Inactivation of C/EBP transcription factors specifically affects the synaptic plasticity of a common snail neuron.

Our previous studies showed that the acquisition of nociceptive sensitization in common snails is accompanied by long-term facilitation of synaptic transmission in defensive behavior command neuron LP11, this being dependent on translation and transcription processes. The characteristics of the neurochemical mechanisms of plasticity in the different sensory inputs of this nerve cell were identified. The mechanisms of induction of synaptic facilitation of the responses of neuron LP11 to chemical sensory stimulation of the snail's head involved NMDA glutamate receptors, serotonin receptors, cAMP, and serotonin-modulated transcription-regulating protein SMP-69. The mechanisms of induction of synaptic facilitation of another sensory input of the neuron--from tactile receptors on the head - involved protein kinase C. The present study addresses the involvement of C/EBP transcription factors (CCAAT-enhancer-binding protein) in the processes of synapse-specific plasticity of neuron LP11 during the acquisition of sensitization in snails. C/EBP was inactivated using oligonucleotides specifically binding to these proteins. The results showed that acquisition of sensitization during intracellular administration of oligonucleotides led to the selective suppression of synaptic facilitation in the responses of neuron LP11 to chemical sensory stimulation of the snail's head. Synaptic facilitation in the responses to tactile stimulation of the head or foot developed as in neurons in control sensitized snails. It is suggested that C/EBP transcription factor is selectively involved in the mechanisms of synapse-specific plasticity of the sensory input of neuron LP11 from chemoreceptors on the head during the acquisition of sensitization in snails.