockade of Voltage-Sensitive Sodium Channels (VSSCs)

Inhibits sustained repetitive neuronal firing by prolonging recovery of voltage-activated Na⁺ channels from their inactivated state
Reduces excessive sodium influx → reduces excitatory (glutamatergic) neurotransmission
This action parallels those of phenytoin and carbamazepine

2. Enhancement of GABAergic Inhibition

Stimulates glutamic acid decarboxylase (GAD) - the enzyme that synthesizes GABA
Inhibits GABA-transaminase (GABA-T) - the main GABA-degrading enzyme
Inhibits succinic semialdehyde dehydrogenase - another enzyme in GABA catabolism
Net result: ↑ GABA levels in the brain → enhanced inhibitory neurotransmission

3. Reduction of T-Type Calcium Currents

Produces a small reduction of T-type Ca²⁺ currents in thalamic neurons (similar to ethosuximide)
This action is thought to explain its efficacy against absence seizures (which depend on thalamo-cortical oscillatory circuits driven by T-type Ca²⁺)

4. Inhibition of Histone Deacetylase (HDAC)

Valproate is a potent HDAC inhibitor → modulates gene expression via epigenetic mechanisms
This may underlie some of its neuroprotective, mood-stabilizing, and anticancer properties

Summary Diagram (Stahl's Psychopharmacology):

"Valproic acid may work by interfering with voltage-sensitive sodium channels, enhancing the inhibitory actions of GABA, and regulating downstream signal transduction cascades."

II. Therapeutic Uses

A. Epilepsy (First-line broad-spectrum antiseizure drug)

Seizure Type	Notes
Generalized tonic-clonic seizures	First-line; highly effective
Absence seizures	First-line (preferred over ethosuximide when patient also has tonic-clonic seizures)
Myoclonic seizures	Drug of choice for juvenile myoclonic epilepsy (JME)
Atonic seizures	Used in Lennox-Gastaut syndrome
Focal (partial) seizures	Effective, though carbamazepine/phenytoin may be superior for complex focal seizures
Status epilepticus	IV formulation available for acute management

B. Bipolar Disorder (Mood Stabilizer)

Acute mania: First-line agent; IV infusion can rapidly stabilize agitated behavior; comparable efficacy to lithium for mixed mania and rapid cycling
Maintenance: Reduces frequency of manic and depressive episodes
Bipolar depression: Less evidence but used

C. Migraine Prophylaxis

Approved for prevention of migraine headaches; reduces frequency and severity
Not used for acute treatment

D. Other (Off-label / Emerging)

Neuropathic pain
Schizoaffective disorder (adjunct)
Post-traumatic stress disorder (PTSD)
HDAC inhibition has prompted investigation in some cancers (e.g., cutaneous T-cell lymphoma)

III. Side Effects

A. Dose-Related (Common)

System	Side Effect
GI	Nausea, vomiting, abdominal pain, heartburn, diarrhea (most common; mitigated by taking with food or using enteric-coated formulation)
CNS	Fine tremor (at higher levels), sedation, dizziness, ataxia
Metabolic	Weight gain, increased appetite
Hair	Transient hair loss (alopecia); hair may regrow curlier
Haematological	Thrombocytopaenia (idiosyncratic), platelet dysfunction
Ammonia	Hyperammonaemia → lethargy, encephalopathy (especially with urea cycle disorders - contraindicated in these patients)

B. Idiosyncratic (Serious / Rare)

Effect	Details
Hepatotoxicity	Most serious; potentially fatal hepatic failure. Risk greatest in children <2 years and those on polypharmacy. Most fatalities within first 4 months of therapy. Monitor LFTs.
Pancreatitis	Rare but life-threatening; can occur at any time in treatment
Thrombocytopaenia	Idiosyncratic; monitor platelet count

C. Teratogenicity (Major Concern)

Valproate is highly teratogenic - it is the most teratogenic of all antiepileptic drugs.

Risk	Detail
Neural tube defects	1-2% risk (spina bifida, anencephaly) - first trimester exposure
Cardiovascular malformations	Atrial/ventricular septal defects
Orofacial clefts	Cleft lip/palate
Digital/limb anomalies
Cognitive impairment	Children exposed in utero have lower IQ scores; learning disabilities
Fetal valproate syndrome	Distinctive facial features + developmental delay

Avoid in women of childbearing age wherever possible. Folic acid supplementation is essential if used.

