Neurons, Synapses, and Neurotransmitters (Vocabulary)
Neurons and Synapses
Neuron components and their terminology
Neuron structure includes the axon and the dendrite. The synapse is the junction between the tips of the sending (presynaptic) neuron and the receiving (postsynaptic) neuron.
The synaptic gap/cleft is the tiny space at that junction.
Chemical communication at the synapse
Neurotransmitters are chemical messengers that cross the synaptic gaps between neurons.
When released by the sending neuron, neurotransmitters travel across the synapse and bind to receptor sites on the receiving neuron, thereby influencing whether that neuron will generate neural impulses.
Neurotransmitters are typically reabsorbed by the sending neuron through reuptake (the neurotransmitter's reabsorption back into the presynaptic neuron).
Key neurotransmitters discussed
Acetylcholine (ACh): one of the best understood neurotransmitters; plays a role in learning and memory.
Endorphins: natural, opiate-like neurotransmitters linked to pain control and to pleasure, explaining good feelings such as runner’s high.
Receptors, binding, and receptor-site interactions
A neurotransmitter binds to a receptor site on the receiving neuron, which can influence the likelihood of a neural impulse being generated.
Agonists are molecules that, by binding to receptor sites, stimulate a response.
Antagonists are molecules that, by binding to receptor sites, inhibit or block a response.
Practical example: endorphins and opiate drugs
Some opiate drugs bind receptor sites to mimic endorphins (agonist effect).
Botulinum toxin as a practical antagonist example
Botulinum toxin (Botox) is used cosmetically to smooth wrinkles by paralyzing underlying facial muscles.
Mechanistically, Botox reduces acetylcholine activity at neuromuscular junctions, leading to muscle relaxation.
Conceptual implications
The balance of excitatory and inhibitory influences at the synapse determines whether a neuron fires.
Disruption to neurotransmitter release, receptor binding, or reuptake can significantly alter mood, perception of pain, muscle control, and learning processes.
Neurotransmitters and the Synaptic Process (step-by-step)
Step 1: Synthesis and storage
Neurotransmitters are synthesized in neurons and stored in vesicles.
Step 2: Release into the synapse
An action potential triggers vesicles to release neurotransmitters into the synaptic gap.
Step 3: Binding to postsynaptic receptors
Neurotransmitters diffuse across the synaptic gap and bind to specific receptor sites on the postsynaptic neuron.
Step 4: Postsynaptic response
Binding can excite or inhibit the postsynaptic neuron, affecting whether it will fire an action potential.
Step 5: Termination of signal
Neurotransmitters are cleared from the synapse via reuptake, enzymatic degradation, or diffusion.
Step 6: Reuptake as regulation
Reuptake returns neurotransmitters to the presynaptic neuron for reuse or breakdown, helping regulate signal strength and duration.
Key Neurotransmitters in Focus
Acetylcholine ({\mathrm{ACh}})
Functions: learning and memory are notably influenced by {\mathrm{ACh}} activity.
Relevance: disruption of {\mathrm{ACh}} signaling is implicated in conditions affecting memory and muscle control.
Endorphins
Functions: natural pain relief and pleasure; contribute to rewarding feelings.
Example effect: runner’s high is associated with endorphin release.
General receptor interactions
Agonists: bind to receptors and imitate the natural neurotransmitter, producing a similar effect.
Antagonists: bind to receptors but do not activate them; instead they block or dampen the effect of the natural transmitter.
Agonists and Antagonists: Definitions and Examples
Agonist
Definition: a molecule that, by binding to a receptor site, stimulates a response.
Example: certain opiate drugs bind to opioid receptors to mimic endorphins.
Antagonist
Definition: a molecule that, by binding to a receptor site, inhibits or blocks a response.
Example (transmission-focused): a molecule that prevents receptor activation, reducing the effect of a neurotransmitter.
Botox as a practical illustration of antagonist effects
Botulinum toxin (Botox) acts to paralyze muscles by preventing acetylcholine release at neuromuscular junctions, producing a decrease in muscle contraction and thereby smoothing wrinkles.
Important nuance: Botox’s effect is largely due to presynaptic blockade of acetylcholine release, not simply receptor antagonism.
Botulinum Toxin (Botox): Mechanism and Implications
Mechanism overview
Botox blocks the release of acetylcholine from presynaptic terminals, reducing stimulation of muscle fibers.
Result: muscle paralysis in targeted areas, leading to cosmetic smoothing of wrinkles.
Practical and ethical considerations
Medical and cosmetic uses vs. potential risks (e.g., unintended muscle weakness, spread of toxin effects).
Societal implications of cosmetic neuropharmacology and questions about dependence on neuromodulation for appearance or mood.