Format

Send to

Choose Destination
Adv Exp Med Biol. 2017;1015:265-277. doi: 10.1007/978-3-319-62817-2_14.

IKD Current in Cold Transduction and Damage-Triggered Cold Hypersensitivity.

Author information

1
Departamento de Biología, Facultad de Química y Biología, and Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD), Universidad de Santiago de Chile, Alameda L. Bdo. O'Higgins 3363, 9160000, Santiago, Chile.
2
Centro Interdisciplinario de Neurociencia de Valparaíso and Instituto de Neurociencia, Facultad de Ciencias, Universidad de Valparaíso, 2340000, Valparaíso, Chile.
3
Departamento de Biología, Facultad de Química y Biología, and Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD), Universidad de Santiago de Chile, Alameda L. Bdo. O'Higgins 3363, 9160000, Santiago, Chile. rodolfo.madrid@usach.cl.

Abstract

In primary sensory neurons of the spinal and trigeminal somatosensory system, cold-sensitivity is strongly dependent on the functional balance between TRPM8 channels, the main molecular entity responsible for the cold-activated excitatory current, and Shaker-like Kv1.1-1.2 potassium channels, the molecular counterpart underlying the excitability brake current IKD. This slow-inactivating outward K+ current reduces the excitability of cold thermoreceptor neurons increasing their thermal threshold, and prevents unspecific activation by cold of neurons of other somatosensory modalities. Here we examine the main biophysical properties of this current in primary sensory neurons, its central role in cold thermotransduction, and its contribution to alterations in cold sensitivity triggered by peripheral nerve damage.

KEYWORDS:

4-AP; Cold hypersensitivity; Cold thermotransduction; Kv1 channels; Primary sensory neurons; TRPM8; α-DTx

PMID:
29080031
DOI:
10.1007/978-3-319-62817-2_14
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center