Synaptic plasticity has long been thought to be the mechanism
by which the brain learns and adapts to experiences. The
neurons of the brain must arrange themselves in specific
connections called synapses that the brain must maintain
over time, yet also allow for plasticity of these connections
such that they can be strengthened or weakened as new
experiences are integrated. Recently, the dendrites of
the neurons have become increasingly recognized as determining
the mechanisms of synaptic plasticity.
One particular area of interest is in back-propagating
action potentials, voltage spikes that travel backwards
up the dendrites towards the inputs from the other neurons.
Johnston's group believes that the ion channels involved
in back-propagating spikes might also be involved in the
plasticity of the synapses. Johnston described one type
of ion channel, the A-type potassium channel, which strongly
controls back-propagation.
Johnston showed that during one of these back-propagating
spikes, the A-type potassium channel opens briefly to
let potassium ions out of the cell. This outward current
is key to keeping the voltage spike that travels up the
dendrite from getting very large.
Johnston also described how the brain's neuromodulators
could change the A-current. Protein kinase A, protein
kinase C and mitogen- activated protein kinase can all
change the effectiveness of this ion channel. Johnston's
group believes that by changing the efficiency of the
ion channel, they can change the size of the back-propagating
spike.
When a synapse is strengthened, such as is suspected
in learning, it is said the synapse has become potentiated.
If this strengthening is long-lasting, it is called long-term
potentiation. When a back- propagating spike occurs at
the same time that input arrives in the dendrites, there
is often long-term potentiation. Johnston's group found
that the same enzymes that manipulate the A-type potassium
channel could indeed change the size of the spike. Moreover,
when they apply inhibitors to these enzymes, they could
prevent long-term potentiation from occurring. Therefore,
it appears that these potassium channels play an important
role in synaptic plasticity.
By having a varied density of these A- type potassium
channels along the dendrites, the neuron can control the
size of the back-propagating spike, and thus control how
much plasticity there is at a synapse. The results described
by Johnston during his lecture emphasized how completely
the cell is able to control its own synaptic strength;
by regulating its ion-channel density, by adjusting any
of several enzyme pathways, or even by responding to the
specific timing of inputs to the synapse. In doing so,
the brain can remember past events and incorporate new
ones as experiences warrant.
