Dendritic Spike - Spike-Timing-Dependent Plasticity

Spike-Timing-Dependent Plasticity

Spike-timing-dependent plasticity (STDP) refers to the functional changes in a neuron and its synapse due to time dependent action potentials. When an action potential reaches the pre-synaptic membrane it opens voltage-gated calcium channels causing an influx of calcium. The influx of calcium releases vesicles filled with neurotransmitters, usually glutamate, into the synaptic cleft. The neurotransmitters bind to receptors on the post-synaptic membrane opening voltage-gated channels causing the membrane to depolarize.

NMDA receptors are found throughout the post-synaptic membrane and act as a coincidence detector. The NMDA detects both glutamate released by pre-synaptic vesicles and depolarization of the post-synaptic membrane. The NMDA receptor exhibits voltage-dependent block by magnesium ions. Depolarization of the post-synaptic membrane (i.e. backward propagating dendritic spike) causes the magnesium ion to be removed from the channel, favoring channel opening. NMDA receptor activation thereby allows calcium influx. Neurons that “fire together wire together” refer to strengthening of synaptic connections through NMDA receptors when glutamate release is coincident with post-synaptic depolarization. This form of wiring is known as long term potentiation. Synaptic connection can also be weakened when the activity of neurons is uncorrelated, also known as long term depression.

The dependence of post-synaptic depolarization in STDP indicates the importance of dendritic spikes. In general, post-synaptic depolarization occurs coincidentally with pre-synaptic activity when a backwards propagating signal reaches the post-synaptic membrane. Dendritic spikes allow backward propagating signals to reach and depolarize the post-synaptic membrane. The strengthening and weakening of synaptic connections is one proposed method of memory formation and learning.