9.5 Effects of Drugs on Nervous System

What are three ways in which drugs can increase the response at a synapse? (3)

- They can increase the amount of neurotransmitter synthesised or increase its release from vesicles.

- They can bind to postsynaptic receptors and activate them, mimicking the effect of the natural neurotransmitter.

- They can prevent the degradation of the neurotransmitter by enzymes or prevent its re-uptake into the presynaptic knob.

How does nicotine affect the synapse? (3)

- Nicotine has a molecular shape that mimics the effects of the neurotransmitter acetylcholine.

- It binds to specific acetylcholine receptors in the postsynaptic membranes known as nicotinic receptors.

- The binding of nicotine to these receptors triggers an action potential in the postsynaptic neurone.

What are the physiological effects of nicotine? (3)

- Nicotine causes a raised heart rate and an increase in blood pressure.

- It also triggers the release of the neurotransmitter dopamine, which is associated with sensations of pleasure.

- Low doses of nicotine typically produce a stimulating effect, while higher doses can block the acetylcholine receptors.

How do organophosphates affect the synapse? (3)

- Organophosphates are known as anticholinesterases as they inhibit the enzyme acetylcholinesterase.

- They competitively inhibit the enzyme by phosphorylating it, which reduces its ability to hydrolyse acetylcholine.

- As a result, the acetylcholine is not broken down, and the transmission signal is continuously stimulated, leading to muscle spasms.

What are three ways in which drugs can decrease the response at a synapse? (3)

- They can block the synthesis of the neurotransmitter.

- They can prevent the release of the neurotransmitter from vesicles at the presynaptic terminal.

- They can block the receptors on the postsynaptic membrane, preventing the neurotransmitter from binding.

How does lidocaine work? (2)

- Lidocaine molecules function by blocking voltage-gated sodium channels in the membranes of neurones.

- This action prevents the production of an action potential, particularly in sensory nerves, which is why it is used as a local anaesthetic.

What is the effect of cobra venom on the nervous system? (3)

- The primary neurotoxin in cobra venom is known as α-bungarotoxin.

- It paralyses acetylcholine receptor channels by binding specifically and irreversibly to them.

- This prevents acetylcholine from having an effect, thereby inhibiting nervous transmission and causing muscle paralysis.

How does botulinum toxin affect the neuromuscular junction? (2)

- Botulinum toxin works by preventing the release of the neurotransmitter acetylcholine from the presynaptic terminal.

- This inhibition of acetylcholine release prevents muscle contraction, resulting in flaccid paralysis.

How does a stimulus lead to a generator potential? (3)

- When a receptor cell receives a stimulus of sufficient strength, sodium ion channels in its membrane open.

- Sodium ions then move rapidly into the cell, down their concentration and electrochemical gradients.

- This movement of positive ions into the cell sets up a change in potential difference known as a generator potential.

What is the relationship between a generator potential and an action potential? (3)

- The larger the generator potential, the shorter the interval between successive action potentials, meaning it determines their frequency.

- Generator potentials are graded and do not obey the all-or-nothing law that action potentials do.

- A generator potential that is sufficient to reach the threshold potential will trigger an action potential in the associated nerve fibre.

What is convergence in a sensory system? (3)

- Convergence occurs when several receptor cells synapse with a single sensory neurone.

- If the generator potential from an individual receptor is insufficient to trigger an action potential, the potentials from several receptors can be combined or summated.

- This summation, known as convergence, can then trigger an action potential, which is an adaptation for increasing sensitivity to low-level stimuli.

How does a neurone communicate the strength of a signal? (3)

- A weak stimulus results in a low frequency of action potentials being generated along the sensory neurone.

- A strong stimulus results in a rapid stream, or high frequency, of action potentials being fired.

- Although each individual action potential obeys the all-or-nothing law, this graded frequency of response indicates the strength of the original signal.

Why does DFP inhibit the activity of acetylcholinesterase? (2)

- DFP binds irreversibly to the active site of the enzyme, which alters the specific three-dimensional shape of the active site.

- As the active site is no longer complementary to the substrate acetylcholine, an enzyme-substrate complex cannot be formed.

Why does a person poisoned with DFP have a slower heart rate? (3)

- DFP inhibits acetylcholinesterase, causing acetylcholine released by the parasympathetic nervous system to accumulate in the synaptic clefts at the sinoatrial node.

- This accumulation leads to the continuous binding of acetylcholine to the receptors on the sinoatrial node.

- The constant stimulation reduces the frequency of impulses generated by the sinoatrial node, which in turn slows down the heart rate.