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BiologyNeural Control
The specific receptors for neurotransmitters in a synapse are present on:
Options
1
Post-synaptic membrane
2
Pre-synaptic membrane
3
Myelin sheath
4
Schwann cell
Correct Answer
Post-synaptic membrane
Solution
1

Synapse structure:

Pre-synaptic terminal (knob) → synaptic cleft (20-50 nm gap) → post-synaptic membrane

2

Pre-synaptic: releases neurotransmitters (from synaptic vesicles)

Post-synaptic membrane: HAS the RECEPTORS for neurotransmitters ✅

Myelin sheath and Schwann cells: insulation — not involved in neurotransmission

Neurotransmitter receptors = POST-SYNAPTIC MEMBRANE
Pre-synaptic releases NT → crosses cleft → binds receptors on POST-synaptic membrane
Theory: Neural Control
1. Synapse — Structure and Function

A synapse is the junction between two neurons (or between a neuron and an effector). Three components: Pre-synaptic terminal (bouton): knob-like ending of the axon. Contains mitochondria (ATP for vesicle release) and synaptic vesicles (store neurotransmitters). Synaptic cleft: narrow gap of 20-50 nm between pre and post-synaptic membranes. Post-synaptic membrane: membrane of the receiving cell (dendrite, cell body, or effector). Contains specific RECEPTORS for neurotransmitters. Process of synaptic transmission: Action potential arrives at pre-synaptic terminal → voltage-gated Ca2+ channels open → Ca2+ influx → synaptic vesicles fuse with pre-synaptic membrane (exocytosis) → neurotransmitters released into cleft → diffuse across cleft → bind to receptors on post-synaptic membrane → receptor-mediated response (depolarisation or hyperpolarisation of post-synaptic cell).

2. Neurotransmitters — Types and Effects

Neurotransmitters are chemical messengers released at synapses. Classification by effect: Excitatory: cause depolarisation of post-synaptic membrane (EPSP — Excitatory Post-Synaptic Potential). Brings membrane potential closer to action potential threshold. Inhibitory: cause hyperpolarisation (IPSP — Inhibitory Post-Synaptic Potential). Moves membrane potential further from threshold. Main neurotransmitters: Acetylcholine (ACh): at neuromuscular junction (NMJ) — excitatory. At some CNS synapses. Broken down by acetylcholinesterase (AChE). Glutamate: main EXCITATORY neurotransmitter in CNS. Binds AMPA, NMDA, kainate receptors. GABA (gamma-aminobutyric acid): main INHIBITORY neurotransmitter in CNS. Dopamine: reward, movement, motivation. Reduced in Parkinson disease. Excessive in schizophrenia. Serotonin (5-HT): mood, sleep, appetite. Low in depression → SSRIs increase it. Noradrenaline (norepinephrine): fight-or-flight, attention. Glycine: inhibitory in spinal cord.

3. Receptor Types — Ionotropic and Metabotropic

Two main types of post-synaptic receptors: Ionotropic receptors (ligand-gated ion channels): neurotransmitter binding directly opens ion channel. Fast response (milliseconds). Examples: Nicotinic ACh receptor (nAChR): ACh → Na+ influx + K+ efflux → depolarisation → action potential. At NMJ (muscle) and some brain synapses. AMPA receptor: glutamate → Na+ influx → EPSP. GABA-A receptor: GABA → Cl- influx → hyperpolarisation → IPSP. Glycine receptor: Cl- influx → inhibition. Metabotropic receptors (G-protein coupled receptors, GPCR): neurotransmitter binds → activates G-protein → second messenger cascade. Slower but longer-lasting effect. Examples: Muscarinic ACh receptor (mAChR): heart, smooth muscle, glands. Coupled to Gi (heart — slows rate) or Gq. GABA-B receptor. Dopamine receptors (D1-D5). Most serotonin receptors.

4. Action Potential and Nerve Impulse

Action potential (AP): the electrical signal that travels along a neuron. Resting membrane potential: -70 mV (inside negative). Maintained by Na+/K+-ATPase (3 Na+ out, 2 K+ in per ATP). K+ channels open → K+ leaks out → inside negative. Depolarisation: stimulus opens voltage-gated Na+ channels → Na+ rushes in → inside becomes positive → membrane depolarises (reaches -55 mV threshold → AP fires). Peak: +30 to +40 mV. Repolarisation: Na+ channels inactivate → K+ channels open → K+ rushes out → membrane repolarises. Hyperpolarisation (afterhyperpolarisation): K+ channels slow to close → membrane overshoots negative resting potential. Refractory period: absolute (no AP possible during Na+ channel inactivation) + relative (AP possible with stronger stimulus). All-or-nothing law: AP is all-or-nothing — once threshold reached, full AP fires regardless of stimulus strength. AP propagates along axon without decay.

