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The Potential Role of Postsynaptic Phospholipase C Activity in Synaptic Facilitation and Behavioral Sensitization in Aplysia

¹Department of Physiological Science, University of California, Los Angeles; ²Interdepartmental PhD Program in Molecular, Cellular and Integrative Physiology; and ³Department of Neurobiology and ⁴Brain Research Institute, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California

Submitted 21 March 2008; accepted in final form 12 May 2008

Previous findings indicate that synaptic facilitation, a cellular mechanism underlying sensitization of the siphon withdrawal response (SWR) in Aplysia, depends on a cascade of postsynaptic events, including activation of inositol triphosphate (IP₃) receptors and release of Ca²⁺ from postsynaptic intracellular stores. These findings suggest that phospholipase C (PLC), the enzyme that catalyzes IP₃ formation, may play an important role in postsynaptic signaling during facilitation and learning in Aplysia. Using the PLC inhibitor U73122 [GenBank] , we found that PLC activity is required for synaptic facilitation following a 10-min treatment with 5-HT, as measured at 20 min after 5-HT washout. Prior work has indicated that facilitation at this time is supported primarily by postsynaptic processes. To determine whether postsynaptic PLC activity is involved in 5-HT–mediated facilitatory actions, we examined the effect of U73122 [GenBank] on enhancement of the response of motor neurons isolated in cell culture to glutamate, the sensory neuron transmitter. A 10-min application of 5-HT induced persistent (>40 min) enhancement of glutamate-evoked potentials (Glu-EPs) recorded from isolated motor neurons, and this enhancement was blocked by U73122. [GenBank] Finally, we showed that injecting U73122 [GenBank] into intact animals before behavioral training impaired intermediate-term sensitization, indicating that PLC activity contributes to this form of nonassociative learning.