At the synapse, a neurone stimulates or inhibits another by releasing a neurotransmitter. The nerve impulse triggers uptake of calcium ions in the presynaptic terminal, this causing synaptic vesicles to move to the presynaptic membrane and release their neurotransmitter molecules. The neurotransmitter then diffuses across the synaptic cleft and binds to specific receptors in the postsynaptic membrane. If the neurotransmitter has a stimulating effect, then when it binds to its receptor it causes sodium channels to open in membrane of the postsynaptic neurone. This entry of sodium ions causes a partial local depolarisation, or excitatory post-synaptic potential (EPSP), and may thus generate a nerve impulse in the post-synaptic cell. Inhibitory transmitters, in contrast, open potassium gates, which then allow potassium ions to diffuse out and result in hyperpolarisation. Once the neurotransmitter has done its work, it is inactivated: it may be broken down enzymatically and/or actively reabsorbed into the presynaptic terminal. This allows the transmitter to be recycled.

Many different neurotransmitters are known to operate in the nervous system. Two of the best understood are acetylcholine (which also acts at the neuromuscular junction) and noradrenaline. Synapses that depend on noradrenaline are described as adrenergic, while acetylcholine synapses are cholinergic. A third important neurotransmitter is serotonin (also known as 5-hydroxytryptamine, or 5-HT).

Many drugs and poisons work by influencing events at synapses. Given the variety of synapses that depend on the same neurotransmitter, the relative predictability of these effects is perhaps surprising. Nicotine, for example, which is chemically similar to acetylcholine, mimics the action of acetylcholine at cholinergic synapses. Other drugs are competitive inhibitors of neurotransmitters, reducing their effectiveness by binding temporarily to the postsynaptic receptors. They do this without causing an EPSP, but they prevent the normal physiological transmitter from working. Beta-blockers operate in this way against noradrenaline, and curare has a similar effect at the neuromuscular junction. There are also drugs that work in yet another way, preventing the breakdown and/or reabsorption of the neurotransmitter after it has been released. Amphetamines have this effect at adrenergic synapses, and Prozac inhibits 5-HT reabsorption. Certain well known poisons (strychnine, and organophosphorus weedkillers, amongst others) are in this group, because they inactivate cholinesterase, the enzyme that hydrolyses acetylcholine. These substances can paralyse by causing maintained muscle contraction: the muscle is in effect unable to switch off, because the acetylcholine transmitter at the neuromuscular junction is never removed.


Question 27
Neurotransmitters "bind to specific receptors in the postsynaptic membrane." What kind of molecules will these receptors be?

A amino-acids
B phospholipids
C proteins
D sodium ions


Question 28
What will be the effect of curare on muscle contraction?

A It will cause a series of uncontrolled twitches
B It will cause a strong, maintained contraction, or tetanus
C It will cause muscle relaxation
D It will prevent nerve impulses from travelling down the motoneurone


Question 29
Of the following, which chemical will not promote extra activity in the postsynaptic neurone of the synapse that it affects?

A amphetamine
B atropine
C nicotine
D Prozac


Question 30
The drug MDMA, or "Ecstasy", blocks 5-HT carrier proteins in the presynaptic membrane. What will be the effect of this?

A accumulation of 5-HT in the presynaptic neurone and at the synapse
B short-term accumulation of 5-HT in the presynaptic neurone, but long-term depletion at the synapse
C short-term accumulation of 5-HT at the synapse, but long-term depletion in the presynaptic neurone
D short-term depletion of 5-HT in the presynaptic neurone and at the synapse

SECTION ANSWERS