How the Central Nervous System Works and Effects of Drugs (Edexcel A-Level Psychology): Revision Notes
How the Central Nervous System Works and Effects of Drugs
The central nervous system (CNS) forms the core processing centre for all human behaviour. It comprises the brain and spinal cord, working together to receive sensory information, process it, and coordinate appropriate responses. Understanding how the CNS functions at a cellular level, particularly through neurons and neurotransmitter systems, is essential for explaining behaviour and the effects of psychoactive substances.
Structure and function of neurons
What is a neuron?
A neuron is a specialised cell within the nervous system designed to transmit information. The CNS contains billions of neurons that communicate with approximately 1,000 other cells simultaneously, forming vast interconnected networks. These networks allow the brain to process incoming sensory data and control behavioural responses.
Each neuron in the CNS can communicate with approximately 1,000 other cells simultaneously, creating incredibly complex networks that enable all our thoughts, feelings, and behaviours.
Components of the neuron
Each neuron consists of four main structural components, each serving a distinct function:
The cell body contains the nucleus, which houses the genetic material specific to that neuron. The cell body also contains mitochondria, the sites where aerobic respiration occurs to release energy from glucose. This energy powers all cellular activities within the neuron.
Dendrites are branch-like structures extending from the cell body. Their primary function is to receive incoming messages from other neurons. When neighbouring neurons send signals, these messages arrive at the dendrites, which then trigger an action potential (electrical impulse) within the receiving cell.
The axon is a long extension from the cell body that carries electrical impulses away from the cell body towards other neurons or target tissues. The point where the axon connects to the cell body is called the axon hillock, where nerve impulses are initiated. Surrounding the axon is the myelin sheath, a fatty insulating layer that serves two purposes: it provides electrical insulation and speeds up the transmission of nerve impulses. The myelin sheath is not continuous; gaps between the myelin-covered sections are called nodes of Ranvier, which allow the electrical signal to jump between sections, further increasing transmission speed.
The myelin sheath is crucial for rapid neural communication. Without it, nerve signals would travel much more slowly, severely impairing our ability to respond quickly to our environment. This is why diseases that damage myelin, such as multiple sclerosis, cause such significant motor and cognitive impairments.
Axon terminals (also called terminal buttons or terminal boutons) are located at the very end of the axon. These bulb-shaped structures contain tiny sacs called vesicles, which store molecules of neurotransmitters. Neurotransmitters are chemicals that transmit messages between neurons. When an electrical impulse reaches the axon terminals, it triggers the release of these neurotransmitters into the space between neurons.
How neurons communicate: the action potential
Resting membrane potential
Neurons maintain a difference in electrical charge between the inside and outside of the cell membrane when at rest. This is called the resting membrane potential, which is approximately . The negative value indicates that the inside of the neuron has a slight negative charge relative to the outside.
When a neuron receives a message from another neuron, this incoming signal is a chemical message that can either stimulate (excite) or inhibit the receiving neuron. An excitatory message causes excitatory postsynaptic potential (EPSP), which slightly depolarises the neuron by reducing its negative charge. This makes the neuron more likely to fire an action potential. Conversely, an inhibitory message causes inhibitory postsynaptic potential (IPSP), which can hyperpolarise the neuron (make it more negative) or prevent depolarisation, making it less likely to fire.
Triggering the action potential
A neuron must receive sufficient excitatory input to reach its threshold before firing. The action potential is triggered when the neuron's charge reaches approximately . This occurs when enough excitatory messages are received, or when excitatory messages sufficiently outnumber inhibitory messages.
Once triggered, the action potential is a rapid electrical impulse that travels along the axon towards the axon terminals. The process occurs in stages:
Worked Example: The Action Potential Sequence
- At rest: The neuron's inside is negatively charged relative to the outside (approximately )
- Depolarisation begins: When stimulated, positively charged particles enter the cell, initiating depolarisation - the action potential begins and the charge rises to approximately and beyond
- Repolarisation: After a brief period, positively charged particles are pushed back outside the neuron, and the neuron begins returning to its polarised resting state
- Return to resting state: The neuron returns to its initial polarised resting state (), ready to fire again
The action potential propagates along the axon like a wave, eventually reaching the axon terminals where it stimulates neurotransmitter release.
