Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Physiology and pathophysiology of nerve fibres
- 1 Ion channels in normal and pathophysiological mammalian peripheral myelinated nerve
- 2 Molecular anatomy of the node of Ranvier: newer concepts
- 3 Delayed rectifier type potassium currents in rabbit and rat axons and rabbit Schwann cells
- 4 Axonal signals for potassium channel expression in Schwann cells
- 5 Ion channels in human axons
- 6 An in vitro model of diabetic neuropathy: electrophysiological studies
- 7 Autoimmunity at the neuromuscular junction
- 8 Immunopathology and pathophysiology of experimental autoimmune encephalomyelitis
- 9 Pathophysiology of human demyelinating neuropathies
- 10 Conduction properties of central demyelinated axons: the generation of symptoms in demyelinating disease
- 11 Mechanisms of relapse and remission in multiple sclerosis
- 12 Glial transplantation in the treatment of myelin loss or deficiency
- Part II Pain
- Part III Control of central nervous system output
- Part IV Development, survival, regeneration and death
- Index
5 - Ion channels in human axons
from Part I - Physiology and pathophysiology of nerve fibres
Published online by Cambridge University Press: 04 August 2010
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Physiology and pathophysiology of nerve fibres
- 1 Ion channels in normal and pathophysiological mammalian peripheral myelinated nerve
- 2 Molecular anatomy of the node of Ranvier: newer concepts
- 3 Delayed rectifier type potassium currents in rabbit and rat axons and rabbit Schwann cells
- 4 Axonal signals for potassium channel expression in Schwann cells
- 5 Ion channels in human axons
- 6 An in vitro model of diabetic neuropathy: electrophysiological studies
- 7 Autoimmunity at the neuromuscular junction
- 8 Immunopathology and pathophysiology of experimental autoimmune encephalomyelitis
- 9 Pathophysiology of human demyelinating neuropathies
- 10 Conduction properties of central demyelinated axons: the generation of symptoms in demyelinating disease
- 11 Mechanisms of relapse and remission in multiple sclerosis
- 12 Glial transplantation in the treatment of myelin loss or deficiency
- Part II Pain
- Part III Control of central nervous system output
- Part IV Development, survival, regeneration and death
- Index
Summary
Some puzzling differences between rat and human myelinated nerve fibres emerged from work in this department some years ago. Rat nerve was being used to investigate the origin of the spontaneous activity which seems to underlie paraesthesiae, a common and disturbing symptom in neuropathies. It proved to be surprisingly difficult to induce rat nerve to become spontaneously active, although this is easily done in human nerve by manoeuvres such as ischaemia. A related finding is that rat nerve fibres accommodate more than those of humans to long stimuli. The electrotonic behaviour of nerve fibres differs between the two species in ways which suggest different populations of K+ channels (Bostock & Baker, 1988).
To try to understand these differences, single-channel and multi-channel patch clamping were applied to human axons, followed by voltage clamping of the node of Ranvier. Much of this work was done in collaboration with groups in Giessen, Hamburg and Munich. The results show that the ion channels in human axons are very similar to those in rat axons, as are the action potential and membrane currents in the node. The species differences are still not understood, but may result from differences in ion channel distribution or density, probably in the paranode or internode rather than the node. This chapter will summarize the information about ion channels in human peripheral myelinated axons which arose from this work, and relate this to descriptions of channels in other species.
- Type
- Chapter
- Information
- The Neurobiology of DiseaseContributions from Neuroscience to Clinical Neurology, pp. 47 - 60Publisher: Cambridge University PressPrint publication year: 1996
- 1
- Cited by