Control of Na+ spike backpropagation by intracellular signaling in the pyramidal neuron dendrites

The integrative function of neurons depends on the somato-dendritic distribution and properties of voltage-gated ion channels. Sodium, potassium, calcium, and hyperpolarization-activated cyclic nucleotide-gated K+ (HCN) channels expressed in the dendrites can be modulated by a number of neurotransmitters and second-messenger systems. For example, activation of protein kinases leads to an increase in dendritic excitability by removing a slow inactivation of Na+ channels and decreasing the activity of transient K+ channels in the apical dendrites of hippocampal pyramidal neurons. Consequently, action potentials propagating along the dendrites can be modified significantly by a variety of neuromodulatory synaptic inputs.