Role of cervical neurons in propriospinal inhibition of thoracic dorsal horn neurons

1992 ◽  
Vol 599 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Lawrence R. Poree ◽  
Lawrence P. Schramm
Keyword(s):  
Dorsal Horn ◽  
Dorsal Horn Neurons

Multiple Firing Patterns in Deep Dorsal Horn Neurons of the Spinal Cord: Computational Analysis of Mechanisms and Functional Implications

2010 ◽  
Vol 104 (4) ◽  
pp. 1978-1996 ◽  
Author(s):  
Yann Le Franc ◽  
Gwendal Le Masson
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Information Transfer ◽  
Network Effects ◽  
Neuronal Response ◽  
Sensory Information ◽  
Firing Patterns ◽  
Dorsal Horn Neurons ◽  
The Impact

Deep dorsal horn relay neurons (dDHNs) of the spinal cord are known to exhibit multiple firing patterns under the control of local metabotropic neuromodulation: tonic firing, plateau potential, and spontaneous oscillations. This work investigates the role of interactions between voltage-gated channels and the occurrence of different firing patterns and then correlates these two phenomena with their functional role in sensory information processing. We designed a conductance-based model using the NEURON software package, which successfully reproduced the classical features of plateau in dDHNs, including a wind-up of the neuronal response after repetitive stimulation. This modeling approach allowed us to systematically test the impact of conductance interactions on the firing patterns. We found that the expression of multiple firing patterns can be reproduced by changes in the balance between two currents (L-type calcium and potassium inward rectifier conductances). By investigating a possible generalization of the firing state switch, we found that the switch can also occur by varying the balance of any hyperpolarizing and depolarizing conductances. This result extends the control of the firing switch to neuromodulators or to network effects such as synaptic inhibition. We observed that the switch between the different firing patterns occurs as a continuous function in the model, revealing a particular intermediate state called the accelerating mode. To characterize the functional effect of a firing switch on information transfer, we used correlation analysis between a model of peripheral nociceptive afference and the dDHN model. The simulation results indicate that the accelerating mode was the optimal firing state for information transfer.

scholarly journals Sensory neuron–derived NaV1.7 contributes to dorsal horn neuron excitability

2020 ◽  
Vol 6 (8) ◽  
pp. eaax4568 ◽  
Author(s):  
Sascha R. A. Alles ◽  
Filipe Nascimento ◽  
Rafael Luján ◽  
Ana P. Luiz ◽  
Queensta Millet ◽  
...  
Keyword(s):  
Dorsal Horn ◽  
Dorsal Horn Neuron ◽  
Mutant Mice ◽  
Afferent Neuron ◽  
Null Mutant ◽  
Dorsal Horn Neurons ◽  
Afferent Nerves ◽  
Horn Neuron ◽  
Null Mutant Mice

Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensation. We examined the role of NaV1.7 in the dorsal horn of the spinal cord using an epitope-tagged NaV1.7 knock-in mouse. Immuno–electron microscopy showed the presence of NaV1.7 in dendrites of superficial dorsal horn neurons, despite the absence of mRNA. Rhizotomy of L5 afferent nerves lowered the levels of NaV1.7 in the dorsal horn. Peripheral nervous system–specific NaV1.7 null mutant mice showed central deficits, with lamina II dorsal horn tonic firing neurons more than halved and single spiking neurons more than doubled. NaV1.7 blocker PF05089771 diminished excitability in dorsal horn neurons but had no effect on NaV1.7 null mutant mice. These data demonstrate an unsuspected functional role of primary afferent neuron-generated NaV1.7 in dorsal horn neurons and an expression pattern that would not be predicted by transcriptomic analysis.

Role of Calcitonin Gene-Related Peptide in the Sensitization of Dorsal Horn Neurons to Mechanical Stimulation After Intradermal Injection of Capsaicin

2004 ◽  
Vol 92 (1) ◽  
pp. 320-326 ◽  
Author(s):  
Rui-Qing Sun ◽  
Nada B. Lawand ◽  
Qing Lin ◽  
William D. Willis
Keyword(s):  
Spinal Cord ◽  
Receptive Field ◽  
Dorsal Horn ◽  
Background Activity ◽  
Calcitonin Gene Related Peptide ◽  
Intradermal Injection ◽  
Dorsal Horn Neurons ◽  
Related Peptide ◽  
Calcitonin Gene

This study was designed to assess the role of calcitonin gene-related peptide (CGRP) and its receptor in the sensitization of dorsal horn neurons induced by intradermal injection of capsaicin in rats. Extracellular recordings were made from wide dynamic range (WDR) dorsal horn neurons with receptive fields on the hindpaw in the lumbar enlargement of anesthetized rats. The background activity and responses to brushing, pressing, and pinching the skin were assessed. A postsuperfusion or a presuperfusion of CGRP8-37 paradigm was followed. When tested 30 min after capsaicin injection, there was an increase in background activity and responses to brush, press, and pinch applied to the receptive field. Superfusion of CGRP8-37 into the spinal cord at 45 min after capsaicin injection significantly reversed the increased background activity and responses to brush, press, and pinch applied to the receptive field. On the other hand, spinal superfusion of CGRP8-37 prior to capsaicin injection prevented the increased background activity and responses to brush, press, and pinch of WDR neurons that occurred following capsaicin injection in control experiments. A sensitization of spinal dorsal horn neurons could also be induced by superfusion of the spinal cord with CGRP. The effect could be blocked by CGRP8-37 dose-dependently. Collectively, these results suggest that CGRP and its receptors are involved in the spinal cord central sensitization induced by intradermal injection of capsaicin.

