The gill withdrawal reflex of Aplysia is generally depicted as a simple behaviour mediated by a simple neural circuit in a simple organism. Such a view has permitted a clear focus upon synapses between relatively small numbers of identified neurones, which are known to participate in the reflex and its plasticity. Ensuing research has provided some of the first and still among the most powerful explanations of the cellular underpinnings of learning and memory. In reality, however, the reflexive withdrawal of the gill and other mantle organs is anything but simple. First, the behaviour itself is complex and varies depending upon the strength of the tactile stimulus and where it is applied. In addition, over 100 central neurones are activated by stimuli, which elicit the withdrawal reflex and likely change their activities during learning (although not all of these cells necessarily contribute to the actual withdrawal response). Moreover, multiple mechanisms are activated at both presynaptic and postsynaptic sites to orchestrate the numerous modifications that underlie observed changes in synaptic efficacy. The picture becomes even more complicated when hundreds of additional peripheral neurones, which are known to participate in various aspects of the response, are also considered. Recent work has shifted attention back to these peripheral cells by suggesting that they might be the previously unidentified light touch receptors that mediate both central and peripheral components of the reflex. While daunting, the complexity of the total circuitry mediating the gill withdrawal reflex may provide yet another important lesson: even in simple systems, memory may not be localized to specific loci, but rather may be an emergent property of physiological mechanisms distributed throughout the entire circuitry.