or by a short-term storage mechanism for short-term memory. Nonsynaptic plasticity can emerge during learning as a result of cellular processes, although the timing, persistence, and the relationship between nonsynaptic plasticity and synaptic output are all poorly understood. Studies have shown that nonsynaptic plasticity plays an indirect but important role in the formation of memories. Learning-induced nonsynaptic plasticity is associated with soma depolarization. Classical conditioning Experiments have revealed that nonsynaptic changes take place during conditional learning. Woody et al. demonstrated that eyeblink conditioning (EBC), a form of classical conditioning for studying neural structures and mechanisms underlying learning and memory, in a cat is associated with increased excitability and input in the neurons in sensorimotor cortical areas and in the facial nucleus. It was observed that increasing excitability from classical conditioning continued after the response stopped. This suggests that increased excitability may function as a mechanism for memory storage. In eyeblink conditioning in rabbits, nonsynaptic changes occurred throughout the dorsal hippocampus. This indicates that although excitability changes alone are not enough to explain memory storage processes, nonsynaptic plasticity might be a storage mechanism for phases of memory limited by time. Nonsynaptic changes influence other types of plasticity involved with memory. For example, a nonsynaptic change such as depolarization of the resting membrane potential resulting from conditional learning could cause synaptic plasticity in future learning. Rule learning and savings The ability to learn rules is dependent on nonsynaptic plasticity. One study sought to teach rats to discriminate between various odors, and it took several days to teach them to distinguish between a first pair of smells. However, after learning this, the rat was able to learn to distinguish between different odors much faster. Changes in excitability of the pyramidal neurons in these rats were observed for three days after training. These changes faded eventually, suggesting that the neurons were involved in learning the rules, not in storing memory. Daoudal and Debanne attempted to determine if the same learning rules and induction mechanisms defined for synaptic plasticity also applied to nonsynaptic plasticity affecting ion channels. They determined that nonsynaptic and synaptic plasticity share common learning rules and induction pathways, e.g., NMDA receptor dependent long-term potentiation (LTP) and long-term depression (LTD). They also showed that nonsynaptic and synaptic plasticity synergistically form a coherent engram to store memory traces. Savings is the ability to relearn forgotten information much faster than it was learned originally. Nonsynaptic