|
| Neurones |
- Soma: nerve cell body / contains nucleus, cell organelles / synthesise of neurotransmitter
- Dendrites: branching extensions from nerve cell soma
Stimulated by other neurones \ transmit impulses towards soma
- Axon: single extension that extends from the soma to the target cell
- Myelinated axon is surrounded by Schwann cells (myelin sheath)
- Have nodes of Ranvier and are rich in myelin (lipid)
|
Table 16-7-1
| NEURONE |
STIMULATED BY |
TRANSMITS IMPULSES TO |
STRUCTURE |
| Sensory |
Receptor |
Relay neurone |
Cell body in root cell ganglion |
| Relay |
Sensory neurone |
Motor neurone |
No axon |
| Motor/effector |
Relay neurone |
Gland, muscle
(effector organ) |
Schwann cells |
|
Action Potentials And Nerve Impulses |
| Change In Membrane Permeability Leading To The Generation Of An Action Potential |
- Stimulus reaches threshold
- Voltage-regulated sodium channels open / influx of Na+ / down electrochemical gradient / +ve feedback
- Depolarisation / inside becomes +ve / membrane potential reverses
- //Depolarisation opens sodium channels in adjacent membrane
- Potassium channels open (slower than Na+ gates) / diffusion of K+ ions out of neurone
- Repolarisation
- Sodium channels close
- Hyperpolarisation due to overshoot in movement of K+out of the cell
- //Membrane potential is lower than resting potential
- //Interior of the cell becomes -ve \ membrane is more permeable to K+ ions than to Na+ ions
- Sodium-potassium pump restores RESTING POTENTIAL
[GRAPH] Highest positive membrane potential is the action potential
|
The Role Of The Neurone Membrane In The Establishment Of A Resting Potential |
- MEMBRANE IS POLARISED: inside of axon is more -ve than outside
- A resting potential of -70mV is maintained by [EXAM BYA7 JUN2002]
- Negatively charged proteins/large anions inside axon
- Membrane more permeable to K+ ions than to Na+ ions / K+ ions move out faster than Na+ ions diffuse in
- Sodium/potassium pump / Na+ ions pumped out faster than K+ ions pumped in
- Electrochemical gradient determines movement of ions
- K+ cannot move down its conc. gradient
- Build up of positive Na+ outside membrane repels K+
- Imbalance of negative ions causes potential difference/voltage
- Cl- cannot move down its conc gradient
- Negatively charged proteins in cytoplasm repel Cl-
|
The All-Or Nothing Nature Of Nerve Impulses |
- Once action potential starts, it travels to a synapse
- Stimulus must cause sufficient movement of Na+ and K+ to depolarise the membrane and
cause an action potential
- Threshold stimulus → impulse that causes an action potential
- Stimulus transmits an impulse at a constant and max strength
- Transmission is independent of any intensity of the stimulus
- High frequency of impulses / more amount of sodium entry / more ATP
- Subthreshold stimulus → stimulus weaker than a threshold stimulus
- Summation → series of subthreshold stimuli cumulate to cause an action potential
|
Refractory Period |
- Represents a time during which the membrane cannot be depolarised again
- During repolarisation and hyperpolarisation
- Membrane is impermeable to Na+ ions / sodium ion channels closed
- Sodium ions cannot enter axon
- K+ ions move out as membrane is more permeable to K+ ions
- Membrane becomes more negative than resting potential
- Nerve impulses can only travel in one direction
- Action potential can only depolarise the membrane in front
- Membrane behind is recovering from refractory period (previous action potential)
- Limits frequency with which neurones can transmit impulses
|
Factors Affecting the Speed of Conductance: Myelin, Axon Diameter, Temperature |
- Impulses travel faster in myelinated neurones → SALTATORY CONDUCTION
- Schwann cells prevent diffusion of ions
- Flow of current between adjacent nodes of Ranvier
- \ depolarisation only at nodes of Ranvier
- Action potential jumps from node to node
- Temp affects speed of conduction of impulses
- Higher temp increases rate of diffusion of ions
- Impulses faster in an axon with larger diameter
- Small cells / large surface area:volume ratio / ion leakage weakens membrane
- Myelin stops ion leakage \ diameter only important for unmyelinated neurones
|
Synaptic Transmission |
- Synaptic cleft (gap) of 20μm separates two neurones at a synapse (junction of 2 neurones)
- Presynaptic membrane is at the end of a neurone
- Postsynaptic membrane is at the next neurone in the chain
- Synaptic knob of a presynaptic neurone contains
- Neurotransmitters in small vesicles
- Mitochondria to produce ATP needed for neurotransmitter synthesis
|
Aspects Of Synaptic Transmission |
| Unidirectional |
- Neurotransmitter always travels from pre- to postsynaptic membrane
- \ Flow in one direction only, action potential only in postsynaptic neurone
|
Summation |
- Several presynaptic neurones release neurotransmitter
- Cumulative effect reaches a threshold to depolarise postsynaptic membrane
- E.g. rod cells when they synapse with relay neurones in the retina
- Spatial summation
- Several impulses arrive at one neurone via
several synapses
- Cause sufficient depolarisation / open sufficient sodium ion channels
- For threshold to be reached
- Temporal summation
- Several impulses arrive at same neurone via
same synapse
- Threshold → action potential
|
Inhibition |
- More inhibitory postsynaptic potentials IPSPs than excitatory postsynaptic potentials EPSPs
- Reduces membrane potential / makes more negative
- Hyperpolarisation of postsynaptic membrane
- Cancels effect of action potential when several synapses
|
The Mechanisms Of Transmission At An Excitatory Synapse |
- Nerve impulse reaches synaptic knob/presynaptic membrane/neurone
- Depolarisation opens Ca2+ gates / calcium ions enter
- Ca2+ causes vesicles containing neurotransmitter to fuse with membrane
- Release of neurotransmitter / into synaptic cleft / by exocytosis
- Diffuse across synaptic cleft
- Neurotransmitter binds to specific receptors in postsynaptic membrane
- Sodium channels open / sodium ions enter
Depolarisation of postsynaptic membrane Threshold causes an action potential along postsynaptic neurone
- Neurotransmitter are quickly removed from the postsynaptic membrane
Diffuse out of the synaptic cleft Taken up by presynaptic membrane by endocytosis Enzymes break down neurotransmitters into inactive substances
|
Knowledge Of Transmitters Limited To Acetylcholine And Noradrenaline |
- Acetylcholine released by
- motor neurones on to muscle cells
- neurones in the parasympathetic division of the ANS (autonomic nervous system)
- Noradrenaline is released in the sympathetic division of the ANS
//The international name for noradrenaline is now norepinephrine
|
The Agonistic And Antagonistic Effects Of Chemicals On Synaptic Transmission |
- Agonists/antagonists are similar in shape to neurotransmitter
- Fit into specific protein receptors of postsynaptic membrane
- Agonists → same effect as neurotransmitter
- Anatoxin produced by some algae and mimics effect of acetylcholine
- Swallowing H2O contaminated with anatoxin causes continuous salvation in mouth
- Antagonists block action of neurotransmitter
- Prevent neurotransmitter from binding with their receptor sites
- High blood pressure can be treated by drugs called β-blockers
- Antagonist of adrenaline-receptors on membrane of muscle cells in heart
- Curare blocks action of acetylcholine at the junction of nerves and muscles
- Useful as a general muscle relaxant in patients undergoing major surgery
|
|
|
