Synapses

Synapses act as junctions. 

They tramsmit impulses from one neurone to another by chemicals known as neurotransmitters.

Neurones are separated by a small gap, called the synaptic cleft.

The neurone that releases the neurotransmitter is called the presynaptic neurone. The axon of this neurone ends in a swollen portion called the synaptic knob.- this has many mitochondria and endoplasmic reticulum, which are required for the manufacture of thhe neurotransmitter. 

The neurotransmitter is stored in synaptic vesicles. when released, the neurotransmitter diffuses across to the postsynaptic neurone, which has receptor molecules on its membrane to recieve it. 

Low-frequency action potentials often produce insufficient amounts of neurotransmitter to trigger a new action potential in the postsynaptic neurone. However, they can generate a new action potential by a process called summation.  

Summation entails the build-up of neurotransmitter in the synapse by one of two methods:

1) Spatial Summation- a number of different presynaptic neurones together release enough neurotransmitter to exceed the threshold value of the postsynaptic neurone. (spatial summation is exemplified in the retina of the human eye in which many rod cells share a single sensory neurone) 

2) Temporal Summation- a single presynaptic neurone releases neurotransmitter many times over a short period. If the total amount of neurotransmitter exceeds the threshold value of the postsynaptic neurone, a new action potential is triggered, i.e high frequency action potentials lead to release of large amounts of neurotransmitter. 

On the postsynaptic membrane of some synapses, the protein channels carrying chloride ions (Cl-) can be made to open.

This leads to an inward diffusion of Cl- ions, making the inside of the postsynaptic membrane even more negative than when it is at resting potential. 

This is called hyperpolarisation and makes it less likely that a new action potential will be generated (it is harder to reach threshold value of around -50mv when the membrane is hyperpolarised, around -90mv, than at resting potential of -70mv). 

Many drugs work on synapses by creating fewer action potentials in postsynaptic neurones, thus inhibiting the nervous system. 

They may do this by inhibiting the release of neurotransmitter or blocking the receptors on sodium/potassium ion channels on the postsynaptic neurone. 

Drugs such as morphine and codeine act like endorphins by binding to pain receptor sites and therefore preventing action potentials being created in the neurones of the pain pathways.

A cholinergic synapse is one in which the neurotransmitter is acetylcholine. 

1) The arrival of an action potential at the end of the presynaptic neurone causes calcium ion channels to open and Ca2+ ions to enter the synaptic knob. 

2) The influx of Ca2+ ions into the presynaptic neurone causes synaptic vesicles to fuse with the presynaptic membrane, so releasing acetylcholine into the synaptic cleft.

3) Acetylcholine molecules fuse with receptor sites on the sodium ion channel in the membrane of the postsynaptic neurone. This causes the Na+ ion channels to open , allowing Na+ ions to diffuse in rapidly along a concentration gradient. 

4) The influx of sodium ions generates a new action potential in the postsynaptic neurone. 

5) Acetylcholinesterase hydrolyses acetylcholine into choline and ethanoic acid (acetyl), which diffuse back across the synaptic cleft into the presynaptic neurone (=recycling). The breakdown of acetylcholine also prevents it from continuously generating a new action potential in the postsynaptic neurone.

6) ATP is used to recombine choline and the ethanoic acid into acetylcholine. This is stored in synaptic vesicles for future use. Sodium ion channels close in the absence of acetylcholine in the receptor sites. 

Synapses transmit impulses from one neurone to another by means of neurotransmitters. Neurotransmitters transmit an action potential from one neurone to another. 

Transmission across a cholinergic synapse:

1) An action potential arrives at the end of the presynaptic neurone- Ca2+ ion channels open, Ca2+ ions enter the synaptic knob. 

2) Synaptic vesicles fuse with the presynaptic membrane- releasing acetylcholine into the synaptic cleft. 

3) Acetylcholine fuses with receptor sites on the sodium ion channel in the membrane of the postsynaptic neurone. Sodium ion channels open. Na+ ions diffuse in along a concentration gradient, generating a new action potential in the postsynaptic neurone. 

4) The enzyme Acetylcholinesterase hydrolyses acetylcholine to choline and ethanoic acid- which diffuse back across the synaptic cleft into the presynaptic neurone, here ATP is used to reform the acetylcholine. 

5) Sodium ion channels close in the absence of acetylcholine in the receptor sites.