scholarly journals Chronic compression of mouse dorsal root ganglion alters voltage-gated sodium and potassium currents in medium-sized dorsal root ganglion neurons

2011 ◽  
Vol 106 (6) ◽  
pp. 3067-3072 ◽  
Author(s):  
Ni Fan ◽  
David F. Donnelly ◽  
Robert H. LaMotte
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Small Diameter ◽  
Radicular Pain ◽  
Dorsal Root Ganglion Neurons ◽  
Delayed Rectifier ◽  
Drg Neurons ◽  
Voltage Dependent ◽  
Ganglion Neurons

Chronic compression (CCD) of the dorsal root ganglion (DRG) is a model of human radicular pain produced by intraforaminal stenosis and other disorders affecting the DRG, spinal nerve, or root. Previously, we examined electrophysiological changes in small-diameter lumbar level 3 (L3) and L4 DRG neurons treated with CCD; the present study extends these observations to medium-sized DRG neurons, which mediate additional sensory modalities, both nociceptive and non-nociceptive. Whole-cell patch-clamp recordings were obtained from medium-sized somata in the intact DRG in vitro. Compared with neurons from unoperated control animals, CCD neurons exhibited a decrease in the current threshold for action potential generation. In the CCD group, current densities of TTX-resistant and TTX-sensitive Na+ current were increased, whereas the density of delayed rectifier voltage-dependent K+ current was decreased. No change was observed in the transient or “A” current after CCD. We conclude that CCD in the mouse produces hyperexcitability in medium-sized DRG neurons, and the hyperexcitability is associated with an increased density of Na+ current and a decreased density of delayed rectifier voltage-dependent K+ current.

scholarly journals Increased Na+ and K+ currents in small mouse dorsal root ganglion neurons after ganglion compression

2011 ◽  
Vol 106 (1) ◽  
pp. 211-218 ◽  
Author(s):  
Ni Fan ◽  
Parul Sikand ◽  
David F. Donnelly ◽  
Chao Ma ◽  
Robert H. LaMotte
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Neuronal Response ◽  
Small Diameter ◽  
Neuronal Cell ◽  
Radicular Pain ◽  
Dorsal Root Ganglion Neurons ◽  
Delayed Rectifier ◽  
Ganglion Neurons

We investigated the effects of chronic compression (CCD) of the L3 and L4 dorsal root ganglion (DRG) on pain behavior in the mouse and on the electrophysiological properties of the small-diameter neuronal cell bodies in the intact ganglion. CCD is a model of human radicular pain produced by intraforaminal stenosis and other disorders affecting the DRG, spinal nerve, or root. On days 1, 3, 5, and 7 after the onset of compression, there was a significant decrease from preoperative values in the threshold mechanical force required to elicit a withdrawal of the foot ipsilateral to the CCD (tactile allodynia). Whole cell patch-clamp recordings were obtained, in vitro, from small-sized somata and, for the first time, in the intact DRG. Under current clamp, CCD neurons exhibited a significantly lower rheobase compared with controls. A few CCD but no control neurons exhibited spontaneous action potentials. CCD neurons showed an increase in the density of TTX-resistant and TTX-sensitive Na+ current. CCD neurons also exhibited an enhanced density of voltage-dependent K+ current, due to an increase in delayed rectifier K+ current, without a change in the transient or “A” current. We conclude that CCD in the mouse produces a model of radicular pain, as we have previously demonstrated in the rat. While the role of enhanced K+ current remains to be elucidated, we speculate that it represents a compensatory neuronal response to reduce ectopic or aberrant levels of neuronal activity produced by the injury.

