Differential expression of alpha-adrenoceptor subtypes in rat dorsal root ganglion after chronic constriction injury / 华中科技大学学报（医学）（英德文版）

mRNAs of alpha-adrenoceptor (α-AR) subtypes are found in neurons in dorsal root ganglion (DRG) and change after peripheral nerve injury. In this study, the distribution of α-AR subtype proteins was studied in L5 DRG of normal rats and rats with chronic constriction injury of sciatic nerve (CCI). Using immunofluorescence technique, it was found that α1A-, α1B-, and α2A-AR proteins were expressed in large, medium, and small size neurons in normal DRG, and significantly increased in all size neurons 14 days after CCI. α1D- and α2C-AR was also expressed in all size neurons in normal DRG. However, α1D-AR was significantly increased and α2C-AR was decreased in small size neurons 14 days post CCI. α2B-AR neurons were not detectable in normal and CCI DRG. Co-expression of α1A- and α2A-AR in the same neuron was observed in normal DRG and increased post CCI. Collectively, these results indicated that there is distinct distribution of α-AR subtypes in DRG neurons, and the distribution and levels of expression of α-AR subtypes change differently after CCI. The up-regulation of α-AR subtypes in DRG neurons may play an important role in the process of generating and transmitting neuropathic pain.

Differential expression of alpha-adrenoceptor subtypes in rat dorsal root ganglion after chronic constriction injury / 华中科技大学学报（医学）（英德文版）

mRNAs of alpha-adrenoceptor (α-AR) subtypes are found in neurons in dorsal root ganglion (DRG) and change after peripheral nerve injury. In this study, the distribution of α-AR subtype proteins was studied in L5 DRG of normal rats and rats with chronic constriction injury of sciatic nerve (CCI). Using immunofluorescence technique, it was found that α1A-, α1B-, and α2A-AR proteins were expressed in large, medium, and small size neurons in normal DRG, and significantly increased in all size neurons 14 days after CCI. α1D- and α2C-AR was also expressed in all size neurons in normal DRG. However, α1D-AR was significantly increased and α2C-AR was decreased in small size neurons 14 days post CCI. α2B-AR neurons were not detectable in normal and CCI DRG. Co-expression of α1A- and α2A-AR in the same neuron was observed in normal DRG and increased post CCI. Collectively, these results indicated that there is distinct distribution of α-AR subtypes in DRG neurons, and the distribution and levels of expression of α-AR subtypes change differently after CCI. The up-regulation of α-AR subtypes in DRG neurons may play an important role in the process of generating and transmitting neuropathic pain.

The effect of niflumic acid on gamma aminobutyric acid activated current in DRG neurons / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the modulatory effect of niflumic acid (NFA) on gamma aminobutyric acid (GABA)-activated currents of dorsal root ganglion (DRG) neurons in rat.</p><p><b>METHODS</b>The whole-cell patch-clamp technique was used to record the NFA- and GABA-activated currents in neurons freshly dissociated from rat DRG neurons.</p><p><b>RESULTS</b>Application of NFA(0.1 - 100 micromol/L) could induce concentration-dependent outward currents in some cells (21/48,43.75%), and GABA (0.1 - 100 micromol/L) could induce concentration-dependent inward currents in some cells(150/159,94.32%). NFA-(100 micromol/L) and GABA-(100 micromol/L) activated currents were (0.27 +/- 0.06) nA (n = 12) and (1.29 +/- 0.72) nA (n = 53) respectively. However, pre-application of NFA (0.1 - 100 micromol/L) could inhibit the GABA-activated inward current which was identified to be GABAA receptor-mediated current. The inhibitory effects of NFA were concentration-dependent. NFA could not alter the EC50 (about 30 micromol/L) and inverse potential (about -10 mV) of GABA-activated current (P > 0.05).</p><p><b>CONCLUSION</b>Pre-application of NFA exerts a more strong inhibitory effect on the peak value of GABA-activated current.</p>

The effect of niflumic acid and blocker of calcium channel on the desensitization of gamma aminobutyric acid-activated current / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the modulatory effect of niflumic acid and blocker of calcium channel on the desensitization of gamma aminobutyric acid (GABA)-activated currents in dorsal root ganglion(DRG) neurons from rat.</p><p><b>METHODS</b>The whole-cell patch-clamp technique was used to observe the modulatory effect of niflumic acid and blocker of calcium channel on the desensitization of GABA-activated currents in neurons freshly dissociated from rat DRG neurons.</p><p><b>RESULTS</b>Application of GABA (0.1-1 000 micromol/L) could induce concentration-dependent inward currents in some cells (212/223, 95.11%). GABA-(100 micromol/L) activated currents was (1.32 +/- 0.74) nA (n = 84). However, pre-application of niflumic acid (1-100 micromol/L) and nitrendipine (specific blocker of L-calcium channel)(0.1-30 micromol/L) could inhibit the GABA-activated inward current which was identified to be GABAA receptor-mediated current. The inhibitory effects of niflumic acid and nitrendipine were concentration-dependent. The suppression rate of 10 micromol/L niflumic acid and nitrendipine to GABA-activated currents were (31.60% +/- 4.87%) (n = 19) and (43.60% < or = 5.10%) (n = 5), respectively. The desensitization of GABA-activated currents had double exponential characteristic. Tau value was (14.68 +/- 5.11) s (n = 6) and (175.8 +/- 42.67) s (n = 6, r = 0.9647), respectively. Pre-application of niflumic acid (100 micromol/L) and nickel chloride (nonspecific blocker of L-calcium channel) (100 micromol/L) altered tau value of the desensitization of GABA-activated currents, tau value reduced for (4.64 +/- 2.21) s (n = 3), (43.70 +/- 14.34) s ( n = 3, r = 0.9548) and (4.64 +/- 2.21) s (n = 3), (43.70 +/- 14.34) s (n = 3, r = 0.9721).</p><p><b>CONCLUSION</b>Pre-application of niflumic acid exerts a more strong inhibitory effect on the peak value of GABA-activated current, which possibly is through blocking the calcium-activated chloride ion channel to accelerate the desensitization of GABA-activated currents.</p>

Effect of nitric oxide on the somatic membrane of rat DRG neurons / 中国应用生理学杂志

<p><b>AIM</b>To observe the role of nitric oxide in dorsal root ganglion (DRG) neurons and its related ionic mechanisms, and explore the function of NO in pain transmission process.</p><p><b>METHODS</b>In freshly isolated rat DRG samples, using intracellular recording technique, we perfused sodium nitroprusside (NO donor) to observe the role of NO in DRG neurons.</p><p><b>RESULTS</b>In 77.45% of the bath cells, application of sodium nitroprusside (10 -100 mmol/L) induced concentration-dependent membrane hyperpolarization (79/102), and remaining neurons had no response. The membrane conductance increased from control value of (21.06 +/- 1.94) nS to (23.08 +/- 0.92) nS during sodium nitroprusside induced hyperpolarization. L-NAME (1 mmol/L), CdCl2 (0.1 mmol/L) and non-sodium BSS failed to change the amplitude of sodium nitroprusside induced hyperpolarization. When BSS containing 10 mmol/L TEA was used, sodium nitroprusside induced hyperpolarization was obviously inhibited.</p><p><b>CONCLUSION</b>Sodium nitroprusside could cause concentration-dependent hyperpolarization in DRG neurons by activating K+ channels.</p>