TY - JOUR
T1 - Lamina specific loss of inhibition may lead to distinct neuropathic manifestations
T2 - A computational modeling approach
AU - Prada, Erick Javier Argüello
AU - Silva Bustillos, Ricardo José
AU - Huerta, Mónica Karel
AU - Martínez, Antonio D’Alessandro
N1 - Publisher Copyright:
© 2015, Sociedade Brasileira de Engenharia Biomedica. All rights reserved.
PY - 2015/7/22
Y1 - 2015/7/22
N2 - 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.
AB - 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.
KW - Computational pain modeling
KW - Inhibitory control
KW - Network model
KW - Superficial dorsal horn circuit
UR - http://www.scopus.com/inward/record.url?scp=84937441497&partnerID=8YFLogxK
U2 - 10.1590/2446-4740.0734
DO - 10.1590/2446-4740.0734
M3 - Article
AN - SCOPUS:84937441497
SN - 1517-3151
VL - 31
SP - 133
EP - 147
JO - Revista Brasileira de Engenharia Biomedica
JF - Revista Brasileira de Engenharia Biomedica
IS - 2
ER -