Calcium currents and transmitter output in cultured spinal cord and dorsal root ganglion neurons

1986 ◽  
Vol 56 (5) ◽  
pp. 1257-1267 ◽  
Author(s):  
M. Jia ◽  
P. G. Nelson
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Calcium Currents ◽  
Dorsal Root Ganglion Neurons ◽  
Ion Concentration ◽  
Drg Neurons ◽  
Voltage Dependent ◽  
Ganglion Neurons

The effects of repetitive activation upon voltage-dependent calcium currents (ICa) and transmitter release were studied in dissociated cell cultures of fetal mouse spinal cord and dorsal root ganglion. Sodium and potassium currents were suppressed with tetrodotoxin (TTX) and tetraethylammonium (TEA) ions, 4-aminopyridine (4-AP), and cesium sulfate. Calcium currents were compared under voltage clamp before and after a series of depolarizing clamp pulses in spinal cord (SC) and dorsal root ganglion (DRG) neurons. Repetitive activation resulted in an exponential decline in ICa, with the decrease in ICa being much more marked in DRG compared with SC neurons. Both voltage-dependent inactivation and inactivation related to the intracellular movement of Ca2+ appeared to be involved in the decrement in ICa with repetitive activation. A decrease in transmitter output occurred with repetitive activation in DRG neurons but not in SC neurons (either excitatory or inhibitory). DRG neuron synaptic boutons had fewer mitochondria than did the boutons of either excitatory or inhibitory of SC neurons. The decrement in both ICa and synaptic transmitter output in DRG neurons could last for prolonged periods (at least minutes) following repetitive activation. We hypothesize that this vulnerability of DRG neurons to repetitive activation may be related, at least in part, to a relative incapacity to maintain a low intracellular calcium ion concentration [Ca]i during periods of increased calcium ingress associated with excitation. Such an incapacity to buffer [Ca]i may be one mechanism leading to the inactive synapses seen in some studies in vitro and in vivo of synaptic transmission.

Variation in IH, IIR, and ILEAK between acutely isolated adult rat dorsal root ganglion neurons of different size

1994 ◽  
Vol 71 (1) ◽  
pp. 271-279 ◽  
Author(s):  
R. S. Scroggs ◽  
S. M. Todorovic ◽  
E. G. Anderson ◽  
A. P. Fox
Keyword(s):  
Dorsal Root Ganglion ◽  
Action Potentials ◽  
Dorsal Root ◽  
Membrane Surface ◽  
Small Diameter ◽  
Reversal Potential ◽  
Dorsal Root Ganglion Neurons ◽  
Time Dependent ◽  
Drg Neurons ◽  
Ganglion Neurons

1. The distribution of IH, IIR, and ILEAK was studied in different diameter rat dorsal root ganglion (DRG) neuron cell bodies (neurons). DRG neurons were studied in three diameter ranges: small (19–27 microns), medium (33–37 microns), and large (44-54 microns). IH was defined as a slowly activating inward current evoked by hyperpolarizing voltage steps from a holding potential (HP) of -60 mV, and blocked by 1 mM Cs2+ but not 1 mM Ba2+. Inward rectifier current (IIR) was defined as a rapidly activating current evoked by hyperpolarizations from HP -60 mV, which rectified inwardly around the reversal potential for potassium (EK), and was completely blocked by 100 microM Ba2+. ILEAK was defined as an outward resting current at HP -60 mV, which did not rectify and was blocked by 100 microM Ba2+ but not by 2 mM Cs+. 2. IH was observed in 23 of 23 large, 11 of 12 medium, and in 9 of 20 small diameter DRG neurons tested. Peak IH normalized to membrane surface area was significantly greater in large than in medium or small diameter DRG neurons expressing IH. All neurons exhibiting IH under voltage clamp conditions had short duration action potentials and exhibited time-dependent rectification under current clamp conditions, properties similar to A-type DRG neurons. The 11 small diameter neurons not expressing IH had long duration action potentials and did not exhibit time-dependent rectification, properties similar to C-type DRG neurons. 3. IIR was detected in 18 of 22 medium diameter neurons tested.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Slow sodium conductances of dorsal root ganglion neurons: intraneuronal homogeneity and interneuronal heterogeneity

1994 ◽  
Vol 72 (6) ◽  
pp. 2796-2815 ◽  
Author(s):  
M. A. Rizzo ◽  
J. D. Kocsis ◽  
S. G. Waxman
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Half Time ◽  
Drg Neurons ◽  
Patch Clamp Technique ◽  
Adult Rat ◽  
Voltage Dependent ◽  
Order Of Magnitude ◽  
Ganglion Neurons

