Premium
PAINFUL NEUROPATHY DECREASES MEMBRANE CALCIUM CURRENT IN MAMMALIAN PRIMARY AFFERENT NEURONS
Author(s) -
Hogan Qh,
McCallum Jb,
Sarantopoulos C,
Aason M,
Mynlieff M,
Kwok Wm,
Bosnjak Zj
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1111/j.1529-8027.2000.22-34.x
Subject(s) - dorsal root ganglion , neuropathic pain , sciatic nerve , calcium , calcium channel , voltage dependent calcium channel , current clamp , nerve injury , patch clamp , sensory system , peripheral nerve injury , neuroscience , t type calcium channel , medicine , chemistry , electrophysiology , anesthesia , biology
Hyperexcitability of the primary afferent neuron leads to neuropathic pain following injury to peripheral axons. Changes in calcium channel function of sensory neurons following injury have not been directly examined at the channel level, even though calcium is a primary second messenger‐regulating neuronal function. We compared calcium currents (I‐Ca) in 101 acutely isolated dorsal root ganglion neurons from 31 rats with neuropathic pain following chronic constriction injury (CCI) of the sciatic nerve, to cells from 25 rats with normal sensory function following sham surgery. Cells projecting to the sciatic nerve were identified with a fluorescent label applied at the CCI site. Membrane function was determined using patch‐clamp techniques in current clamp mode, and in voltage‐clamp mode using solutions and conditions designed to isolate I‐Ca. Somata of peripheral sensory neurons from hyperalgesic rats demonstrated decreased I‐Ca. Peak calcium channel current density was diminished by injury from 3.06 +/− 0.30 pS/pF to 2.22 +/− 0.26 pS/pF in medium neurons, and from 3.93 +/− 0.38 pS/ pF to 2.99 +/− 0.40 pS/pF in large neurons. Under these voltage and pharmacologic conditions, medium‐sized neuropathic cells lacked obvious T‐type calcium currents which were present in 25% of medium‐sized cells from control animals. Altered Ca2+ signalling in injured sensory neurons may contribute to hyperexcitability leading to neuropathic pain.