Long-term potentiation (LTP) in a particular synapse, results in an increase in excitability of the dendritic branches specific to that synapse. Dendritic excitability is important for the propagation and integration of synaptic signals. Dendritic excitability is thought to contribute to E-S potentiation, or an increase in the probability that a given input will result in the firing of an action potential. It is known that changes in dendritic excitability affect action potential back propagation. Action potentials begin near the axon hillock and propagate down the length of the axon, but they also propagate backward through the soma into the dendritic arbor. Active back propagation is dependent on ion channels and changing the densities or properties of these channels can influence the degree to which the signal is attenuated. Plasticity of back-propagation in the dendrites occurs in less than one minute and lasts longer than 25 minutes. Back propagation is a method of signaling to the synapses that an action potential was fired. This is important for spike-timing-dependent plasticity. Fast dendritic adaptation on timescales of few seconds was experimentally observed indicating a potential meaningful global learning mechanism Intrinsic plasticity Intrinsic plasticity is a form of activity-dependent plasticity distinct from synaptic plasticity, which involves changes at the synapse between two neurons rather than changes in the electrical properties within a single neuron. There are some closely related phenomena that can affect a neuron's excitability – such as neuromodulation, structural plasticity, short-term plasticity due to channel kinetics, and neural development. There is no consensus on the quantity that intrinsic plasticity regulates, e.g. the firing rate of a neuron, its gain or its internal calcium concentration. Functionally, intrinsic plasticity might allow neurons to learn the intensity of stimuli and represent those intensity statistics in their excitabilities. Intrinsic plasticity contributes to encoding memory and complements other forms of activity-dependent plasticity including synaptic plasticity. Higher brain function Long-term associative memory Experimental evidence The experiment of Kemenes et al. demonstrated that in an extrinsic modulatory neuron, nonsynaptic plasticity influences the expression of long-term associative memory. The relationship between nonsynaptic plasticity and memory was assessed using cerebral giant cells (CGCs). Depolarization from conditioned stimuli increased the neuronal network response. This depolarization lasted as long as the long-term memory. Persistent depolarization and behavioral memory expression occurred more than 24 hours after training, indicating long-term effects. In this experiment, the electrophysiological expression of the long-term memory trace was a conditioned