Neurones and nerve impulses

> Cell body - contains nucleus and large amounts of RER, associated with the production of proteins and neurotransmitters.

> Dendrons - small extensions of cell body - branch into smaller fibres called dendrites, which carry nerve impulses along the cell body.

> Axon - single long fibre that carries nerve impulses away from the cell body.

> Schwann cells - surround the axon, protecting it and providing electrical insulation. Carry out Phagocytosis and aid nerve regeneration. Wrap themselves around the axon many times > layers of their memebranes build up around it.

> Myelin Sheath - forms covering to axon, made up of membranes of Schwann cells, rich in lipid, myelin. Myelinated neurones transmit nerve impulses faster.

> Nodes of Ranvier - gaps between adjacent Schwann cells where there is no myelin sheath.

Sensory neurone - transmit nerve impulse from receptor to intermediate or motor neurone. Have one dendron that carries impulse towards cell body and one axon to carry it from the cell body.

Motor neurone - transmit impulse from intermediate or sensory neurone to an effector, such as a gland or muscle. Have long axon and many short dendrites.

Intermediate neurone - transmit impulses between neurones. Have numerous short processes.

Nerve impulse = A self-propagating wave of electrical disturbance that travels along the surface of the axon membrane.

Movement of ions across axon membrane, controlled by:

> Phospholipid bilayer of the axon plasma - prevents sodium and potassium ions diffusing across it.

> Intrinsic proteins - contain ion channels (some gated) control when sodium and potassium ions can move through them. Different channels for sodium and potassium. Some remain open all the time.

> Sodium-potassium pump = intrinsic proteins that actively transport potassium ions into and sodium ions out of the axon.

As a result the inside of the axon is negatively charged relative to the outside = Resting Potential, is usually 65mV. The axon is polarised. 

1. Sodium ions are actively transported out of the axon by sodium-potassium pumps.

2. Potassium ions are actively transported into the axon by sodium-potassium pumps.

3. Three Sodium ions move out for every two potassium ions moved in.

4. As a result there are more sodium ions in the TF surrounding the axon than in the cytoplasm and more potassium ions in the axon cytoplasm than the TF surrounding it = chemical gradient.

5. Sodium ions begin to diffuse back into the axon, while potassium ions begin to move back out.

6. Most of the Potassium-gated channels are open and most of the Sodium-gated channels are closed.

7. The axon membrane is 100 times more permeable to potassium ions, which diffuse back out faster than sodium ions diffuse back in. Increases potential difference.

8. Also an electrical gradient - as more potassium ions move out > outside becomes more positive > ions are attracted by the overall negative charge of the axon cytoplasm and repelled by the positive charge of the outside.

9. Equilibrium established = chemical and electrical gradients balanced = no net movement of ions. Resting potential = Axom membrane is not transmitting a nerve impulse.

1. Some potassium voltage-gated channels are permanently open, so open at resting potential, but the sodium voltage-gated channels are closed.

2. Energy of stimulus causes some sodium voltage-gated channels to open, so sodium ions siffuse back in along their electrochemical gradient. Trigger a reversal in the potential difference across the membrane.

3. As sodium ions diffuse back in it causes more sodium channels to open > greater influx of sodium ions by diffusion.

4. Once an action potential of +40mV has been reached, the sodium ion channels close. The voltage gates on the potassium ion channels begin to open.

5. The electrical gradient is reversed so more potassium ion channels open. More potassium ions diffuse out, causing repolarisation of the axon.

6. Outward movement of potassium ions causes a temporary overshoot of the electrical gradient, so the inside of the axon is more negative than usual = hyperpolarisation. Gates on potassium ion channels now close and sodium-potassium pumps cause sodium ions to be pumped out and potassium ions to be pumped in. Resting potential re-established = repolarised.

Action Potential = Axon membrane is transmitting a nerve impulse.

The reversal of the electrical charge is reproduced at different points along the axon membrane.

As one region of the axon is depolarised, it acts as a stimulus for the depolarisation of the next region. Then the previous region of the axon membrane can return to its resting potential, it undergoes repolarisation.

1. At RP, the conc of sodium ions outside the axon membrane is high relative to the inside. Conc of potassium ions high inside relative to the outside. Axon membrane is polarised because there is a greater overall concentration of positive ions outside.

2. Stimulus causes a sudden influx of sodium ions > reversal of charge on the axon membrane = Action Potential > axon depolarised.

3. Influx of sodium ions causes sodium voltage-gated channels to open , further along the axon > influx further along causes depolarisation > behind this region the sodium voltage-gated channels close and potassium ones open. Potassium ions begin to leave the axon.

4. The action potential is propagated further along the axon. The outward movement of potassium ions continues so the axon membrane behind the action potential returns to normal (repolarised).

5. Repolarisation of the axon allows sodium ions to be actively transported out, returning the axon to its resting potential, ready for a new stimulus.

Fatty myelin sheath acts as an electrical insulator and prevents action potentials from forming.

At intervals of 1-3mm there are gaps = nodes of Ranvier, where action potentials can occur.

Localised circuits arise between adjacent nodes of Ranvier, so the AP's effectively 'jump' from one node to the next  = Saltatory conduction.

Nerve impulse = transmission of an action potential along the axon of a neurone.

