Dendritic spike
Depolarization of the dendritic membrane causes sodium and potassium voltage-gated ion channels to open.
Nav1.1, Nav2.2, and Nav1.6 are three isoforms of the voltage-gated sodium channels that are present at high levels in the central nervous system of an adult rat brain.
However, increased density of voltage-gated sodium channels may reduce the amplitude of a signal needed to initiate a spike.
N- and P/Q-type voltage-gated calcium channels are the primary subtypes found to support synaptic transmission.
[11] The relative strength of LVA calcium currents is significantly more concentrated at the distal end of dendrites.
The ability of voltage-gated potassium channels to modulate dendritic signaling may have significant effects on synaptic plasticity.
For example, backward propagation of action potentials is very limited in cerebellar Purkinje cells[14] but is quite prevalent in interneurons of the medium ganglionic layer of the cerebellum-like lobe of some fish.
[15] Action potentials may be first generated at the dendrite if stimulated by strong synchronous synaptic inputs.
Hippocampal CA1 neurons have been shown to produce reliable dendritic spike propagation through spatial summation of multiple synaptic inputs.
In the hippocampus, the CA1 neurons contain two distinctive regions that receive excitatory synaptic inputs: the perforant path (PP) through the apical dendritic tuft (500-750 μm from soma) and the Schaffer-collateral (SC) through the basal and apical dendrites (250-500 μm from soma).
[17] Studies show that individual stimulation of either the PP or SC was not sufficient to allow a dendritic spike to initiate an action potential.
Forward propagation of dendritic spikes initiates due to synaptic activity, and refers to the transmission of the signal towards the soma.
[17] The strength of synaptic stimulation required to generate a dendritic spike varies among neuronal types.
Spike-timing-dependent plasticity (STDP) refers to the functional changes in a neuron and its synapse due to time dependent action potentials.
Neurons that “fire together wire together” refer to strengthening of synaptic connections through NMDA receptors when glutamate release is coincident with post-synaptic depolarization.
Two-photon glutamate uncaging, a type of photostimulation, has become the premier tool for studying dendritic spikes due to its high level of precision.
The technique uses a one micrometer diameter open tip glass micropipette to suction the membrane of a cell.
The ion solution can be varied and drugs can be delivered through the micropipette to study the effects of current under various conditions.
[20] Interestingly, the chronic recording paradigm that demonstrated this also showed that dendritic voltage properties exhibited egocentric spatial maps comparable to pyramidal neurons.
This rare phenomenon may be due to a glial sheath[21] forming around the tetrode tips, creating a high impedance sea, similar to a gigaohm seal in patch recordings, that allows for such small and localized voltage measurement to be made.
In the case of dendritic spikes, staining and labeling are used to identify and quantify the presence of certain voltage-gated channels.
For example, rabbit polyclonal antibodies raised against synthetic peptide sequences have been used to identify the presence of Nav1.2, Nav1.3, and Nav1.6 sodium channels in dendrites of the globus pallidus neuron.
This field has generated much interest and serves as a tool for all branches of neuroscience research including dendritic spike initiation.
