Long-term sensitization training produces spike narrowing in Aplysia sensory neurons.

Both short- and long-term sensitization of withdrawal reflexes of Aplysia are attributable at least in part to facilitation of the sensorimotor synapse. Previously, short-term synaptic facilitation has been associated with spike broadening and no change in temporal dynamics of burst transmission. In the present study, we examined whether long-term sensitization (LTS) is also associated with spike broadening and whether long-term synaptic facilitation is accompanied by changes in temporal dynamics.

Learning insights transmitted by glutamate.

Plasticity of the Aplysia sensorimotor synapse plays a crucial role in learning and memory of withdrawal reflexes. During the past ten years, a growing body of evidence has indicated that the sensorimotor synapse is glutamatergic. This new information has guided several studies that implicate AMPA and NMDA receptors in synaptic plasticity.

Desensitization of postsynaptic glutamate receptors contributes to high-frequency homosynaptic depression of aplysia sensorimotor connections.

Withdrawal reflexes of Aplysia are mediated in part by a monosynaptic circuit of sensory (SN) and motor (MN) neurons. A brief high-frequency burst of spikes in the SN produces excitatory postsynaptic potentials (EPSPs) that rapidly decrease in amplitude during the burst of activity. It is generally believed that this and other (i.

Burst-induced synaptic depression and its modulation contribute to information transfer at Aplysia sensorimotor synapses: empirical and computational analyses.

The Aplysia sensorimotor synapse is a key site of plasticity for several simple forms of learning. Plasticity of this synapse has been extensively studied, albeit primarily with individual action potentials elicited at low frequencies. Yet, the mechanosensory neurons fire high-frequency bursts in response to even moderate tactile stimuli delivered to the skin.