Factors...

Myelin Sheath - prevents action potentials from forming in the part of the axon covered by myelin, so that saltatory conduction has to take place instead. 

Diameter of the axon - greater the diameter the faster the speed of conductance. Due to less leakage of ions from a large axon.

Temperature - higher temperature, faster the nerve impulse. Energy for active transport comes from respiration, which is controlled by enzymes > function more rapidly at higher temperature, up until a point. Above certain temperature, enzymes and plasma membrane proteins denature and impulses cannot be conducted.

Period during which the membrane  of the axon of a neurone cannot be depolarised and no new action potential can be initiated. Sodium voltage-gated channels closed. The refractory period ensures...

> Action potential propagated in one direction only - an action potential cannot be propagated in a region that is refractory. Prevents action potential from spreading out in both directions.

> It produces discrete impulses - a new action potential cannot be formed immediately after the first one. Ensures the action potentials are separated from each other.

> Limits the number of action potentials - As they are separated from each other this limits the number of action potentials that can pass along an axon in a given time.

All-or-Nothing principle = the threshold value triggers an action potential - any stimulus below the threshold value will fail to generate an action potential. Any stimulus above this value will generate an action potential. To perceive size of a stimulus...

> Number of impulses passing in a given time. Larger stimulus = more impulses in given time.

> Different neurones with different threhold values - brain interprets number & type of neurones that pass impulses.

Synapse = Junction between neurones in which they do not touch but have a narrow gap, the synaptic cleft, across which a neurotransmitter can pass. / Point at which the axon of one neurone connects with the dendrite of another, or an effector.

Neurotransmitter - chemical involved in communication between adjacent neurones.

Neurones separated by synaptic cleft 20-30nm wide. 

Presynaptic neurone releases neurotransmitter - the swollen ending of this neurone is known as the synaptic knob - processes mitochondria and large amounts of ER - required in the manufacture of neurotransmitter. 

Neurotransmitter is stored in the synaptic vesicles. Once released from the vesicles, the neurotransmitter diffuses across to the postsynaptic neurone, which has receptor molecules on its membrane to receive it.

> Allows a single impulse to be transmitted to a number of different neurones at a synapse. So a single stimulus can create a number of simultaneous responses.

> Allows a number of impulses to be combined at a synapse - so stimuli from different receptors can interact and produce a single response.

 - Neurotransmitter is made only in the presynaptic neurone.

 - Neurotransmitter which is stored in the synaptic vesicles is released into the synapse when an action potential reaches the synaptic knob.

 - Once released the neurotransmitter diffuses across the synapse to the receptor molecules on the postsynaptic neurone.

 - The neurotransmitter then binds with the receptor molecules and sets up a new action potential in the postsynaptic neurone.

Unidirectionality - can only pass impulses in one direction. Synapses act like valves.

Summation - Low-frequency action potentials produce insufficient amounts of neurotransmitter to trigger a new AP in the postsynaptic neurone. However, summation ensures they can by...

  > Spatial summation - a number of different presynaptic neurones release enough neurotransmitter to exceed the threshold value of the postsynaptic neurone. Together they trigger a new AP.

  > Temporal summation - single presynaptic neurone releases neurotransmitter many times over a short perod of time - if total amount of neurotransmitter released exceeds threshold value of postsynaptic neurone > new AP triggered.

Inhibition - On postsynaptic membrane of some synapses, the Chloride ion channels can be made to open > inward diffusion of chloride ions > inside of postsynaptic membrane more negative than resting potential = hyperpolarisation - less likely a new AP will be created = Inhibitory synapse.

Cholinergic synapse- uses acetylcholine- common in CNS/neuromuscular junctions.

1. AP arrives at presynaptic neurone > Calcium ion channels open > to synaptic knob

2. Influx of calcium ions causes synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft.

3. Acetylcholine molecules fuse with receptor sites on the sodium ion channels in the membrane of the postsynaptic neurone > sodium ion channels open > Sodium ions diffuse in rapidly.

4. Influx of sodium ions generates a new AP in the postsynaptic neurone.

5. Acetylcholinesterase hydrolyses acetylcholine back to ethanoic acid and choline > diffuse back to presynaptic neurone. Breakdown prevents it from continuously generating a new action potential in the postsynaptic neurone.

6. ATP released by mitochondria used to recombine ethanoic acid and choline > acetylcholine stored synaptic vesicles. Sodium ion channels close in absence of acetylcholine in its receptor sites.

Receptors and neurotransmitters are either...

Excitatory - create a new AP in the postsynaptic neurone 

Inhibitory - make it less likely that a new action potenital will be created in the postsynaptic neurone. 

Drugs either...

> Stimulate nervous system by creating more action potentials in the portsynaptic neurones. Mimick a neurotransmitter - stimulate release of more neurotransmitter - inhibit enzyme that breaks down neurotransmitter > enhances body's responses to impulses passed along the portsynaptic neurone.

> Inhibit nervous system by creating fewer AP's in the postsynaptic neurone - inhibit the release of neurotransmitter - block receptors on ion channels of postsynaptic neurone > reduces body's responses to impulses passed along the postsynaptic neurone.

Effect of drug depends on type of transmitter.