scholarly journals Bidirectional Neuron–Glia Interactions Triggered by Deficiency of Glutamate Uptake at Spinal Sensory Synapses

2010 ◽  
Vol 104 (2) ◽  
pp. 713-725 ◽  
Author(s):  
Hui Nie ◽  
Haijun Zhang ◽  
Han-Rong Weng
Keyword(s):  
Dorsal Horn ◽  
Glial Cells ◽  
Synaptic Input ◽  
Spinal Dorsal Horn ◽  
Glutamate Uptake ◽  
Glutamate Transporters ◽  
Spinothalamic Tract ◽  
Dorsal Horn Neurons ◽  
Spinal Dorsal

Bidirectional interactions between neurons and glial cells are crucial to the genesis of pathological pain. The mechanisms regulating these interactions and the role of this process in relaying synaptic input in the spinal dorsal horn remain to be established. We studied the role of glutamate transporters in the regulation of such interactions. On pharmacological blockade of glutamate transporters, slow inward currents (SICs) appeared spontaneously and/or were evoked by peripheral synaptic input in the spinal superficial dorsal horn neurons, including the spinothalamic tract neurons. We showed that the SICs were induced by the release of glutamate from glial cells. On inhibition of glutamate uptake, the stimulation-induced, synaptically released glutamate activated glial cells and caused glial cells to release glutamate. Glial-derived glutamate acted on extrasynaptic N-methyl-d-aspartate (NMDA) receptors mainly composed of NR2B receptors and generated SICs, which led to depolarization and action potential generation in superficial spinal dorsal horn neurons. Thus glutamate transporters regulate glutamatergic neuron–glia interactions at spinal sensory synapses. When glutamate uptake is impaired, glial cells function like excitatory interneurons—they are activated by peripheral synaptic input and release glutamate to activate postsynaptic neurons in spinal pain pathways.

scholarly journals Peripheral and central hyperexcitability: Differential signs and symptoms in persistent pain

1997 ◽  
Vol 20 (3) ◽  
pp. 404-419 ◽  
Author(s):  
Terence J. Coderre ◽  
Joel Katz
Keyword(s):  
Neuropathic Pain ◽  
Postoperative Pain ◽  
Experimental Evidence ◽  
Dorsal Horn ◽  
Central Sensitization ◽  
Signs And Symptoms ◽  
Persistent Pain ◽  
Dorsal Horn Neurons ◽  
Target Article

This target article examines the clinical and experimental evidence for a role of peripheral and central hyperexcitability in persistent pain in four key areas: cutaneous hyperalgesia, referred pain, neuropathic pain, and postoperative pain. Each suggests that persistent pain depends not only on central sensitization, but also on inputs from damaged peripheral tissue. It is instructive to think of central sensitization as comprised of both an initial central sensitization and an ongoing central sensitization driven by inputs from peripheral sources. Each of these factors, initial sensitization, ongoing central sensitization, and inputs from peripheral sources, contributes to the net activity in dorsal horn neurons and thus influences the expression of persistent pain or hyperalgesia. Since each factor, peripheral inputs and central sensitization (initial or ongoing), can contribute to both the initiation and maintenance of persistent pain, therapies should target both peripheral and central sources of pathology.

scholarly journals Sensory neuron-derived Nav1.7 contributes to dorsal horn neuron excitability

2019 ◽  
Author(s):  
Sascha R.A. Alles ◽  
Filipe Nascimento ◽  
Rafael Luján ◽  
Queensta Millet ◽  
Ali Bangash ◽  
...  
Keyword(s):  
Dorsal Horn ◽  
Functional Role ◽  
Dorsal Horn Neuron ◽  
Spiking Neurons ◽  
Pain Sensation ◽  
Tonic Firing ◽  
Dorsal Horn Neurons ◽  
Immuno Electron Microscopy ◽  
Horn Neuron

SummaryExpression of the voltage-gated sodium channel Nav1.7 in sensory neurons is required for pain sensation. We examined the role of Nav1.7 in the dorsal horn of the spinal cord using an epitope-tagged knock-in mouse. Immuno-electron microscopy showed the presence of Nav1.7 in dendrites of lamina II neurons, despite the absence of mRNA. Peripheral nervous system-specific Nav1.7 KO mice showed central deficits with lamina II dorsal horn tonic firing neurons more than halved and single spiking neurons more than doubled. Nav1.7 blocker PF05089771 diminished excitability in dorsal horn neurons, but had no effect on Nav1.7 KO mice. These data demonstrate an unsuspected functional role of peripherally generated Nav1.7 in dorsal horn neurons and an expression pattern that would not be predicted by transcriptomic analysis.

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