1. Voltage-dependent Na+ conductances were studied in small (18-25 microns diam) adult rat dorsal root ganglion (DRG) neurons with the use of the whole cell patch-clamp technique. Na+ currents were also recorded from larger (44-50 microns diam) neurons and compared with those of the small neurons. 2. The predominant Na+ conductance in the small neurons was selective over tetramethylammonium by at least 10-fold and was resistant to 1 microM external tetrodotoxin (TTX). Na+ conductances in many larger DRG neurons were kinetically faster and, in contrast, were blocked by 1 microM TTX. 3. The Na+ conductance in the small neurons was kinetically slow. Activation half-times were voltage dependent and ranged from 2 ms at -20 mV to 0.7 ms at +50 mV. Approximately 50% of the activation half-time was comprised of an initial delay. Inactivation half-times were voltage dependent and ranged from 11 ms at -20 mV to 2 ms at +50 mV. 4. Peak slow Na+ conductances were near maximal with conditioning potentials negative to -120 mV and were significantly reduced or eliminated with conditioning potentials positive to -40 mV. The slow Na+ conductance increased gradually with test potentials extending from -40 to +40 mV. In some cells the conductance could be saturated at +10 mV. Peak conductance/voltage relationships, although stable in a given neuron, revealed marked variability among neurons, spanning > 20- and 50-mV domains for steady-state activation and inactivation (current availability), respectively. 5. Kinetics remained stable within a given neuron over the course of an experiment. However, considerable kinetic variation was exhibited from neuron to neuron, such that the half-times of activation and of inactivation spanned an order of magnitude. In all small neurons studied there appeared to be a singular kinetic component of the current, based on sensitivity to the conditioning potential, voltage dependence of activation, and inactivation half-time. 6. Unique closing properties were exhibited by Na+ channels of the small neurons. Hyperpolarization following a depolarization-induced fully inactivated state resulted in tail currents that appeared to be the consequence of reactivation of the slow Na+ conductance. Tail currents recorded at various times during a fixed level of depolarization revealed that the underlying channels accumulated into a volatile inactivated state over the course of the preceding depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Permeation of Na+ through a delayed rectifier K+ channel in chick dorsal root ganglion neurons.

1994 ◽  
Vol 104 (4) ◽  
pp. 747-771 ◽  
Author(s):  
M J Callahan ◽  
S J Korn
Keyword(s):  
Dorsal Root Ganglion ◽  
Binding Site ◽  
Dorsal Root ◽  
Reversal Potential ◽  
Dorsal Root Ganglion Neurons ◽  
K Channel ◽  
Delayed Rectifier ◽  
Cation Binding Site ◽  
Voltage Dependent ◽  
Ganglion Neurons

In whole-cell patch clamp recordings from chick dorsal root ganglion neurons, removal of intracellular K+ resulted in the appearance of a large, voltage-dependent inward tail current (Icat). Icat was not Ca2+ dependent and was not blocked by Cd2+, but was blocked by Ba2+. The reversal potential for Icat shifted with the Nernst potential for [Na+]. The channel responsible for Icat had a cation permeability sequence of Na+ > Li+ > TMA+ > NMG+ (PX/PNa = 1:0.33:0.1:0) and was impermeable to Cl-. Addition of high intracellular concentrations of K+, Cs+, or Rb+ prevented the occurrence of Icat. Inhibition of Icat by intracellular K+ was voltage dependent, with an IC50 that ranged from 3.0-8.9 mM at membrane potentials between -50 and -110 mV. This voltage-dependent shift in IC50 (e-fold per 52 mV) is consistent with a single cation binding site approximately 50% of the distance into the membrane field. Icat displayed anomolous mole fraction behavior with respect to Na+ and K+; Icat was inhibited by 5 mM extracellular K+ in the presence of 160 mM Na+ and potentiated by equimolar substitution of 80 mM K+ for Na+. The percent inhibition produced by both extracellular and intracellular K+ at 5 mM was identical. Reversal potential measurements revealed that K+ was 65-105 times more permeant than Na+ through the Icat channel. Icat exhibited the same voltage and time dependence of inactivation, the same voltage dependence of activation, and the same macroscopic conductance as the delayed rectifier K+ current in these neurons. We conclude that Icat is a Na+ current that passes through a delayed rectifier K+ channel when intracellular K+ is reduced to below 30 mM. At intracellular K+ concentrations between 1 and 30 mM, PK/PNa remained constant while the conductance at -50 mV varied from 80 to 0% of maximum. These data suggest that the high selectivity of these channels for K+ over Na+ is due to the inability of Na+ to compete with K+ for an intracellular binding site, rather than a barrier that excludes Na+ from entry into the channel or a barrier such as a selectivity filter that prevents Na+ ions from passing through the channel.

