Neuronal communication is frequently described simply as an
all-or-nothing event. If a neuron is depolarized enough, it will fire
and release neurotransmitters to communicate with another neuron; if it
doesn't reach the threshold to fire, it doesn't send a signal at all.
However, depolarizations that don't reach the threshold to make the
neuron fire can still impact neurotransmission. The depolarization
spreads throughout the neuron, and when the neuron does eventually reach
the threshold to fire, it releases a stronger signal with more
neurotransmitters. This is known as analog-to-digital facilitation, a
type of short-term plasticity.
‘How neurons in the cerebellum, a region in the back of the brain that controls movement, interact with each other is being studied by scientists at Max Planck Florida Institute for Neuroscience.’
Researchers were already aware that this type of short-term
plasticity exists, but had struggled to view it directly because the
axons that utilize this type of plasticity are difficult for scientists
to access. This means that some of the molecular mechanisms behind the
phenomenon remain mysterious.
In a study published in Cell Reports
in February 2017, Matt
Rowan, a Post-doctoral researcher in the lab of Dr. Jason
Christie, sought to understand the molecular mechanisms behind a type of
short-term neuronal plasticity that may have importance for motor
The team showed that this type of plasticity can impact
neurotransmission in as little as 100 milliseconds and depends upon
inactivation of Kv3 channels. Interestingly, the team also found that
this type of plasticity occurs more readily in juvenile brains than in
"This has been seen before, and we're adding a molecular mechanism
showing exactly the molecule you need to get this sort of facilitation,"
For the current study, the team used novel
techniques for voltage imaging and patch clamp recordings that allowed
them to visualize and record from these tiny sections of individual
The researchers observed analog-to-digital facilitation as it
occurred in experimental models. They showed that subthreshold
depolarization spreads from the body of the neuron down its axon, the
long extension through which action potentials travel before causing the
neurons to release neurotransmitters into a synapse. Here, subthreshold
depolarizations impacted neurotransmission in the juvenile models by
briefly making Kv3.4 channel unavailable thereby increasing the duration
of the presynaptic spike. The fact that the group observed less of this
same plasticity in mature models suggests that learning and experience
may temper this type of plasticity as an animal matures.
The team chose to study inhibitory interneurons in the cerebellum
because they play an especially important role in the function of
circuits throughout the cerebellum as well as the rest of the brain.
Understanding this type of neuronal plasticity may have important
implications for understanding motor disorders such as cerebellar
ataxia, a disorder that can cause a variety of motor problems in humans
ranging from increased falling to difficulty with speech and swallowing.