D. Drug Interactions

Interaction	Effect
Phenobarbital	Valproate inhibits phenobarbital metabolism → ↑ phenobarbital levels → stupor/coma
Phenytoin	Displaces phenytoin from plasma proteins → ↑ free phenytoin → toxicity
Lamotrigine	Valproate dramatically reduces lamotrigine clearance (2-3× prolonged t½) → lamotrigine toxicity; require halving of lamotrigine dose
Carbamazepine	↑ carbamazepine epoxide (toxic metabolite) levels
Warfarin	Displacement from protein binding → ↑ anticoagulant effect

Quick Reference Summary

Property	Detail
Class	Short-chain branched fatty acid / Broad-spectrum AED + Mood stabilizer
MOA	Na⁺ channel blockade + ↑ GABA (GAD activation + GABA-T inhibition) + ↓ T-type Ca²⁺ + HDAC inhibition
Main uses	All seizure types, Bipolar mania/prophylaxis, Migraine prophylaxis
Characteristic side effects	GI distress, tremor, weight gain, alopecia
Serious toxicity	Fatal hepatotoxicity (esp. <2 yr), pancreatitis, teratogenicity
Contraindications	Urea cycle disorders, hepatic disease, pregnancy (relative)
Therapeutic range	50-100 mcg/mL (up to 150 mcg/mL in some cases)

Goodman & Gilman's Pharmacological Basis of Therapeutics, 14th Ed.
Katzung's Basic and Clinical Pharmacology, 16th Ed.
Stahl's Essential Psychopharmacology, 5th Ed.

Glutamate

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Glutamate as a Neurotransmitter

1. Overview

Glutamate (glutamic acid) is the principal excitatory neurotransmitter in the CNS. Key facts:

Mediates fast excitatory neurotransmission at ~80% of all brain synapses, particularly those innervating dendritic spines
Brain concentration is 10 mM - the highest of all amino acids; ~20% of this constitutes the neurotransmitter pool
Repolarization of membranes after glutamatergic depolarization accounts for up to 80% of the brain's total energy expenditure
Virtually every neuron in the CNS is innervated by glutamatergic neurons

2. Synthesis

Glutamate cannot cross the blood-brain barrier - it must be synthesised de novo inside the CNS:

Primary pathway:

Glucose → TCA cycle → α-Ketoglutarate → (transamination) → Glutamate

The Glutamine Cycle (Glutamate-Glutamine Cycle): This is the dominant recycling pathway, accounting for ~40% of brain glutamate turnover:

Presynaptic terminal          Astrocyte (glia)
     Glutamate   →  released into synapse
                          ↓  taken up by EAAT1/EAAT2
                     Glutamate
                          ↓  Glutamine synthetase (ATP-dependent, glia only)
                     Glutamine  →  released to neuron
                          ↓  Phosphate-activated glutaminase (mitochondrial)
     Glutamate  ←  recycled

Astrocytes (not neurons) express the reuptake transporters EAAT1 and EAAT2 that clear glutamate from the synapse
Glutamine synthetase is expressed only in glia - neurons lack it
This astrocyte-neuron metabolic cooperation is called the glutamate-glutamine shuttle

Storage: The neurotransmitter pool (~20%) is packaged into vesicles by the vesicular glutamate transporter (vGluT)

3. Glutamatergic Pathways in the Brain

Pathway	Details
Primary sensory afferents	Retinal ganglion cells, cochlear cells, trigeminal nerve, spinal afferents - all glutamatergic
Thalamocortical projections	Distribute sensory information to cortex via glutamate
Corticolimbic pyramidal neurons	Major source of intrinsic, associational, and efferent cortical projections
Hippocampal circuit (memory)	Perforant path → Granule cells (dentate gyrus) → CA3 pyramidal cells → CA1 pyramidal cells (4 sequential glutamatergic synapses)
Climbing fibres	Cerebellar cortex - glutamatergic
Corticospinal tract	Glutamatergic

4. Glutamate Receptors

Glutamate acts on two broad families of receptors:

A. Ionotropic Glutamate Receptors (iGluRs) — Fast Transmission

These are ligand-gated ion channels (tetramers). Three subtypes:

Ionotropic glutamate receptor diagram showing AMPA/kainate and NMDA channel properties

1) AMPA Receptors

Property	Detail
Agonist	α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)
Subunits	GluR1–GluR4 (4 subunits); tetramers
Ion permeability	Na⁺ and K⁺ primarily; GluR2 subunit restricts Ca²⁺ entry (via Q/R editing: Arg at position 607 of GluR2 blocks Ca²⁺)
Function	Mediate the fast EPSP (excitatory postsynaptic potential); primary mediators of fast excitatory transmission
Antagonist	CNQX (6-cyano-7-nitroquinoxaline-2,3-dione)
LTP/LTD	Trafficking of AMPA receptors into/out of the postsynaptic membrane underlies long-term potentiation (LTP) and long-term depression (LTD)

2) Kainate Receptors

Property	Detail
Subunits	GluR5–GluR7, KA1, KA2 (5 subunits)
Ion permeability	Na⁺ and K⁺
Location	Presynaptically on glutamatergic terminals (auto-receptors)
Function	Reduce glutamatergic neurotransmission when activated (negative feedback); role less defined than AMPA
Antagonist	CNQX

3) NMDA Receptors (Most complex and clinically important)

Property	Detail
Agonist	N-Methyl-D-aspartate (NMDA)
Subunits	NR1 (channel-forming) + NR2A-D (glutamate-binding); 7 genes
Ion permeability	Ca²⁺, Na⁺, K⁺ - highly Ca²⁺ permeable
Antagonist	APV (2-amino-5-phosphonovaleric acid); MK-801; Phencyclidine (PCP); Ketamine; Mg²⁺ (voltage-dependent)

Unique features of the NMDA receptor - it is a "coincidence detector":

Three conditions must be met simultaneously for the channel to open:

Glutamate binds to the NR2 subunit
Glycine or D-serine binds to the glycine modulatory site (GMS) on NR1 (co-agonist; mandatory)
Membrane depolarisation sufficient to expel the Mg²⁺ block from within the channel (provided by prior AMPA activation)

This triple requirement makes NMDA receptors act as molecular coincidence detectors - they only activate when both presynaptic and postsynaptic neurons are simultaneously active. This is the cellular basis of Hebbian learning ("neurons that fire together, wire together").