scholarly journals Role of CaMK II α in the Injury of Dorsal Root Ganglion Neurons Induced by Ropivacaine Hydrochloride in the Dorsal Root Ganglion of Rats

2021 ◽  
pp. 1-7
Author(s):  
Wu Zhaoxia ◽  
Chen Meixin ◽  
Li Yiqun ◽  
Yang Shuxuan ◽  
Wen Xianjie
Keyword(s):  
Dorsal Root Ganglion ◽  
Cell Viability ◽  
Intracellular Calcium ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Drg Neurons ◽  
Apoptosis Rate ◽  
Ganglion Neurons ◽  
Ropivacaine Hydrochloride

Objective: To investigate whether CaMKⅡα participates in the dorsal root ganglion neurotoxicity induced by ropivacaine hydrochloride. Methods: DRG neurons were isolated from 1-day-old SD rats and cultured in vitro. pAd-shRNA-CaMKⅡα-DRG cells were constructed by RNA interference technique to inhibit the expression of CaMKⅡα. The experiment was divided into six groups: DRG group (DRG group), vector DRG group (vector group), pAd-shRNA- CaMKIIα-DRG group (pAd-shRNA group), DRG + ropivacaine group (DRG + R group), vector DRG + ropivacaine group (vector + R group), pAd-shRNA-CaMKII α - DRG + ropivacaine group (pAd-shRNA + R group), and the last three groups were treated with 3 mM ropivacaine hydrochloride for 4 hours. MTT assay was used to detect cell viability, flow cytometry was used to detect cell apoptosis rate, laser confocal microscopy was used to detect intracellular calcium level, and real-time PCR was used to detect the mRNA expression of CaMKⅡα, Cav3.2 and Cav3.3. Results: The cell viability of DRG+R group, vector+R group and pAd-shRNA+R group decreased significantly after 3 mM ropivacaine hydrochloride treatment for 4 h. Compared with DRG+R group, the cell viability of pAd-shRNA+R group was significantly higher. After 3 mM ropivacaine hydrochloride treatment for 4 h, the apoptosis rate of DRG + R group, vector + R group and pAd-shRNA + R group increased significantly. Compared with DRG+R group, the apoptosis rate in pAd shRNA+R group was significantly lower. After 3 mM ropivacaine hydrochloride treatment for 4 h, the intracellular calcium levels in DRG + R group, vector + R group and pAd-shRNA + R group were significantly increased, and the intracellular calcium levels in pAd-shRNA + R group were significantly lower than those in DRG + R group. The mRNA expressions of CaMKⅡα, Cav3.2 and Cav3.3 were significantly decreased in pAd- shRNA group. The mRNA expressions of CaMK Ⅱ α, Cav3.2 and Cav3.3 were up-regulated in DRG + R group, vector + R group and pAd-shRNA + R group after 3 mm ropivacaine treatment for 4 h. The mRNA expressions of CaMKⅡα, Cav3.2 and Cav3.3 in pAd-shRNA + R group were significantly lower than those in DRG + R group. Conclusion: Inhibition of CaMKⅡα expression can down regulate the expression of Cav3.2 and Cav3.3 mRNA, increase cell viability of DRG neurons, reduce the apoptosis rate, and improve the dorsal root ganglion neurotoxicity induced by ropivacaine hydrochloride.

