Dendritic spike

In neurophysiology, a dendritic spike refers to an action potential generated in the dendrite of a neuron. Dendrites are branched extensions of a neuron. They receive electrical signals emitted from projecting neurons and transfer these signals to the cell body, or soma. Dendritic signaling has traditionally been viewed as a passive mode of electrical signaling. Unlike its axon counterpart which can generate signals through action potentials, dendrites were believed to only have the ability to propagate electrical signals by physical means: changes in conductance, length, cross sectional area, etc. However, the existence of dendritic spikes was proposed and demonstrated by W. Alden Spencer, Eric Kandel, Rodolfo Llinás and coworkers in the 1960s and a large body of evidence now makes it clear that dendrites are active neuronal structures. Dendrites contain voltage-gated ion channels giving them the ability to generate action potentials. Dendritic spikes have been recorded in numerous types of neurons in the brain and are thought to have great implications in neuronal communication, memory, and learning. They are one of the major factors in long-term potentiation. In neurophysiology, a dendritic spike refers to an action potential generated in the dendrite of a neuron. Dendrites are branched extensions of a neuron. They receive electrical signals emitted from projecting neurons and transfer these signals to the cell body, or soma. Dendritic signaling has traditionally been viewed as a passive mode of electrical signaling. Unlike its axon counterpart which can generate signals through action potentials, dendrites were believed to only have the ability to propagate electrical signals by physical means: changes in conductance, length, cross sectional area, etc. However, the existence of dendritic spikes was proposed and demonstrated by W. Alden Spencer, Eric Kandel, Rodolfo Llinás and coworkers in the 1960s and a large body of evidence now makes it clear that dendrites are active neuronal structures. Dendrites contain voltage-gated ion channels giving them the ability to generate action potentials. Dendritic spikes have been recorded in numerous types of neurons in the brain and are thought to have great implications in neuronal communication, memory, and learning. They are one of the major factors in long-term potentiation. A dendritic spike is initiated in the same manner as that of an axonal action potential. Depolarization of the dendritic membrane causes sodium and potassium voltage-gated ion channels to open. The influx of sodium ions causes an increase in voltage. If the voltage increases past a certain threshold, the sodium current activates other voltage-gated sodium channels transmitting a current along the dendrite. Dendritic spikes can be generated through both sodium and calcium voltage-gated channels. Dendritic spikes usually transmit signals at a much slower rate than axonal action potentials. Local voltage thresholds for dendritic spike initiation are usually higher than that of action potential initiation in the axon; therefore, spike initiation usually requires a strong input. Voltage-gated sodium channels are proteins found in the membrane of neurons. When electrically activated, they allow the movement of sodium ions across a plasma membrane. These channels are responsible for propagation of electrical signals in nerve cells. Voltage-gated sodium channels can be divided into two subunits: alpha and beta. A variety of alpha subunit voltage-gated sodium channels have been identified. Voltage-gated sodium channels found in mammals can be divided into three types: Nav1.x, Nav2.x, and Nav3.x. Nav1.x sodium channels are associated with the central nervous system. 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. These channels have been well documented in the axonal membrane of the central nervous system. Nav1.2 has been primarily identified in unmyelinated axons while high concentrations of Nav1.6 have been observed at nodes of Ranvier of axons. Nav1.6 has been identified in the dendrites of hippocampal CA1 neurons that generate dendritic spikes; the density of Nav1.6 in these neurons is 35-80 times lower than in the initial segments of axons. Distribution of voltage-gated sodium channels along the dendritic membrane plays a crucial role in a dendrites ability to propagate a signal. High dendritic membrane thresholds often make it harder for initiation of dendritic spikes. However, increased density of voltage-gated sodium channels may reduce the amplitude of a signal needed to initiate a spike. Clustering of voltage-gated sodium channels have been observed at the synapses of the globus pallidus neuron. It has also been demonstrated through dendritic computational models that the threshold amplitude of a synaptic conductance needed to generate a dendritic spike is significantly less if the voltage-gated sodium channels are clustered at the synapse. The same type of voltage-gated channels may differ in distribution between the soma and dendrite within the same neuron. There seems to be no general pattern of distribution for voltage-gated channels within dendrites. Different neuronal dendrites exhibit different density patterns which are subject to change during development and can be modulated by neurotransmitters. Like voltage-gated sodium channels, voltage-gated calcium channels are also integral membrane proteins found in the plasma membrane. Voltage-gated calcium channels generate action potentials by the same mechanisms as voltage-gated sodium channels. Various voltage-gated calcium channels have been identified in neurons. N- and P/Q-type voltage-gated calcium channels are the primary subtypes found to support synaptic transmission. These channels are concentrated at nerve terminals. T-type and R-type voltage-gated calcium channels have been found in basal dendrites, and it is thought that the activation of these channels during action potential bursts lead to the generation of dendritic calcium spikes. T-type and R-type channels are all part of the alpha 1 subunit class of calcium channels. The various types of voltage-gated calcium channels result in two forms of voltage activation: low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium currents. In deep cerebellar nuclei, calcium currents are not uniformly distributed along a dendrite. The relative strength of LVA calcium currents are significantly more concentrated at the distal end of dendrites. The uneven distribution of LVA calcium currents suggests the important role of LVA calcium currents in dendritic integration at synaptic inputs.