RESUMEN
Using steady-state electrical properties of non-ohmic dendrite based on cable theory, we derive electrotonic potentials that do not change over time and are localized in space. We hypothesize that clusters of such stationary, local and permanent pulses are the electrical signatures of enduring memories which are imprinted through nonsynaptic plasticity, encoded through epigenetic mechanisms, and decoded through electrotonic processing. We further hypothesize how retrieval of an engram is made possible by integration of these permanently imprinted standing pulses in a neural circuit through neurotransmission in the extracellular space as part of conscious recall that acts as a guiding template in the reconsolidation of long-term memories through novelty characterized by uncertainty that arises when new fragments of memories reinstate an engram by way of nonsynaptic plasticity that permits its destabilization. Collectively, these findings seem to reinforce this hypothesis that electrotonic processing in non-ohmic dendrites yield insights into permanent electrical signatures that could reflect upon enduring memories as fragments of long-term memory engrams.
Asunto(s)
Dendritas/fisiología , Memoria a Largo Plazo/fisiología , Modelos Neurológicos , Plasticidad Neuronal/fisiología , Animales , Electricidad , Epigénesis Genética , Espacio Extracelular/fisiología , Iones/metabolismo , Consolidación de la Memoria/fisiología , Transmisión Sináptica/fisiologíaRESUMEN
Although decision making is a ubiquitous function, the understanding of its underlying mechanisms remains limited, particularly at the single-cell level. In this study, we used the decision not to feed that follows satiation in the marine mollusk Aplysia to examine the role of putative decision-making neuron B51 in this process. B51 is a neuron in the feeding neural circuit that exhibits decision-making characteristics in vitro, which bias the circuit toward producing the motor programs responsible for biting behavior. Once satiated, Aplysia decided not to bite for a prolonged period of time (≥24h) when presented with a food stimulus that normally elicits feeding in non-satiated animals. Twenty-four hours after satiation, suppressed feeding was accompanied by a significant decrease of B51 excitability compared to the control group of unfed animals. No differences were measured in B51 resting membrane properties or synaptic input to B51 between the satiated and control groups. When B51 properties were measured at a time point in which feeding had recovered from the suppressive effects of satiation (i.e., 96 h after satiation), no difference in B51 excitability was observed between satiated and control groups. These findings indicate that B51 excitability changes in a manner that is coherent with the modifications in biting resulting from food satiation, thus implicating this neuron as a site of plasticity underlying the decision not to bite following food satiation in Aplysia.