Similar Electrophysiological Changes in Axotomized and Neighboring Intact Dorsal Root Ganglion Neurons

2003 ◽  
Vol 89 (3) ◽  
pp. 1588-1602 ◽  
Author(s):  
Chao Ma ◽  
Yousheng Shu ◽  
Zheng Zheng ◽  
Yong Chen ◽  
Hang Yao ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Receptive Fields ◽  
Input Resistance ◽  
Spinal Nerve ◽  
Dorsal Root Ganglion Neurons ◽  
Drg Neurons ◽  
Ganglion Neurons

We investigated electrophysiological changes in chronically axotomized and neighboring intact dorsal root ganglion (DRG) neurons in rats after either a peripheral axotomy consisting of an L5 spinal nerve ligation (SNL) or a central axotomy produced by an L5 partial rhizotomy (PR). SNL produced lasting hyperalgesia to punctate indentation and tactile allodynia to innocuous stroking of the foot ipsilateral to the injury. PR produced ipsilateral hyperalgesia without allodynia with recovery by day 10. Intracellular recordings were obtained in vivo from the cell bodies (somata) of axotomized and intact DRG neurons, some with functionally identified peripheral receptive fields. PR produced only minor electrophysiological changes in both axotomized and intact somata in L5 DRG. In contrast, extensive changes were observed after SNL in large- and medium-sized, but not small-sized, somata of intact (L4) as well as axotomized (L5) DRG neurons. These changes included (in relation to sham values) higher input resistance, lower current and voltage thresholds, and action potentials with longer durations and slower rising and falling rates. The incidence of spontaneous activity, recorded extracellularly from dorsal root fibers in vitro, was significantly higher (in relation to sham) after SNL but not after PR, and occurred in myelinated but not unmyelinated fibers from both L4 (9.1%) and L5 (16.7%) DRGs. We hypothesize that the changes in the electrophysiological properties of axotomized and intact DRG neurons after SNL are produced by a mechanism associated with Wallerian degeneration and that the hyperexcitability of intact neurons may contribute to SNL-induced hyperalgesia and allodynia.

scholarly journals Intra-articular AAV-PHP.S mediated chemogenetic targeting of knee-innervating dorsal root ganglion neurons alleviates inflammatory pain in mice

2020 ◽  
Author(s):  
Sampurna Chakrabarti ◽  
Luke A. Pattison ◽  
Balint Doleschall ◽  
Rebecca H. Rickman ◽  
Helen Blake ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Knee Joint ◽  
Joint Pain ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Drg Neurons ◽  
Neuron Excitability ◽  
Ganglion Neurons

AbstractObjectiveJoint pain is the major clinical symptom of arthritis that affects millions of people. Controlling the excitability of knee-innervating dorsal root ganglion (DRG) neurons (knee neurons) could potentially provide pain relief. Therefore, our objective was to evaluate whether the newly engineered adeno-associated virus (AAV) serotype, AAV-PHP.S, can deliver functional artificial receptors to control knee neuron excitability following intra-articular knee injection.MethodsAAV-PHP.S virus packaged with dTomato fluorescent protein and either excitatory (Gq) or inhibitory (Gi) designer receptors activated by designer drugs (DREADDs) was injected into the knee joint of adult mice. Labelling of DRG neurons by AAV-PHP.S from the knee was evaluated using immunohistochemistry. Functionality of Gq- and Gi-DREADDs was evaluated using whole-cell patch clamp electrophysiology on acutely cultured DRG neurons. Pain behavior in mice was assessed using a digging assay, dynamic weight bearing and rotarod, before and after intra-peritoneal administration of the DREADD activator, Compound 21.ResultsWe show that AAV-PHP.S can deliver functional genes into the DRG neurons when injected into the knee joint in a similar manner to the well-established retrograde tracer, fast blue. Short-term activation of AAV-PHP.S delivered Gq-DREADD increases excitability of knee neurons in vitro, without inducing overt pain in mice when activated in vivo. By contrast, in vivo Gi-DREADD activation alleviated complete Freund’s adjuvant mediated knee inflammation-induced deficits in digging behavior, with a concomitant decrease in knee neuron excitability observed in vitro.ConclusionsWe describe an AAV-mediated chemogenetic approach to specifically control joint pain, which may be utilized in translational arthritic pain research.

scholarly journals Cryopreservation of Canine Primary Dorsal Root Ganglion Neurons and Its Impact upon Susceptibility to Paramyxovirus Infection

