The Effects of Drugs on Nervous TransmissionThe ...
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  • What general part of the nervous system do many drugs affect by altering events at synapses?

    • The brain and nervous system
    drugs synapse

  • Name one way drugs can increase transmission of impulses at a synapse.

    • Causing more neurotransmitter to be released at the presynaptic membrane
    synapse increase

  • Name one way drugs can decrease transmission of impulses at a synapse.

    • Preventing the release of neurotransmitter at the presynaptic membrane
    synapse decrease

  • How can drugs imitate the effect of a neurotransmitter at a synapse?

    • By binding to and activating receptors on the postsynaptic membrane
    synapse agonist

  • How can drugs prevent removal of neurotransmitter from a synapse to increase transmission?

    • By preventing the breakdown of neurotransmitters by enzymes
    synapse reuptake

  • What is one mechanism by which a synaptic knob can lose neurotransmitter before an action potential arrives?

    • Neurotransmitter gradually leaks out of the presynaptic knob and is destroyed by enzymes
    synapse leakage

  • How does nicotine act at cholinergic synapses?

    • It mimics acetylcholine by binding to nicotinic acetylcholine receptors on the postsynaptic neurone
    nicotine receptors

  • What effect does nicotine binding to nicotinic receptors have on those receptors after stimulation?

    • It causes a prolonged period of unresponsiveness to further stimulation
    nicotine desensitisation

  • What reward-related neurotransmitter does nicotine stimulate the release of?

    • Dopamine
    nicotine dopamine

  • State one cardiovascular effect of nicotine described in the text.

    • Increases heart rate and blood pressure
    nicotine cardiovascular

  • How does lidocaine prevent an action potential in a postsynaptic neurone?

    • By blocking voltage gated sodium channels, preventing a large influx of sodium ions
    lidocaine ionchannels

  • Where is lidocaine commonly used clinically as given in the text?

    • As a local anaesthetic for numbing small areas, e.g. before dental procedures
    lidocaine clinical

  • How does straight alpha-cobratoxin affect synaptic transmission?

    • It binds to acetylcholine receptors on the postsynaptic membrane, preventing an influx of sodium ions and action potential generation
    cobratoxin antagonist

  • What is a major risk when straight alpha-cobratoxin blocks neuromuscular junctions?

    • Paralysis of muscles that control breathing, which can lead to death
    cobratoxin neuromuscular

  • What therapeutic use of small quantities of straight alpha-cobratoxin is mentioned?

    • Used as a muscle relaxant during asthma attacks
    cobratoxin therapy

  • What is L-dopa converted into after transport into the brain?

    • Dopamine
    l-dopa parkinsons

  • Why cannot dopamine be given directly to people with Parkinson's disease?

    Because dopamine cannot cross the barrier between the blood and the brain.

    pharmacology dopamine parkinsons

  • What is the effect of increasing dopamine levels in the brain for Parkinson's sufferers?

    More nerve impulses are transmitted in brain areas that control movement, improving movement control and lessening Parkinson's symptoms.

    dopamine parkinsons neurophysiology

  • What is MDMA commonly known as?

    MDMA is a recreational drug also known as 'ecstasy'.

    drugs mdma recreational

  • What is the legal status of MDMA in most parts of the world?

    Its use and sale are criminal offences in most parts of the world.

    legal mdma drugs

  • Which neurotransmitter is most notably affected by MDMA?

    MDMA most notably affects the neurotransmitter 'serotonin'.

    neurotransmitters serotonin mdma

  • How does MDMA inhibit serotonin reuptake?

    MDMA binds to specific proteins on the presynaptic membrane that enable serotonin reuptake, inhibiting reuptake and increasing serotonin in the brain.

    mechanism serotonin mdma

  • What normally happens to serotonin after release into the synapse?

    Serotonin is usually reabsorbed into the presynaptic neurone to be recycled for future action potentials.

    serotonin synapse reuptake

  • Besides inhibiting reuptake, what additional effect does MDMA have on serotonin levels?

    MDMA triggers the release of further serotonin from presynaptic neurones, further increasing serotonin levels.

    mdma serotonin release

  • What aspects of experience can serotonin affect?

    Serotonin can affect mood, anxiety and sleep.

    serotonin behavior neurochemistry

  • What subjective effects may an individual feel after taking MDMA?

    They may feel extreme euphoria and enhanced touch and bodily sensations.

    mdma effects euphoria
ํ•™์Šต ๋…ธํŠธ

Overview

  • Drugs alter nervous transmission primarily by acting at synapses, changing how signals are passed between neurons.
  • Effects can increase or decrease synaptic transmission and have clinical or harmful consequences depending on the mechanism.

