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E Kandel

Publications and source records attributed to E Kandel.

27 records · Page 2Linked to original sources
PubMed1970

Habituation and dishabituation of the gill-withdrawal reflex in Aplysia.

A behavioral reflex mediated by identified motor neurons in the abdominal ganglion of Aplysia undergoes two simple forms of shortterm modification. When the gill-with-drawal reflex was repeatedly evoked by a tactile stimulus to the siphon or mantle shelf, the amplitude of the response showed marked decrement (habituation). After a period of rest the response showed spontaneous recovery. The amplitude of a habituated response was facilitated by the presentation of a strong tactile stimulus to another part of the animal (dishabituation). Many characteristics of habituation and dishabituation in Aplysia are similar to those in vertebrates.

Animals↗
PubMed1970

Neuronal correlates of habituation and dishabituation of the gill-withdrawal reflex in Aplysia.

We have examinived the nieural correlates of habittuatiotn atid dishabitiuation of tlhe gill-withdrwal reflex in Aplysia. We obtained intracelllular recordings from identified gill motor neurons in the abdominal ganglionz of a semi-intact preparation of Aplysia wlhile we simultaneously recorded behavior responises of the gill. Habituation and dishabituation were not due to peripheral changes in either the sensory receptors or the gill musculature butt were caused by changes in the amplitlude of the excitatory synaptic potentials produced at the gill motor neurons.

Animals↗
PubMedDate not supplied

A genetic switch for long-term memory.

Current models of brain function hold that learning corresponds to changes in the efficacy of single synapses. The study of learning and of a variety of forms of synaptic plasticity has revealed that both have at least two phases: an early phase that is not dependent on protein synthesis and a late phase that depends on new transcription and translation. Our laboratory has examined synaptic plasticity in Aplysia and in mice to better understand the regulatory events that lead to the induction of the late, protein synthesis-dependent phase of synaptic plasticity. Our recent studies of Aplysia have revealed that the genes that control the late phase of synaptic facilitation are controlled by both an activator, ApCREB1, and a repressor, ApCREB2. This leads to a model in which the late phase of synaptic facilitation is initiated by a perturbation of the balance between activators and repressors of transcription; this perturbation can be accomplished by regulating the activator, the repressor, or both. We, and others, have shown that this transcriptional switch is conserved, at least in part, in the regulation of synaptic plasticity in mice: CREB is implicated in activation of genes required for LTP, a model for synaptic plasticity in the mammalian hippocampus. We speculate that a similar balance between activators and repressors may regulate the genes required for long-term memory in mammals.

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