Synaptic transmission
From electrical to chemical signalling
The neuron's electrical impulse remains electrical only while travelling along the axon. When it reaches the terminal button, a transformation occurs: the electrical signal converts into a chemical message. This conversion is necessary because neurons do not physically touch each other; there is a tiny gap between them called the synaptic gap (or synaptic cleft).
The neuron sending the message is termed the presynaptic neuron, whilst the one receiving the message is the postsynaptic neuron.
The process of synaptic transmission
When the action potential reaches the axon terminal, calcium channels open, allowing calcium ions to flood into the terminal button. This calcium influx triggers vesicles containing neurotransmitters to move toward the outer membrane of the terminal button. The vesicle casing then fuses with this membrane, releasing neurotransmitter molecules into the synaptic gap/cleft through a process called exocytosis.
The neurotransmitter molecules diffuse across the synaptic gap and bind to specialised receptors on the postsynaptic neuron. These receptors are designed to recognise and bind to specific neurotransmitter molecules, much like a lock and key. When the neurotransmitter binds to its receptor, it either stimulates or inhibits the postsynaptic neuron, depending on the type of neurotransmitter and receptor involved.
The lock-and-key mechanism ensures specificity in neural communication. Each neurotransmitter can only bind to its specific receptor type, ensuring that messages are delivered accurately and to the correct locations in the nervous system.
Reuptake
Not all released neurotransmitter molecules bind to postsynaptic receptors. Some are broken down by enzymes in the synaptic gap/cleft. Others are reabsorbed by the presynaptic neuron through a process called reuptake. During reuptake, unused neurotransmitter molecules are absorbed back into the presynaptic neuron. Once inside, enzymes destroy these molecules, effectively "turning off" the neuron in preparation for the next action potential. This reuptake mechanism is important for regulating neurotransmitter levels and ensuring neurons can respond to new signals.
Reuptake is a critical regulatory mechanism. Many psychiatric medications, such as selective serotonin reuptake inhibitors (SSRIs) used to treat depression, work by blocking reuptake to increase neurotransmitter availability in the synapse.
Neurotransmitters and their functions
Each neuron produces a particular neurotransmitter, and different neurotransmitters serve different functions in the nervous system. Understanding these functions helps explain how drugs can affect behaviour by altering neurotransmitter systems.
| Neurotransmitter | Functions |
|---|---|
| Acetylcholine | Stimulates muscle contractions and plays a key role in motor control and movement. Essential for memory and cognitive functions such as attention and wakefulness/alertness. Involved in expressions of emotions including anger and sexuality. |
| Noradrenaline | Associated with emotion, particularly mood control. Involved in functions such as sleeping and dreaming, as well as learning. |
| Dopamine | A chemical precursor to noradrenaline, with similar functions. Related to emotion and cognitive functions, as well as posture and control of movement. Associated with reinforcement in learning and linked to dependency and addictions. Used in hormonal regulation, including control of the menstrual cycle in women. |
| Serotonin | Most commonly associated with mood control, particularly within the limbic system in the brain (a set of structures associated with drives, emotions and mood). Involved in many other functions such as feeling pain, sleep, regulating body temperature and hunger. |
Each of these neurotransmitters plays multiple roles in the nervous system. This explains why drugs that affect a single neurotransmitter system can have such wide-ranging effects on behaviour, mood, and cognition.
The effect of recreational drugs on the central nervous system
What are recreational drugs?
Recreational drugs are substances used without medical justification, typically for personal enjoyment. Often called psychoactive drugs, these substances alter brain function, changing mood, perception or conscious experience. Examples include caffeine, nicotine, alcohol, cannabis, amphetamines, LSD, cocaine and heroin, though many others exist.
The use of such substances has long been known to alter consciousness, but only relatively recently has it become possible to investigate how drugs affect the nervous system at a cellular level.
The dopamine reward pathway
The brain contains a reward pathway that, when activated, produces pleasant and rewarding feelings. This system encourages us to repeat behaviours that activate it, serving an adaptive function in learning. For example, the rewarding feeling we experience after eating high-calorie foods encourages fat storage for potential periods of famine.
The dopamine system is a neural pathway operating on the neurotransmitter dopamine, whose release produces feelings of reward. This system primarily involves the nucleus accumbens and ventral tegmental areas of the midbrain, which are associated with the brain's reward system.
