Experimental neurology
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Experimental neurology · Jun 2004
The role of capsaicin-sensitive afferent fibers in the lower urinary tract dysfunction induced by chronic spinal cord injury in rats.
The role of capsaicin-sensitive afferents in neurogenic voiding dysfunction was studied in chronic spinal cord injured rats (SCI). Cystometry and external urethral sphincter (EUS) electromyography were performed on 2 consecutive days after induction of urethane anesthesia in SCI rats 6-8 weeks after spinal cord injury. SCI rats exhibited voiding abnormalities including: non-voiding contractions (NVCs) before micturition, increased volume threshold (VT) for initiating voiding, increased amplitude and duration of voiding contractions, decreased voiding efficiency, increased residual urine, and changes in the pattern of the EUS-EMG. ⋯ Capsaicin treatment increased the percentage of animals (from 55% to 80%) that voided on day 1. The results indicate that capsaicin-sensitive C-fiber bladder afferents are not essential for reflex micturition in SCI rats. However, these afferents do contribute to overactivity of the bladder and detrusor sphincter dyssynergia in deeply anesthetized SCI rats.
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Experimental neurology · May 2004
Suppression of neuropathic pain by peripheral electrical stimulation in rats: mu-opioid receptor and NMDA receptor implicated.
Peripheral electrical stimulation (PES) has been utilized to manage chronic pain associated with nerve injury. However, the data on clinical effectiveness are conflicting and the neurophysiological mechanism is not well known. This study was designed to assess whether PES relieved neuropathic pain and its possible mechanisms. ⋯ The results are as follows: (1) PES relieved neuropathic pain and the effect was blocked by 1.0 mg/kg naloxone. (2) The effect of one session of PES lasted up to 12 h. (3) Repetitive PES showed a cumulative effect and no tolerance was observed. (4) There was a significant increase of NR1 immunoreactivity in the superficial laminae of the spinal cord of neuropathic pain rats as compared with naive rats. This increase could be reversed by repetitive 2 Hz PES. These results suggest that PES can relieve neuropathic pain, and that mu-opioid receptors and NMDA receptors are involved in the effect of PES.
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Experimental neurology · Apr 2004
Comparative StudyNociceptive response to innocuous mechanical stimulation is mediated via myelinated afferents and NK-1 receptor activation in a rat model of neuropathic pain.
Peripheral nerve injury in humans can produce a persistent pain state characterized by spontaneous pain and painful responses to normally innocuous stimuli (allodynia). Here we attempt to identify some of the neurophysiological and neurochemical mechanisms underlying neuropathic pain using an animal model of peripheral neuropathy induced in male Sprague-Dawley rats by placing a 2-mm polyethylene cuff around the left sciatic nerve according to the method of Mosconi and Kruger. von Frey hair testing confirmed tactile allodynia in all cuff-implanted rats before electrophysiological testing. Rats were anesthetized and spinalized for extracellular recording from single spinal wide dynamic range neurons (L(3-4)). ⋯ A result of this is that tonic release of substance P from the central terminals of these phenotypically altered neurons would lead to ongoing excitation of NK-1-expressing nociceptive spinal neurons. In addition, these spinal neurons would also exhibit exaggerated responses to innocuous pressure stimulation. The data in this study put forth a possible neurophysiological and neurochemical basis of neuropathic pain and identify substance P and the NK-1 receptor as potential neurochemical targets for its management.
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Experimental neurology · Jan 2004
Cyclooxygenase inhibition in nerve-injury- and TNF-induced hyperalgesia in the rat.
After nerve injury, cyclooxygenase-2 (COX-2) is upregulated in spinal cord and peripheral nerve, the latter being dependent on tumor necrosis factor-alpha (TNF). Here we asked whether COX inhibitors attenuate pain behavior induced by chronic constrictive sciatic nerve injury (CCI) or intraneural injection of TNF (2.5 pg/ml). Rats received either 0.9% saline, the nonselective COX inhibitor ibuprofen (40 mg/kg) or the selective COX-2 inhibitor celecoxib (10 or 30 mg/kg) twice daily by gavage started 2 days before, 12 h or 7 days after surgery. ⋯ In spinal cord, no change in PGE2 levels was observed. In contrast to the marked inhibition of nerve-injury-induced upregulation of PGE2 by COX inhibitors, the effect on pain behavior was modest. Nerve-injury- and TNF-induced pain-related behavior seem to be only partly dependent on peripheral prostaglandins.
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Experimental neurology · Nov 2003
Thyroid hormone reduces the loss of axotomized sensory neurons in dorsal root ganglia after sciatic nerve transection in adult rat.
We have shown that a local administration of thyroid hormones (T3) at the level of transected rat sciatic nerve induced a significant increase in the number of regenerated axons. To address the question of whether local administration of T3 rescues the axotomized sensory neurons from death, in the present study we estimated the total number of surviving neurons per dorsal root ganglion (DRG) in three experimental group animals. Forty-five days following rat sciatic nerve transection, the lumbar (L4 and L5) DRG were removed from PBS-control, T3-treated as well as from unoperated rats, and serial sections (1 microm) were cut. ⋯ In addition, the volume of ganglia showed a similar tendency. These results suggest that T3 rescues a high number of axotomized sensory neurons from death and allows these cells to grow new axons. We believe that the relative preservation of neurons is important in considering future therapeutic approaches of human peripheral nerve lesion and sensory neuropathy.