*P< 0

*P< 0.05, Truncated Poisson distribution) The incidence of coupling between SGCs was defined as the percentage of recordings in which the dye was present in more than one SGC (Fig. currents, but not sodium currents, were detected in individual SGCs. SGCs enveloping differently sized neurons had comparable electrophysiological properties. SGCs in the compressed vs. control DRG exhibited significantly reduced inwardly rectifying potassium currents (Kir), increased input resistances and positively shifted resting membrane potentials. The reduction in Kir was greater for nociceptive medium-sized neurons compared to non-nociceptive neurons. Kir currents of SGCs around spontaneously active neurons were significantly reduced one day after compression but recovered by 7 days. These Avarofloxacin data demonstrate rapid alterations in glial membrane currents and GFAP expression in close temporal association with the development of neuronal hyperexcitability in the CCD model of europathic pain. However, these alterations are not fully sustained and suggest other mechanisms for the maintenance of the hyperexcitable state. Keywords:GFAP, gap junction, Kir current, DRG, intraforaminal stenosis == INTRODUCTION == Satellite glial cells (SGCs) form a distinct sheath around the cell bodies of individual sensory neurons in the dorsal root ganglion (Hanani, 2005;Pannese, 1981). Inwardly rectifying potassium (Kir) channels in SGCs may play an important role in maintaining ionic homeostasis by taking up potassium ions released during action potential activity in sensory neurons (Hanani 2005). Such activity will differ according to the functional properties of the neuron, for example whether its peripheral receptors discharge frequently (e.g. muscle spindles) or infrequently (nociceptors). In addition, ectopic spontaneous activity can originate within the dorsal root ganglion (DRG) after peripheral axotomy or after an injury of the ganglion itself. For example, after a chronic compression of the DRG (CCD) in the rat, ectopic discharges are generated from the neuronal axon or cell body (Ma and LaMotte 2007). However, there is little information regarding the SELL participation of satellite glial cells during the period of hyperexcitability or even the relationship between satellite glial cell electrophysiological parameters and the functional properties of the neuron enveloped by the glial cell. In the present study, we examined the effects of CCD around the expression of GFAP in SGCs, using GFAP as a marker, on the formation of gap junctional connections in SGCs, and on the electrophysiological characteristics of SGCs including their expression of Kir currents. We also explored the possible relationships between the electrophysiological properties of the single SGC and its associated neuron. == MATERIALS AND METHODS == == Animals == Adult, female Sprague-Dawley rats, weighing 120150g, were housed in groups of three or four under a 12 hr light/dark cycle. The use and handling of animals were approved by the Avarofloxacin Institutional Animal Care and Use Committee of the Yale University School of Medicine and were in accordance with guidelines provided by the National Institute of Health and the International Association for the Study of Pain. == Rod Implantation == The procedure for a chronic compression of the DRG (CCD) has been described (Hu and Xing, 1998; Song et al., 1999;Zhang et al., 1999). Under pentobarbital sodium anesthesia (Nembutal, 50 mg/kg i.p.), the right transverse process and intervertebral foramina were uncovered at L4and L5. Two L-shaped stainless rods (42 mm length and 0.4 mm diameter) were inserted into the L4and L5foramina, separately. After each rod was in place, the muscle and skin were sutured. == Immunocytochemical Labeling == Glutamine synthetase (GS), which catalyzes the conversion of glutamate to glutamine (Norenberg and Martinez-Hermandez, 1979), is usually selective for SGCs in DRG and trigeminal ganglia (Hanani, 2005). Thus, GS staining was used in the present study as a marker for SGCs. GFAP was used as a marker for glial cell activation. Injured and control rats were deeply anesthetized with isoflurane and transcardially perfused with saline followed by 4% paraformaldehyde at 6 Avarofloxacin hrs, 12 hrs, 1 day, 3 days, 7 days, 10 days and 21 days after surgery (n = Avarofloxacin 2 for each group). The L3 and L4 DRGs from both sides were removed and post-fixed in the same fixative for 4 hrs and then cryoprotected in 30% sucrose overnight. The tissue was frozen and sectioned at 10 Avarofloxacin m thickness on a cryostat. Tissuesections were washed three times with PBS, incubated with blocking buffer (10% normal horse serum and 0.2% Triton X-100 in.