How Drugs Hijack the Reward System
Drugs hijack this reward system, producing pleasurable feelings without serving any adaptive function. Most psychoactive drugs of addiction affect the dopamine system. For instance, heroin increases dopamine levels in the reward pathways of the brain (the nucleus accumbens and ventral tegmental areas), intensifying dopaminergic synaptic activation. This produces an intensely pleasurable experience or feeling of euphoria whilst the drug remains active.
However, the brain naturally reacts to sudden dopamine increases by reducing (down-regulating) its own natural dopamine production. When drug effects wear off, the person has less dopamine than before the drug use, causing impaired normal brain functioning. This leads to an unpleasurable experience called dysphoria (intense dissatisfaction, anxiety or depression, discomfort and distress), motivating the person to take more of the drug to stop feeling negative and reproduce the high they initially experienced.
Repeated drug use causes further down-regulation of dopamine production, making the person physically dependent on the drug to avoid the negative withdrawal experience. Lack of dopamine produced by the brain leads to addiction.
Mode of action of recreational drugs
Different drugs affect neurotransmitter systems through various mechanisms:
| Drug | Mode of action |
|---|---|
| Alcohol | Acts as a depressant on the nervous system by inhibiting neural transmission. Increases the action of GABA (an inhibitory neurotransmitter). |
| Opioids (e.g. heroin and morphine) | Reduce GABA activity, leading to overactivity of dopaminergic neurotransmission in the reward pathways of the brain. |
| Amphetamines (e.g. methamphetamines) | Increase dopamine and noradrenaline in the synapse by reversing the reuptake process. Force the release of these neurotransmitters, block reuptake, and in high doses can inhibit their breakdown by enzymes. |
| Cocaine | Increases activity in the dopamine pathway by blocking the reuptake of dopamine. |
| Nicotine | Targets aspects of the dopamine pathway, increasing the amount and transmission of dopamine by blocking the enzyme that breaks it down. Also mimics acetylcholine and binds to nicotinic receptors. |
Individual differences in drug effects
Although drugs have common biological mechanisms, they produce different effects in different people. This variation may result from physiological differences in brain chemistry or from the mediating effect of environment. In some cases, effects are determined by where the drug is taken. For example, in situations where the user has never experienced drug-taking before, even regular doses can lead to overdose. This occurs because the brain becomes conditioned to expect increased chemical levels in certain situations; this expectation causes down-regulation of neurotransmitter release in anticipation of the drug. The sudden rush of chemicals caused by the drug explains why people who have overcome addiction often develop cravings and relapse when they return to places where they previously used drugs.
Environmental cues play a powerful role in addiction. The brain's conditioned responses to drug-related environments help explain why recovery programs often emphasize avoiding places, people, and situations associated with previous drug use.
How these processes lead to addiction
Withdrawal occurs when a drug is no longer active in the nervous system, resulting in unpleasant and sometimes dangerous symptoms. Withdrawal happens when the brain adapts to changes imposed by the drug and no longer operates normally without it. This adaptation leads to tolerance, where users must take increasingly larger doses to achieve the same effect as previously experienced.
The brain adapts to high dopamine levels caused by drugs and down-regulates its natural dopamine production. The baseline measure of dopamine becomes lower than before drug use, meaning that to achieve the same 'high', users require more dopamine and therefore more of the drug.
Common Misconception: Addiction as a Choice
Tolerance and withdrawal are physiological adaptations that occur at the neurological level. This is why addiction is recognized as a medical condition rather than simply a matter of willpower. The brain's chemistry has been fundamentally altered, making it extremely difficult to stop using without experiencing severe withdrawal symptoms.
Remember!
Key Points to Remember:
- The CNS consists of the brain and spinal cord; neurons are the specialised cells that transmit information through electrical and chemical signals.
- Action potentials are electrical impulses triggered when a neuron reaches threshold ( from resting ); they travel down the axon to stimulate neurotransmitter release.
- Synaptic transmission converts electrical signals to chemical messages; neurotransmitters cross the synaptic gap, bind to receptors, and are then subject to reuptake or enzymatic breakdown.
- Different neurotransmitters (acetylcholine, noradrenaline, dopamine, serotonin) have distinct functions in motor control, emotion, memory and mood regulation.
- Recreational drugs alter neurotransmitter systems, particularly the dopamine reward pathway, leading to euphoria but also down-regulation of natural dopamine production, which can result in tolerance, dependence and addiction.