The Neuroid revisited: A heuristic approach to model neural spike trains

AbstractIntroduction: Since it was introduced in 2012, the Neuroid has been used to aid in understanding how functionally different neural populations contribute to sensory information processing. However, insights about whether this neuron-model could perform better than others or about when its utilization should be considered have not been provided yet. Methods In an attempt to address this issue, a comparison between the Neuroid and the leaky-integrate-and-fire (LIF) model in terms of accuracy and computational cost was performed. Both models were tested for different stimulation amplitudes and stimulation periods, with time step sizes ranging from 10-4 to 1 ms. Results It was found that, although the Neuroid was able to produce more accurate results than its original version, its accuracy was lower than the achieved with the LIF model solved by the forward Euler method. On the other hand, the Neuroid performed its calculations in an amount of time significantly lower (Mulfactorial ANOVA test, p < 0.05) than that required by the LIF model when it was solved by using the forward Euler method. Moreover, it was possible to use Neuroid-based networks to replicate biologically relevant firing patterns produced by low-scale networks composed of more detailed neuron-models. Conclusion Results suggest that the Neuroid could be an interesting choice when computational resources are limited, although its use might be restricted to a narrow band of applications.

Lamina specific loss of inhibition may lead to distinct neuropathic manifestations: a computational modeling approach

Introduction It has been reported that inhibitory control at the superficial dorsal horn (SDH) can act in a regionally distinct manner, which suggests that regionally specific subpopulations of SDH inhibitory neurons may prevent one specific neuropathic condition. Methods In an attempt to address this issue, we provide an alternative approach by integrating neuroanatomical information provided by different studies to construct a network-model of the SDH. We use Neuroids to simulate each neuron included in that model by adapting available experimental evidence. Results Simulations suggest that the maintenance of the proper level of pain sensitivity may be attributed to lamina II inhibitory neurons and, therefore, hyperalgesia may be elicited by suppression of the inhibitory tone at that lamina. In contrast, lamina III inhibitory neurons are more likely to be responsible for keeping the nociceptive pathway from the mechanoreceptive pathway, so loss of inhibitory control in that region may result in allodynia. The SDH network-model is also able to replicate non-linearities associated to pain processing, such as Aβ-fiber mediated analgesia and frequency-dependent increase of the neural response. Discussion By incorporating biophysical accuracy and newer experimental evidence, the SDH network-model may become a valuable tool for assessing the contribution of specific SDH connectivity patterns to noxious transmission in both physiological and pathological conditions.