Introduction to synaptic transmission

Synaptic transmission is the process by which information passes from one neurone to another in the nervous system. This occurs at specialised junctions called synapses, allowing signals to travel efficiently through neural networks.

Synapses act as bridges between neurones, enabling the transfer of electrical signals in the form of chemical messages. This transmission begins when an electrical impulse, known as an action potential, reaches the end of one neurone and triggers a series of chemical events.

Key structures in a synapse

• Presynaptic neurone - The neurone that sends the signal, with its axon terminal containing small sacs called synaptic vesicles.
• Postsynaptic neurone - The receiving neurone, which has dendrites or a cell body that picks up the signal.
• Synaptic cleft - A small gap between the presynaptic and postsynaptic neurones, where chemical messengers are released.
• Synaptic vesicles - Tiny sacs in the axon terminal of the presynaptic neurone that store neurotransmitters.
• Receptors - Specialised protein molecules on the postsynaptic neurone that bind to neurotransmitters.
• Neurotransmitters - Chemical messengers released from synaptic vesicles that carry signals across the synaptic cleft.

The process of synaptic transmission

Synaptic transmission follows a step-by-step sequence that converts an electrical signal into a chemical one and back to electrical. This process allows information to flow from the presynaptic neurone to the postsynaptic neurone without direct physical contact.

Steps in synaptic transmission

1. Arrival of action potential - An action potential, which is an electrical impulse, travels down the axon of the presynaptic neurone and reaches the axon terminal.
2. Release of neurotransmitters - The action potential triggers synaptic vesicles to release neurotransmitters into the synaptic cleft.
3. Diffusion across the cleft - The neurotransmitters diffuse across the synaptic cleft towards the postsynaptic neurone.
4. Binding to receptors - Neurotransmitters bind to specific receptors on the dendrites or cell body of the postsynaptic neurone.
5. Generation of new signal - If the binding generates enough excitation, it triggers a new action potential in the postsynaptic neurone, continuing the signal transmission.
6. Reuptake and breakdown - Remaining neurotransmitters in the synaptic cleft undergo reuptake, where they are absorbed back into the presynaptic neurone, or they are broken down by enzymes to prevent continuous signalling.

How recreational drugs affect synaptic transmission

Recreational drugs influence synaptic transmission by altering how neurotransmitters function in the central nervous system (CNS), which includes the brain and spinal cord. Many drugs target the brain's reward pathway, a network of neurones that releases dopamine - a neurotransmitter associated with pleasure and motivation - in response to rewarding experiences.

Drugs can mimic natural neurotransmitters, block their actions, or interfere with processes like reuptake. This often leads to increased dopamine levels, creating a 'feel-good' effect that can result in cravings and addiction.

Common ways drugs alter transmission

• Mimicking neurotransmitters - Some drugs bind to receptors in place of natural neurotransmitters, activating them artificially and sending exaggerated signals.
• Blocking reuptake - Drugs can prevent the reabsorption of neurotransmitters into the presynaptic neurone, leaving more in the synaptic cleft to prolong effects.
• Increasing neurotransmitter release - Certain drugs boost the release or levels of neurotransmitters like dopamine or noradrenaline, enhancing stimulation.
• Boosting reward pathways - By overactivating dopaminergic synapses (synapses using dopamine), drugs create euphoria, but this can lead to dysphoria (a state of unease or dissatisfaction) when effects wear off, motivating further use.

Effects of specific recreational drugs on transmission

Different recreational drugs target specific neurotransmitters and processes, affecting the CNS in unique ways.

Key recreational drugs and their mechanisms

• Caffeine - Blocks adenosine receptors, preventing adenosine (a chemical that signals sleepiness) from binding. This results in increased alertness and, in moderate doses, improved reaction times, memory, and reasoning skills.
• Nicotine - Mimics acetylcholine (a neurotransmitter involved in muscle action and cognition) by binding to its receptors. This increases dopamine transmission, activating the brain's pleasure centre and creating a rewarding sensation.
• Amphetamines - Reverse the reuptake of noradrenaline and dopamine, leaving higher levels in the synapse. This produces a strong 'feel-good' factor and heightened energy.
• Cocaine - Blocks the reuptake of dopamine and noradrenaline in the presynaptic neurone, causing more to remain in the synaptic cleft. This exaggerates alertness and euphoria.
• Heroin - Boosts dopamine in reward pathways by enhancing dopaminergic synapse activation, leading to intense euphoria. As effects fade, dysphoria sets in, encouraging repeated use to recapture the high and avoid negative feelings.