Monosynaptic connections made by the sensory neurons of the gill- and siphon-withdrawal reflex in Aplysia participate in the storage of long-term memory for sensitization (original) (raw)

A Simplified Preparation for Relating Cellular Events to Behavior: Contribution of LE and Unidentified Siphon Sensory Neurons to Mediation and Habituation of the Aplysia Gill- and Siphon-Withdrawal Reflex

The Journal of Neuroscience the Official Journal of the Society For Neuroscience, 1997

We have begun to analyze several elementary forms of learning in a simple preparation consisting of the isolated mantle organs and abdominal ganglion of Aplysia. Previous studies suggested that plasticity at siphon sensory neuron synapses contributes to habituation and dishabituation of the gill-and siphonwithdrawal reflex in this preparation. We next wished to identify the sensory neurons that participate in the reflex and examine their plasticity more directly. To investigate the contribution of the LE siphon mechanosensory cells, we recorded from them and gill or siphon motor neurons during the same siphon stimulation that has been used in behavioral experiments in this preparation. Our results indicate that the LE cells make a substantial contribution to the evoked response in the motor neurons under these conditions, but they suggest that other as yet unidentified siphon sensory neurons with lower thresholds and shorter latencies also contribute. In addition, we find that homosynaptic depression of monosynaptic postsynaptic potentials (PSPs) from LE sensory cells makes an important contribution to habituation of the response in the motor neurons. To investigate plasticity of PSPs from the unidentified sensory neurons, we recorded the PSP that was produced in a motor neuron by water-movement stimulation of the siphon, which does not cause firing of LE cells. Our results suggest that PSPs from the unidentified sensory neurons and the LE neurons undergo similar plasticity during habituation and dishabituation training. These results support the idea that plasticity at synapses of both LE and unidentified sensory neurons contributes to habituation and dishabituation of the reflex response in this preparation.

Synaptic Mechanisms of Induction and Maintenance of Long-Term Sensitization Memory in Aplysia

Handbook of Behavioral Neuroscience, 2013

The marine snail Aplysia californica exhibits a simple defensive withdrawal reflex that can undergo several forms of learning. In particular, the reflex can exhibit long-term sensitization (LTS), a form of nonassociative memory. LTS is mediated by long-term facilitation (LTF) of the monosynaptic connection between the sensory and motor neurons that mediate the withdrawal reflex. LTS and LTF represent one of the bestunderstood model systems of long-term memory extent. Furthermore, discoveries from work on this system have provided fundamental insights into the cellular and molecular mechanisms that mediate the induction and maintenance of long-term memory. The present chapter reviews this work; it concludes with a discussion of recent studies of the role of protein kinase M in the persistence of the long-term memory and of memory reconsolidation in Aplysia. It is suggested that the study of LTS and LTF can provide important mechanistic information these two intriguing memory phenomena.

Complexities of a simple system: new lessons, old challenges and peripheral questions for the gill withdrawal reflex of Aplysia

Brain Research Reviews, 2003

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. D

Synaptic plasticity in vitro: cell culture of identified Aplysia neurons mediating short-term habituation and sensitization

The Journal of neuroscience : the official journal of the Society for Neuroscience, 1986

The gill withdrawal reflex of the marine mollusk, Aplysia californica, shows habituation and sensitization, two simple forms of learning. In order to extend the cellular studies on synaptic plasticity underlying the changes in the reflex behavior, and to explore further the development of synaptic plasticity during synapse formation, we have sought to establish the neural circuit of the gill withdrawal reflex in vitro. We report here the reconstruction of the elementary gill withdrawal circuit in cell culture and find that the cells show short-term homosynaptic depression and heterosynaptic facilitation, the cellular mechanisms of habituation and sensitization, respectively.