2019 ◽  
Vol 20 (5) ◽  
pp. 1058 ◽  
Author(s):  
Sarah Schwarz ◽  
Ingo Spitzbarth ◽  
Wolfgang Baumgärtner ◽  
Annika Lehmbecker
Keyword(s):  
Dorsal Root Ganglion ◽  
Neurite Outgrowth ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Virus Infections ◽  
Drg Neurons ◽  
Rodent Host ◽  
Promising Tool ◽  
Ganglion Neurons

Canine dorsal root ganglion (DRG) neurons, isolated post mortem from adult dogs, could provide a promising tool to study neuropathogenesis of neurotropic virus infections with a non-rodent host spectrum. However, access to canine DRG is limited due to lack of donor tissue and the cryopreservation of DRG neurons would greatly facilitate experiments. The present study aimed (i) to establish canine DRG neurons as an in vitro model for canine distemper virus (CDV) infection; and (ii) to determine whether DRG neurons are cryopreservable and remain infectable with CDV. Neurons were characterized morphologically and phenotypically by light microscopy, immunofluorescence, and functionally, by studying their neurite outgrowth and infectability with CDV. Cryopreserved canine DRG neurons remained in culture for at least 12 days. Furthermore, both non-cryopreserved and cryopreserved DRG neurons were susceptible to infection with two different strains of CDV, albeit only one of the two strains (CDV R252) provided sufficient absolute numbers of infected neurons. However, cryopreserved DRG neurons showed reduced cell yield, neurite outgrowth, neurite branching, and soma size and reduced susceptibility to CDV infection. In conclusion, canine primary DRG neurons represent a suitable tool for investigations upon the pathogenesis of neuronal CDV infection. Moreover, despite certain limitations, cryopreserved canine DRG neurons generally provide a useful and practicable alternative to address questions regarding virus tropism and neuropathogenesis.

Kv3 channels contribute to the delayed rectifier current in small cultured mouse dorsal root ganglion neurons

2012 ◽  
Vol 303 (4) ◽  
pp. C406-C415 ◽  
Author(s):  
Elke Bocksteins ◽  
Gerda Van de Vijver ◽  
Pierre-Paul Van Bogaert ◽  
Dirk J. Snyders
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Neuronal Excitability ◽  
Dorsal Root Ganglion Neurons ◽  
Delayed Rectifier ◽  
Drg Neurons ◽  
M Current ◽  
Delayed Rectifier Current ◽  
Mouse Dorsal Root Ganglion ◽  
Ganglion Neurons

Delayed rectifier voltage-gated K+ (KV) channels are important determinants of neuronal excitability. However, the large number of KV subunits poses a major challenge to establish the molecular composition of the native neuronal K+ currents. A large part (∼60%) of the delayed rectifier current ( IK) in small mouse dorsal root ganglion (DRG) neurons has been shown to be carried by both homotetrameric KV2.1 and heterotetrameric channels of KV2 subunits with silent KV subunits (KVS), while a contribution of KV1 channels has also been demonstrated. Because KV3 subunits also generate delayed rectifier currents, we investigated the contribution of KV3 subunits to IK in small mouse DRG neurons. After stromatoxin (ScTx) pretreatment to block the KV2-containing component, application of 1 mM TEA caused significant additional block, indicating that the ScTx-insensitive part of IK could include KV1, KV3, and/or M-current channels (KCNQ2/3). Combining ScTx and dendrotoxin confirmed a relevant contribution of KV2 and KV2/KVS, and KV1 subunits to IK in small mouse DRG neurons. After application of these toxins, a significant TEA-sensitive current (∼19% of total IK) remained with biophysical properties that corresponded to those of KV3 currents obtained in expression systems. Using RT-PCR, we detected KV3.1–3 mRNA in DRG neurons. Furthermore, Western blot and immunocytochemistry using KV3.1-specific antibodies confirmed the presence of KV3.1 in cultured DRG neurons. These biophysical, pharmacological, and molecular results demonstrate a relevant contribution (∼19%) of KV3-containing channels to IK in small mouse DRG neurons, supporting a substantial role for KV3 subunits in these neurons.

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