Anatomy of the synapse
In the CNS, a synapse is a structural part of a neuron that passes an electrical or chemical signal to another neuron or to a target cell.
- Cell membrane
- Cell body
- Myelin sheath
- Nodes of Ranvier (between myelin sheaths)
At a synapse:
- A signal-passing neuron (the presynaptic neuron)
- The target neuron (the postsynaptic neuron)
- The 2 neural membranes create a synaptic cleft that carries out the signaling process (neurotransmission)
Synapses by location
- Axodendritic: axon to a dendrite
- Axosomatic: axon to a soma
- Axosecretory: axon to a blood vessel
- Axoaxonic: axon to another axon
- Dendrodendritic: dendrite to another dendrite
- Axoextracellular: axon with no connection
Types of synapses
- Gap with channel proteins connecting 2 neurons so that an electrical signal can travel over the synapse.
- 2 neurons connected through special channels called gap junctions
- Allow signals to be transferred rapidly between cells
- Found in specialized locations:
- Smooth muscle
- Pulp of the tooth
- Retina of the eye
- Gap between 2 neurons where information passes chemically in the form of neurotransmitter molecules
- Presynaptic membrane
- Synaptic cleft
- Postsynaptic membrane
- Most common chemical synapse:
- Neuromuscular junction
- Formed by the contact between a motor neuron and a muscle fiber
- Postsynaptic conductance or postsynaptic potentials (PSPs)
- Excitatory postsynaptic potentials (EPSPs): PSPs that ↑ the likelihood of a postsynaptic action potential occurring
- Inhibitory postsynaptic potentials (IPSPs): PSPs that ↓ the likelihood of a postsynaptic action potential occurring
- Whether a postsynaptic response is an EPSP or an IPSP depends on:
- The type of channel that is coupled to the receptor.
- The concentration of permanent ions inside and outside the cell.
> 500 unique neurotransmitters have been identified in humans. Neurotransmitters are:
- Proteins stored in the synaptic vesicles
- Chemical messengers that transmit signals from a neuron to a target cell
- Clustered close to the cell membrane of the axon terminal
- Released into the synaptic cleft as a result of a threshold action potential in the presynaptic neuron
- Either excitatory or inhibitory
- Amino acid:
- Soluble gases:
Common neurotransmitters and their actions
|Neurotransmitter||Characteristics||Site of synthesis|
|Dopamine||Excitatory and inhibitory||CNS: substantia nigra, ventral tegmental area, and others|
|Norepinephrine||Excitatory||CNS: locus coeruleus, sympathetic nervous system, and adrenal medulla|
|Serotonin||CNS: raphe nuclei and enterochromaffin cells|
|Histamine||Excitatory and inhibitory|
|Acetylcholine||Excitatory (usually)||Neuromuscular junctions, presympathetic synapses, and preganglionic sympathetic synapses|
|Glutamate||CNS: almost every part of the nervous system|
|Glycine||Inhibitory||CNS: spinal cord, brain stem, and retina|
|Endorphins||Inhibitory||CNS and PNS|
|Neurokinins||GI tract: modulate motility, fluid, and electrolyte secretion||Intrinsic enteric neurons and extrinsic primary afferent nerve fibers|
|Substance P||Modulates vasodilation, inflammation, pain, and the process of vomiting||Intrinsic enteric neurons and extrinsic primary afferent nerve fibers|
|Gastrin-releasing peptide||Stimulates the release of gastrin from the G cells||Postganglionic fibers of the vagus nerve|
- Vesicles filled with neurotransmitters arrive from cell soma and reside in the presynaptic knob.
- Action potential arrives via the axon.
- Voltage-gated Ca2+ channels open.
- Vesicles are stimulated.
- Neurotransmitter vesicles fuse with synaptic membranes and release the neurotransmitter contents in the synaptic cleft.
- Postsynaptic receptor binds the transmitter and opens.
- Unbound transmitter is degraded, recycled, or diffused out of the cleft.
- Myasthenia gravis: autoimmune disease characterized by a production of autoantibodies against acetylcholine receptors on the postsynaptic membrane. When these receptors are blocked, muscle contraction is inhibited. Individuals with myasthenia gravis report exhaustion and fatigue as the day ends. The classic early symptom is drooping of the eyelids as nighttime approaches.
- Parkinson’s disease: neurodegenerative disorder in which the production of dopamine is decreased owing to destruction of the cells producing it in the substantia nigra. This destruction results in symptoms such as tremors, loss of movement control, hypokinesia, rigidity, dementia, and depression.
- Tetanus toxin: prevents the release of GABA, an inhibitory neurotransmitter. This release results in unchecked excitatory signals to the skeletal muscles, which go into spasm. The jaw muscles are specifically affected, giving the classic sign of lockjaw. As the disease progresses, the respiratory muscles also get involved, causing death.
- Botulism: Botulinum toxin is among the most toxic proteins known. This toxin is produced by the bacterium Clostridium botulinum. When botulinum toxin binds to the synaptic vesicle proteins and gangliosides, it prevents the release of acetylcholine, a stimulatory neurotransmitter, inhibiting stimulatory effects, preventing muscle contraction, and causing flaccid paralysis.
- Autism spectrum disorder: neurodevelopmental disorder marked by poor social skills, restricted interests and social interactions, and repetitive and stereotyped behaviors. This condition is termed a “spectrum” because of the wide variability in the severity of symptoms exhibited. Some individuals suffer from severe impairment in language and intellectual levels, while others may have normal or even advanced intellect.
- Huntington disease: progressive neurodegenerative disorder with an autosomal dominant mode of inheritance. It is caused by CAG (cytosine-adenine-guanine) trinucleotide repeats in the huntingtin (HTT) gene. A common clinical presentation in adulthood is a movement disorder known as chorea—abrupt, involuntary movements of the face, trunk, and limbs. Management is supportive.
- Schizophrenia: serious chronic mental health disorder. Schizophrenia is characterized by the presence of psychotic symptoms, disorganized speech or behavior, flat affect, avolition, anhedonia, poor attention, and alogia. Management includes antipsychotics in conjunction with behavioral therapy.
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