5. Saltatory Conduction in Myelinated Nerves

Myelinated nerve fibres conduct signals faster and more efficiently than unmyelinated fibres. Myelin sheath: formed by Schwann cells (PNS) or oligodendrocytes (CNS) wrapping around the axon. Composed mainly of lipids (sphingomyelin) and proteins. Provides electrical insulation. Nodes of Ranvier: short gaps (1-2 micrometres) in the myelin sheath where axon membrane is exposed. Voltage-gated Na+ channels concentrated at nodes. Saltatory conduction: action potential jumps from node to node (saltatory = Latin for jumping). Current flows through myelinated internodal segments instantly (capacitative current) to next node → depolarises next node → fires AP → jumps to next node. Speed: myelinated fibres up to 120 m/s. Unmyelinated: 0.5-2 m/s. Myelinated fibres are also more energy-efficient (Na+/K+-ATPase only needs to restore ions at nodes). Demyelinating diseases: Multiple Sclerosis (MS) — autoimmune destruction of myelin in CNS → slowed/blocked conduction → variable neurological symptoms. Guillain-Barre syndrome — demyelination of PNS → ascending paralysis.

6. Neuromuscular Junction (NMJ)

The NMJ is a specialised synapse between a motor neuron and skeletal muscle fibre. Pre-synaptic: terminal bouton of motor neuron. Contains ACh in synaptic vesicles. Post-synaptic: motor end plate of muscle fibre (sarcolemma). Contains nicotinic ACh receptors (nAChR) — ionotropic. Process: AP reaches motor terminal → Ca2+ influx → ACh released → ACh diffuses across synaptic cleft → ACh binds nAChR on motor end plate → nAChR opens (Na+ in, K+ out) → end plate potential (EPP) → triggers AP in sarcolemma → muscle contraction. Termination: acetylcholinesterase (AChE) in synaptic cleft breaks ACh → choline + acetate → choline taken up for new ACh synthesis. Clinical importance: Myasthenia gravis: autoimmune attack on nAChR → fewer functional receptors → muscle weakness. Treated with AChE inhibitors (neostigmine, pyridostigmine) → more ACh available. Botulinum toxin (Botox): blocks ACh release from pre-synaptic terminal → flaccid paralysis. Organophosphate pesticides: inhibit AChE → ACh accumulates → continuous muscle stimulation → spasm.

7. Reflex Arc

Reflex: automatic, rapid, stereotyped response to a stimulus that does not require conscious thought. Components of a reflex arc: Receptor: detects stimulus. Sensory (afferent) neuron: carries impulse from receptor to spinal cord (via dorsal root). Integration centre: spinal cord (or brain). Interneuron: connects sensory and motor neurons (in polysynaptic reflexes). Motor (efferent) neuron: carries impulse from spinal cord to effector (via ventral root). Effector: muscle or gland. Types of reflexes: Monosynaptic (stretch reflex): only one synapse (sensory → motor). Example: knee-jerk reflex (patellar tendon tap → quadriceps contraction). Polysynaptic: two or more synapses. Most reflexes. Example: withdrawal reflex (pain → flexor muscles contract, extensor relax). Spinal reflexes: mediated by spinal cord. Do not need brain. Can occur even after spinal cord injury (spinal shock then reflex recovery). Cranial reflexes: mediated by brainstem. Pupillary light reflex, gag reflex, blink reflex.

8. Central vs Peripheral Nervous System

CNS (Central Nervous System): brain + spinal cord. Brain parts: Forebrain: cerebrum (highest functions — thought, language, voluntary movement, sensory), limbic system (emotion, memory, smell), thalamus (relay station), hypothalamus (homeostasis, autonomic). Midbrain: visual and auditory reflexes, reticular activating system. Hindbrain: pons (breathing rhythm, sleep), cerebellum (coordination, balance, fine motor), medulla oblongata (vital functions — heart rate, blood pressure, breathing). Spinal cord: 31 segments (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal). Reflex centre. Ascending (sensory) and descending (motor) tracts. PNS (Peripheral Nervous System): Somatic: voluntary (skeletal muscle control). Motor: CNS → skeletal muscle. Sensory: receptors → CNS. Autonomic: involuntary (smooth muscle, cardiac muscle, glands). Sympathetic (fight-or-flight): thoracolumbar. Parasympathetic (rest-and-digest): craniosacral.