D-Serine is the dominant co-agonist in the forebrain - synthesised in the postsynaptic spine and released as an autocrine signal to prime NMDA receptors.

B. Metabotropic Glutamate Receptors (mGluRs) — Modulatory

Property	Detail
Type	G protein-coupled receptors (GPCRs)
Groups	Group I (mGluR1, 5) - postsynaptic, Gq-coupled → ↑IP₃/DAG → ↑Ca²⁺; Group II (mGluR2, 3) - presynaptic auto-receptors, Gi-coupled → ↓cAMP; Group III (mGluR4, 6, 7, 8) - presynaptic, Gi-coupled → ↓cAMP
Function	Primarily modulate (fine-tune) glutamatergic and GABAergic transmission; do not mediate fast EPSPs
Agonist	ACPD (trans-1-amino-1,3-cyclopentanedicarboxylic acid)

5. Synaptic Transmission Sequence

1. Action potential arrives at presynaptic terminal
2. Voltage-gated Ca²⁺ channels open → Ca²⁺ influx
3. Glutamate-containing vesicles fuse with membrane → glutamate released into cleft
4. Glutamate binds AMPA receptors → rapid Na⁺ influx → EPSP (fast depolarisation)
5. If depolarisation sufficient → Mg²⁺ expelled from NMDA channel
6. Glutamate + D-serine bind NMDA receptor → Ca²⁺ influx (slower, sustained)
7. Ca²⁺ activates kinases (CaMKII, PKC) → LTP, gene expression, synaptic plasticity
8. Glutamate cleared by astrocytic EAAT1/EAAT2 → converted to glutamine → recycled

6. Role in Synaptic Plasticity

Process	Mechanism
Long-Term Potentiation (LTP)	↑ AMPA receptors inserted into postsynaptic membrane (via PSD-95 scaffold expansion) + NMDA-dependent Ca²⁺ signalling → CaMKII activation
Long-Term Depression (LTD)	↓ AMPA receptors removed from postsynaptic membrane (PSD-95 scaffold shrinks)
Memory formation	LTP at hippocampal synapses (CA3→CA1 Schaffer collaterals) is the leading cellular model of learning and memory

AMPA receptor trafficking is continuous: half the synaptic AMPA receptors are replaced every ~15 minutes. LTP/LTD disrupt this equilibrium to strengthen or weaken synapses.

7. Clinical Relevance

Condition	Glutamate's Role
Excitotoxicity	Excess glutamate (stroke, trauma, hypoxia) → sustained NMDA activation → massive Ca²⁺ influx → mitochondrial dysfunction, free radical generation, neuronal death
Epilepsy	Excessive glutamatergic excitation; AMPA receptor autoantibodies (anti-GluA3) can cause seizures; NMDA antagonists have antiseizure properties
Schizophrenia	NMDA receptor hypofunction hypothesis: NMDA blockade (by PCP/ketamine) mimics positive and negative symptoms of schizophrenia; GWAS data link glutamate pathway genes to schizophrenia risk
Alzheimer's Disease	Tonic NMDA activation by low-level glutamate leak → synaptic noise → memantine (NMDA antagonist) used therapeutically
Depression	Ketamine (NMDA antagonist) produces rapid antidepressant effects; glutamate dysregulation implicated in MDD
Bipolar disorder	Glutamatergic hyperactivity; valproate and lithium modulate NMDA/glutamate signalling
ALS / Stroke	Motor neuron loss and ischaemic neuronal death involve excitotoxic glutamate mechanisms

8. Summary Diagram of Receptor Types

Receptor	Type	Ions	Speed	Key Feature
AMPA	iGluR	Na⁺, K⁺	Fast	Mediates EPSP
Kainate	iGluR	Na⁺, K⁺	Fast	Presynaptic auto-receptor
NMDA	iGluR	Ca²⁺, Na⁺, K⁺	Slower	Needs Glu + Gly/D-Ser + depolarisation; coincidence detector; LTP/learning
mGluR (Gp I)	mGluR (Gq)	—	Slow	Postsynaptic; ↑Ca²⁺ via IP₃
mGluR (Gp II/III)	mGluR (Gi)	—	Slow	Presynaptic; ↓glutamate release (auto-inhibition)

Kaplan & Sadock's Comprehensive Textbook of Psychiatry
Eric Kandel's Principles of Neural Science, 6th Ed.
Neuroscience: Exploring the Brain, 5th Ed.
Stahl's Essential Psychopharmacology, 5th Ed.

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