Paroxysmal depolarizing shift

IPSPs) and ionic conductances (persistent sodium current and high-threshold calcium current) and the post-PDS hyperpolarization is governed by multiple potassium currents, activated by calcium or sodium entry, as well as by leak current. The next cycle of depolarization is initiated by both synaptic drive and the hyperpolarization-activated IH current.^{[citation needed}

electrical or chemical stimulation of single neurons.^{[citation needed}

synaptic transmission.^{[citation needed]}. The amount of calcium entry through ion channels is critical in determining the physiological or pathological state of individual neurons,^[3]). For example, high concentration of calcium perturbs Ca-signalling cascades, leading to the death of neurons and circuits, while adequate amount of calcium will help in maintaining normal physiological function.^{[citation needed}

heavy metals such as Ni²⁺.^[1] Further evidence for Na⁺ dependent PDS is highlighted in leeches with the possibility of studying PDS in detail.^[1][4] It is likely that such type of PDS is sustained in the absence of Calcium, the case represents the non-synaptic nature of PDS. Finally, the Na/K pump and calcium activated potassium channel might play a role in terminating PDS. Paradoxically, there might arise the argument whether intracellular calcium could be able to repolarize the single neuron while blocking this calcium entry from the extracellular milieu. However, the other opportunity such as Na⁺-Ca²⁺ exchange as well as small contribution from intracellular stores need to be explored.^{[citation needed}

epileptic seizure if there is an underlying predisposition, and recording the spike can be an important aid in distinguishing seizure types.^{[citation needed}