Frequently Asked Questions
1. What are the components of a synapse? ⌄
A synapse has three main components: Pre-synaptic terminal (bouton): bulb-like ending of the transmitting neuron (usually axon terminal). Contains: mitochondria (ATP production for vesicle fusion), synaptic vesicles (membrane-bound sacs containing neurotransmitters), voltage-gated Ca2+ channels (open when AP arrives). Synaptic cleft: fluid-filled gap between pre and post-synaptic membranes. Width: 20-50 nm. Contains: synaptic basement membrane, enzymes for neurotransmitter breakdown (e.g., AChE), extracellular matrix proteins. Post-synaptic membrane: membrane of the receiving cell. Contains: specific receptor proteins for the neurotransmitter (this is what the question asks about). Ion channels associated with receptors. Amplification machinery (G-proteins, second messengers for metabotropic receptors). The specificity of neurotransmission: each neurotransmitter has specific receptors on the post-synaptic membrane that recognise only that neurotransmitter.
2. What is the difference between EPSP and IPSP? ⌄
EPSP (Excitatory Post-Synaptic Potential): depolarisation of post-synaptic membrane (inside becomes less negative). Caused by: Na+ influx through ionotropic receptors (e.g., AMPA receptor responding to glutamate). K+ efflux or Ca2+ influx can also contribute. Effect: brings membrane closer to threshold for action potential. Does not itself cause AP unless threshold reached. IPSP (Inhibitory Post-Synaptic Potential): hyperpolarisation of post-synaptic membrane (inside becomes more negative). Caused by: Cl- influx through GABA-A or glycine receptors. K+ efflux through GABA-B or other receptors. Effect: moves membrane further from threshold → harder to fire AP. Spatial and temporal summation: a single EPSP usually not enough to fire AP. Multiple EPSPs summate: Temporal summation: rapid successive EPSPs from same synapse add up. Spatial summation: EPSPs from multiple synapses add up simultaneously. If total depolarisation reaches threshold: AP fires.
3. What is acetylcholinesterase and why is it important? ⌄
Acetylcholinesterase (AChE) is an enzyme located in the synaptic cleft (and on post-synaptic membrane) that rapidly breaks down acetylcholine (ACh) after it has bound to its receptor. Reaction: ACh → choline + acetate. Speed: one of fastest enzymes known, breaks down ~25,000 ACh molecules per second. Importance: without AChE, ACh would remain bound → continuous receptor stimulation → sustained muscle contraction or gland secretion → uncontrolled. AChE terminates the signal → allows rapid ON-OFF cycling of the synapse. Clinical/toxicological relevance: Nerve agents (sarin, VX, tabun): irreversible AChE inhibitors → ACh accumulates → overstimulation → SLUDGE symptoms (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis) → eventually respiratory failure. Treatment: atropine (blocks muscarinic ACh receptors) + pralidoxime (if given quickly, reactivates AChE). Organophosphate pesticides (malathion, parathion): reversible AChE inhibitors. Same mechanism. Agricultural workers exposure risk.
4. What happens at the neuromuscular junction when a nerve impulse arrives? ⌄
Detailed sequence at NMJ: (1) Action potential propagates along motor neuron axon to the terminal bouton. (2) Depolarisation of terminal membrane → voltage-gated Ca2+ channels open → Ca2+ enters terminal from extracellular fluid. (3) Elevated intracellular Ca2+ → triggers fusion of synaptic vesicles containing ACh with pre-synaptic membrane (SNARE protein-mediated exocytosis). (4) ACh released into synaptic cleft in quanta (~10,000 molecules per vesicle). (5) ACh diffuses across 20-50 nm cleft to motor end plate. (6) ACh binds to nicotinic ACh receptors (nAChR) on post-synaptic sarcolemma. (7) nAChR opens (it is an ion channel itself) → Na+ rushes in, K+ out → end plate potential (EPP) generated. (8) EPP spreads along sarcolemma → reaches threshold → triggers AP in muscle fibre → propagates along T-tubules → Ca2+ release from SR → muscle contraction. (9) Meanwhile: AChE breaks down ACh → signal terminated → receptor closes → sarcolemma repolarises ready for next signal.
5. What drugs affect synaptic transmission? ⌄
Many drugs work by modifying synaptic transmission: Drugs that increase neurotransmitter activity: AChE inhibitors: neostigmine (myasthenia gravis), physostigmine, organophosphates. SSRIs: block serotonin reuptake transporter → more serotonin in cleft (antidepressants: fluoxetine, sertraline). Cocaine/amphetamines: block monoamine reuptake transporters. L-DOPA: precursor to dopamine → increases dopamine (Parkinson treatment). Drugs that decrease neurotransmitter activity: Atropine: blocks muscarinic ACh receptors. Used for bradycardia, organophosphate poisoning. Botulinum toxin: blocks ACh vesicle release at NMJ → flaccid paralysis → cosmetically used for wrinkles. Haloperidol/chlorpromazine: block dopamine receptors → antipsychotics (schizophrenia). Beta-blockers: block beta-adrenergic receptors → heart rate reduction. Benzodiazepines: enhance GABA-A receptor → more Cl- → sedation, anxiolysis, anticonvulsant. Anaesthetics (local): block Na+ channels → prevent AP → local anaesthesia (lidocaine, bupivacaine).
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