Synaptic Transmission and Neural Communication
Neurons must constantly communicate with one another to coordinate everything from feeling a mosquito bite to memorizing exam notes. Neural communication is an elegant electrochemical relay system:
- Electrical transmission: Conduction of an electrical wave (Action Potential) along the length of a single neuron’s axon.
- Chemical transmission: Release of chemical messengers (Neurotransmitters) across the microscopic microscopic gap (Synapse) to trigger or inhibit neighboring neurons.
1. Electrical Signaling: The Action Potential
Before a neuron transmits a message, it maintains a state of electrical polarization.
The Three Electrical Phases of an Action Potential
01
Resting Potential
Polarized at -70 mV. Sodium outside, Potassium inside. Maintained by Na+/K+ pump.
→ Threshold (-55mV) →
02
Depolarization
Voltage-gated Sodium channels open; Na+ rushes in. Voltage shoots up to +30 mV.
→
03
Repolarization
Na+ channels close; K+ channels open. Potassium rushes out, restoring negative charge.
Essential Electrical Principles:
- Resting Membrane Potential (-70 mV): The interior of a resting neuron has a net negative charge relative to the extracellular fluid. The Sodium-Potassium Pump actively pumps out 3 Sodium ions (Na+) for every 2 Potassium ions (K+) pumped in, burning metabolic ATP.
- The Threshold of Excitation (-55 mV): If incoming excitatory signals depolarize the membrane to -55 mV, voltage-gated sodium channels burst open.
- The All-or-None Law: An action potential is like firing a gun or flushing a toilet — it either fires at 100% full electrical intensity or does not fire at all. A stronger stimulus (e.g., slamming a door vs dropping a pin) does not produce a larger action potential; instead, it triggers a higher frequency of firing across more neurons.
- Refractory Periods:
- Absolute Refractory Period: Milliseconds immediately following a spike where sodium channels are inactivated; the neuron cannot fire under any condition.
- Relative Refractory Period: Hyperpolarized phase where an exceptionally powerful stimulus can trigger a new spike.
2. Chemical Signaling: Synaptic Transmission
Neurons do not physically touch. There is a microscopic fluid-filled gap approximately 20 to 30 nanometers wide separating neurons called the Synaptic Cleft (discovered by British physiologist Sir Charles Sherrington).
The 5-Step Cycle of Synaptic Transmission
01
Arrival
Action potential reaches presynaptic axon terminal button.
→
02
Calcium Influx
Voltage-gated Calcium (Ca2+) channels open; Ca2+ enters terminal.
→
03
Exocytosis
Synaptic vesicles fuse with membrane, dumping neurotransmitters into cleft.
→
04
Receptor Binding
Molecules diffuse across cleft and bind to postsynaptic receptors like a lock & key.
→
05
Termination
Excess molecules are cleared by Reuptake or enzymatic destruction.
3. Postsynaptic Potentials: EPSP vs IPSP
When a neurotransmitter binds to a postsynaptic receptor, it can trigger one of two opposing electrical effects:
Excitatory vs Inhibitory Postsynaptic Potentials
EPSP (Excitatory Postsynaptic Potential)
- Mechanism: Opens sodium (Na+) or calcium channels, causing slight depolarization (moves inside voltage closer to -55 mV threshold).
- Effect: Increases the likelihood that the receiving neuron will fire an action potential (e.g., triggered by Glutamate).
IPSP (Inhibitory Postsynaptic Potential)
- Mechanism: Opens potassium (K+) or chloride (Cl-) channels, causing hyperpolarization (voltage drops to -80 mV, further from threshold).
- Effect: Decreases the likelihood that the receiving neuron will fire, calming neural circuits (e.g., triggered by GABA).
4. Major Neurotransmitters and Behavioral Impact
| Neurotransmitter | Primary Functional Role | Psychological / Clinical Relevance |
|---|---|---|
| Acetylcholine (ACh) | Muscle contraction, attention, memory consolidation. | Deficits linked to Alzheimer’s Disease; Botox blocks ACh release causing paralysis. |
| Dopamine (DA) | Voluntary motor control, reward pathway, motivation, pleasure. | Excess linked to Schizophrenia; deficiency causes motor tremors in Parkinson’s Disease. |
| Serotonin (5-HT) | Mood stabilization, sleep regulation, appetite, impulsivity. | Deficits strongly associated with Clinical Depression and anxiety (treated with SSRI drugs). |
| Norepinephrine (NE) | Alertness, arousal, fight-or-flight cardiovascular stress response. | Low levels seen in depression; high levels trigger panic attacks and PTSD flashbacks. |
| GABA | Primary inhibitory neurotransmitter in the brain; dampens anxiety. | Anti-anxiety drugs (Valium, Xanax) and alcohol enhance GABA to calm neural agitation. |
| Glutamate | Primary excitatory neurotransmitter; learning and synaptic plasticity. | Excessive release during strokes causes cytotoxic brain damage (Excitotoxicity). |
| Endorphins | Natural endogenous pain relievers, feelings of euphoria (“runner’s high”). | Chemically mirrored by opiate painkiller drugs (morphine, codeine). |
5. How Neurotransmitter Action is Terminated
If neurotransmitters remained stuck to postsynaptic receptors, the receiving neuron would fire endlessly. Transmission is terminated by two mechanisms:
- Reuptake: The presynaptic terminal reabsorbs intact neurotransmitter molecules through specialized transporter proteins for repackaging into vesicles (e.g., SSRI antidepressants block serotonin reuptake, keeping serotonin active longer).
- Enzymatic Degradation: Specialized enzymes in the cleft break down neurotransmitters into inactive pieces (e.g., Acetylcholinesterase instantly hydrolyzes acetylcholine).