Unequal branch point filtering action in different types of dorsal root ganglion neurons of frogs

Stoney, Susan

doi:10.1016/0304-3940(85)90208-3

Cited by 25 publications

(19 citation statements)

References 14 publications

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“…However, there is one site within the axon of a somatosensory neuron where propagation of the peripherally‐derived action potentials can be effectively disrupted by M channel activation, and it is the point at which the axon, emanating from the cell body, bifurcates into the peripheral and central branches, the t‐junction (Figures and A). The bifurcation of an afferent axon is a point of lowest safety factor for action potential propagation (Stoney, ; Luscher et al, ; Debanne, ; Gemes et al, ; Du et al, ; Sundt et al, ), and both experiments and computer modelling suggest that hyperpolarization of a t‐junction (e.g. with retigabine) can result in the failure of an action potential to propagate (Du et al, ; Sundt et al, ; Figure ).…”

Section: Where Is the Site Of Analgesic Action Of M Channel Openers?mentioning

confidence: 99%

M‐type K⁺ channels in peripheral nociceptive pathways

Gao

Jaffe

et al. 2017

British J Pharmacology

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Pathological pain is a hyperexcitability disorder. Since the excitability of a neuron is set and controlled by a complement of ion channels it expresses, in order to understand and treat pain, we need to develop a mechanistic insight into the key ion channels controlling excitability within the mammalian pain pathways and how these ion channels are regulated and modulated in various physiological and pathophysiological settings. In this review, we will discuss the emerging data on the expression in pain pathways, functional role and modulation of a family of voltage‐gated K+ channels called ‘M channels’ (KCNQ, Kv7). M channels are increasingly recognized as important players in controlling pain signalling, especially within the peripheral somatosensory system. We will also discuss the therapeutic potential of M channels as analgesic drug targets.Linked ArticlesThis article is part of a themed section on Recent Advances in Targeting Ion Channels to Treat Chronic Pain. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.12/issuetoc/

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Section: Where Is the Site Of Analgesic Action Of M Channel Openers?mentioning

confidence: 99%

M‐type K⁺ channels in peripheral nociceptive pathways

Gao

Jaffe

et al. 2017

British J Pharmacology

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“…Accordingly, we used the shortest interstimulus interval that evoked a second S-spike as the soma's ARP. The least conduction interval (LCI) was the interspike interval at the ARP, measured peak-to-peak (Ito and Saiga, 1959;Stoney, 1985Stoney, , 1990. Both ARP and LCI were determined to 0.01-ms accuracy.…”

Section: Entire Cell Modelmentioning

confidence: 99%

Electrical Excitability of the Soma of Sensory Neurons Is Required for Spike Invasion of the Soma, but Not for Through-Conduction

Amir

Devor

2003

Biophysical Journal

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The cell soma of primary sensory neurons is electrically excitable, and is invaded by action potentials as they pass from the peripheral nerve, past the dorsal root ganglion (DRG) and toward the spinal cord. However, there are virtually no synapses in the DRG, and no signal processing is known to occur there. Why, then, are DRG cell somata excitable? We have constructed and validated an explicit model of the primary sensory neuron and used it to explore the role of electrical excitability of the cell soma in afferent signaling. Reduction and even elimination of soma excitability proved to have no detectable effect on the reliability of spike conduction past the DRG and into the spinal cord. Through-conduction is affected, however, by major changes in neuronal geometry in the region of the t-junction. In contrast to through-conduction, excitability of the soma and initial segment is essential for the invasion of afferent spikes into the cell soma. This implies that soma invasion has a previously unrecognized role in the physiology of afferent neurons, perhaps in the realm of metabolic coupling of the biosynthesis of signaling molecules required at the axon ends to functional demand, or in cell-cell interaction within sensory ganglia. Spike invasion of the soma in central nervous system neurons may play similar roles.

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“…In contrast to this excitatory influence, ionic conductance through I h channels reduces the input resistance of neurons and thereby limits AP initiation in response to a depolarizing current (Doan et al, 2004;Gasparini and DiFrancesco, 1997;Maccaferri and McBain, 1996). Since I h is expressed in axons (Birch et al, 1991;Takigawa et al, 1998), reduced input resistance may increase conductance failure through points of impedance mismatch, such as the T-branch where the central and peripheral limbs of the sensory neuron axon meet with the axonal stem that leads to the neuronal soma (Luscher et al, 1994;Stoney, 1985).…”

Section: Introductionmentioning

confidence: 99%

Hyperpolarization-activated current (Ih) contributes to excitability of primary sensory neurons in rats

Hogan

Poroli

2008

Brain Research

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In various excitable tissues, the hyperpolarization-activated, cyclic nucleotide-gated current (I h ) contributes to burst firing by depolarizing the membrane after a period of hyperpolarization. Alternatively, conductance through open channels I h channels of the resting membrane may impede excitability. Since primary sensory neurons of the dorsal root ganglion show both loss of I h and elevated excitability after peripheral axonal injury, we examined the contribution of I h to excitability of these neurons. We used a sharp electrode intracellular technique to record from neurons in nondissociated ganglia to avoid potential artefacts due to tissue dissociation and cytosolic dialysis. Neurons were categorized by conduction velocity. I h induced by hyperpolarizing voltage steps was completely blocked by ZD7288 (approximately 10μM), which concurrently eliminated the depolarizing sag of transmembrane potential during hyperpolarizing current injection. I h was most prominent in rapidly conducting Aα/β neurons, in which ZD7288 produced resting membrane hyperpolarization, slowed conduction velocity, prolonged action potential (AP) duration, and elevated input resistance. The rheobase current necessary to trigger an AP was elevated and repetitive firing was inhibited by ZD7288, indicating an excitatory influence of I h . Less I h was evident in more slowly conducting Aδ neurons, resulting in diminished effects of ZD7288 on AP parameters. Repetitive firing in these neurons was also inhibited by ZD7288, and the peak frequency of AP transmission during tetanic bursts was diminished by ZD7288. Slowly conducting C-type neurons showed minimal I h , and no effect of ZD7288 on excitability was seen. After spinal nerve ligation, axotomized neurons had less I h compared to control neurons and showed minimal effects of ZD7288 application. We conclude that I h supports sensory neuron excitability, and loss of I h is not a factor contributing to increased neuronal excitability after peripheral axonal injury.

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Unequal branch point filtering action in different types of dorsal root ganglion neurons of frogs

Cited by 25 publications

References 14 publications

M‐type K⁺ channels in peripheral nociceptive pathways

M‐type K⁺ channels in peripheral nociceptive pathways

Electrical Excitability of the Soma of Sensory Neurons Is Required for Spike Invasion of the Soma, but Not for Through-Conduction

Hyperpolarization-activated current (Ih) contributes to excitability of primary sensory neurons in rats

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Unequal branch point filtering action in different types of dorsal root ganglion neurons of frogs

Cited by 25 publications

References 14 publications

M‐type K+ channels in peripheral nociceptive pathways

M‐type K+ channels in peripheral nociceptive pathways

Electrical Excitability of the Soma of Sensory Neurons Is Required for Spike Invasion of the Soma, but Not for Through-Conduction

Hyperpolarization-activated current (Ih) contributes to excitability of primary sensory neurons in rats

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M‐type K⁺ channels in peripheral nociceptive pathways

M‐type K⁺ channels in peripheral nociceptive pathways