Basic synaptic mechanisms (quick refresher)

  • A synapse transfers an electrical impulse from a presynaptic neuron to a postsynaptic cell using neurotransmitters.
  • Key steps: neurotransmitter synthesis โ†’ storage in vesicles โ†’ release at presynaptic membrane โ†’ binding to postsynaptic receptors โ†’ removal by enzymatic breakdown or reuptake.
  • Altering any of these steps changes the size or duration of the postsynaptic response.

How drugs increase synaptic transmission

Common mechanisms that enhance signalling:

  • Increase neurotransmitter synthesis in presynaptic terminals, raising available transmitter.
  • Promote release of neurotransmitter at the presynaptic membrane.
  • Mimic neurotransmitter by binding and activating postsynaptic receptors (agonists).
  • Block enzymatic breakdown, so neurotransmitter persists longer in the synaptic cleft.
  • Block reuptake into the presynaptic cell, increasing extracellular transmitter concentration.

How drugs decrease synaptic transmission

Common mechanisms that reduce signalling:

  • Inhibit neurotransmitter synthesis, leaving less transmitter available.
  • Prevent release of neurotransmitter from the presynaptic terminal.
  • Cause leakage or depletion of transmitter so little remains when an action potential arrives; leaked transmitter is degraded by enzymes.
  • Block receptors on the postsynaptic membrane (antagonists), preventing normal transmitter binding.

Example drugs and toxins โ€” mechanisms and consequences

Nicotine

  • Source / role: Addictive compound in tobacco.
  • Mechanisms: Acts as an agonist at nicotinic acetylcholine receptors on postsynaptic neurons, initiating action potentials; also causes prolonged receptor unresponsiveness after stimulation.
  • Secondary effect: Stimulates dopamine release in brain "reward" centers, reinforcing smoking behavior.
  • Physiological effects: Raises heart rate and blood pressure; contributes to addiction and long-term health risks (e.g., circulatory disease, cancer via smoking).

Lidocaine

  • Use: Local anaesthetic and antiarrhythmic.
  • Mechanism: Blocks voltage-gated sodium channels, preventing the large sodium influx needed for action-potential generation.
  • Effect: Local numbness (blocks sensory nerve firing) and can stabilise abnormal cardiac rhythms.

Cobra alpha-cobratoxin (straight alpha-cobratoxin)

  • Mechanism: Binds to acetylcholine receptors at the postsynaptic membrane and prevents their activation, blocking sodium influx.
  • Effect: At neuromuscular junctions this causes muscle paralysis; paralysis of respiratory muscles can be fatal.
  • Clinical note: Very small amounts can be repurposed as a muscle relaxant in specific cases (historical/controlled uses).

Lโ€‘Dopa (levodopa)

  • Use: Treatment for Parkinson's disease symptoms.
  • Rationale: Parkinson's involves low dopamine in parts of the brain that control movement; dopamine itself cannot cross the bloodโ€“brain barrier.
  • Mechanism: Lโ€‘Dopa crosses from blood into the brain and is converted into dopamine by dopa-decarboxylase, increasing central dopamine levels.
  • Effect: Improves motor control and reduces Parkinsonian symptoms by restoring dopaminergic signalling.

MDMA (ecstasy)

  • Type: Recreational psychoactive drug; often illegal.
  • Primary actions: Inhibits serotonin reuptake by binding presynaptic reuptake proteins and also causes extra serotonin release.
  • Consequences: Raises extracellular serotonin, producing euphoria and enhanced sensory perception; affects mood, anxiety, and sleep.
  • Risks: Neurochemical disruption and potential long-term effects on mood regulation.

Clinical and safety implications (summary)

  • Drugs that increase synaptic transmission can be therapeutic (Lโ€‘Dopa) or addictive/harmful (nicotine, MDMA).
  • Drugs that decrease transmission can relieve pain or stop unwanted activity (lidocaine, certain toxins) but may also be lethal (cobra toxin causing respiratory paralysis).
  • Understanding the precise synaptic target (synthesis, release, receptor activation, reuptake, degradation) predicts both therapeutic uses and side effects.

Quick study tips

  • Memorise the five key synaptic targets: synthesis, release, receptor activation, reuptake, breakdown.
  • Link each drug to its main synaptic action and primary clinical or toxic effect.
  • For exam answers, state the mechanism and then the physiological consequence (e.g., "blocks Na+ channels โ†’ prevents AP โ†’ numbness").