Selective Spike Propagation in the Central Processes of an Invertebrate Neuron

Within a neuron, spike propagation can occur in a complex manner, with spikes propagating into some processes but not others. We study this phenomenon in an experimentally advantageous mechanoafferent in Aplysia, neuron B21. B21 has two processes within the CNS. One is ipsilateral to the soma and is referred to as the lateral process. The second travels into the contralateral hemiganglion and is referred to as the contralateral process. Previously we characterized spike propagation to the lateral process, which is an output region that contacts follower motor neurons. Spikes fail to actively propagate to the lateral process when B21 is peripherally activated at its resting potential. This propagation failure can be relieved if the medial regions of B21 are centrally depolarized during peripheral activation. This study examines spike propagation to the contralateral process. We show that, unlike the lateral process, active spike propagation in the contralateral process occurs when B21 is peripherally activated at its resting membrane potential. Thus spike propagation occurs selectively, favoring the contralateral process. Interestingly, the contralateral process of one B21 is immediately adjacent to the medial region of the bilaterally symmetrical cell. The B21 neurons are electrically coupled, suggesting that spikes propagating in the contralateral process of one cell could modify propagation in the sister neuron. Consistent with this idea, we show that lateral process propagation failures observed when a single B21 is peripherally activated can be relieved by central coactivation of the contralateral cell. These results imply that stimuli that coactivate the B21 neurons bilaterally are more apt to generate afferent activity that is transmitted to followers than stimuli that activate one cell.

Modeling Interactions Between Electrical Activity and Second-Messenger Cascades in Aplysia Neuron R15

The biophysical properties of neuron R15 in Aplysia endow it with the ability to express multiple modes of oscillatory electrical activity, such as beating and bursting. Previous modeling studies examined the ways in which membrane conductances contribute to the electrical activity of R15 and the ways in which extrinsic modulatory inputs alter the membrane conductances by biochemical cascades and influence the electrical activity. The goals of the present study were to examine the ways in which electrical activity influences the biochemical cascades and what dynamical properties emerge from the ongoing interactions between electrical activity and these cascades. The model proposed by Butera et al. in 1995 was extended to include equations for the binding of Ca2+ to calmodulin (CaM) and the actions of Ca2+/CaM on both adenylyl cyclase and phosphodiesterase. Simulations indicated that levels of cAMP oscillated during bursting and that these oscillations were approximately antiphasic to the oscillations of Ca2+. In the presence of cAMP oscillations, brief perturbations could switch the electrical activity between bursting and beating (bistability). Compared with a constant-cAMP model, oscillations of cAMP substantially expanded the range of bistability. Moreover, the integrated electrical/biochemical model simulated some early experimental results such as activity-dependent inactivation of the anomalous rectifier. The results of the present study suggest that the endogenous activity of R15 depends, in part, on interactions between electrical activity and biochemical cascades.

Modeling Slowly Bursting Neurons via Calcium Store and Voltage-Independent Calcium Current

Recent experiments indicate that the calcium store (e.g., endoplasmic reticulum) is involved in electrical bursting and [Ca2+]i oscillation in bursting neuronal cells. In this paper, we formulate a mathematical model for bursting neurons, which includes Ca2+ in the intracellular Ca2+ stores and a voltage-independent calcium channel (VICC). This VICC is activated by a depletion of Ca2+ concentration in the store, [Ca2+]CS. In this model, [Ca2+]CS oscillates slowly, and this slow dynamic in turn gives rise to electrical bursting. The newly formulated model thus is radically different from existing models of bursting excitable cells, whose mechanism owes its origin to the ion channels in the plasma membrane and the [Ca2+]i dynamics. In addition, this model is capable of providing answers to some puzzling phenomena, which the previous models could not (e.g., why cAMP, glucagon, and caffeine have ability to change the burst periodicity). Using mag-fura-2 fluorescent dyes, it would be interesting to verify the prediction of the model that (1) [Ca2+]CS oscillates in bursting neurons such as Aplysia neuron and (2) the neurotransmitters and hormones that affect the adenylate cyclase pathway can influence this oscillation.