Urotensin Ⅱ inhibits electrical activity of hippocampal CA1 neurons by potentiating the GABAA receptor-mediated Cl^- current

Objective To examine the effects of urotensin Ⅱ （UⅡ） on the discharges of neurons in CA1 area of hippocampal slices by using extracellular recording technique. Results ①In response to the application of UⅡ （0.3, 3.0, 30.0,300.0 nmol/L, n = 77） into the perfusate for 2 min, the spontaneous discharge rates （SDR） of 63/77 （81.8% ） neurons were significantly decreased in a dose-dependent manner. ②Pretreatment with bicuculline（BIC, 100 μmol/L）, a specific GABAs receptor antagonist, led to a marked increase in the SDR of 6/7 （85.71%） neurons in an epileptiform pattern. The increased discharges were not significantly changed after UⅡ （30.0 nmol/L） was applied into the perfusate for 2 min. ③Pretreatment with picrotoxin （ PIC, 50 μmol/L）, a selective blocker of Cl^- channel, led to an increase in the SDR of all 8/8（ 100% ） neurons. The increased discharges were not influenced by the UⅡ （30.0 nmol/L） applied. ④Application of nitric oxide synthase （NOS） inhibitor N^G nitro-L-arginine methyl ester （L-NAME, 50μmol/L） into the perfusate for 2 min also significantly augmented the SDR of 14/16 （87.5 % ） neurons , then UⅡ （30.0 nmol/L） applied into the perfusate reduced the increased the SDR of all 14/14 （ 100% ） neurons. Conclusion These results suggest that UⅡ may decrease neuronal activity by potentiating GABAA receptor-mediated CI current in hippocampal CA1 neurons, and involved with the mediation of nitric oxide.

Urotensin II inhibits electrical activity of hippoCampal CA1 neurons by potentiating the GABA(A) receptor-mediated Cl(-) current

Objective To examine the effects of urotensin II (UII) on the discharges of neurons in CA1 area of hippocampal slices by using extracellular recording technique. Results (1) In response to the application of UII (0.3, 3.0, 30.0, 300.0 nmol/L, n =77) into the perfusate for 2 min, the spontaneous discharge rates (SDR) of 63/77 (81.8%) neurons were significantly decreased in a dose-dependent manner. (2) Pretreatment with bicuculline (BIC, 100 mu mol/L), a specific GABA(A) receptor antagonist, led to a marked increase in the SDR of 6/7 (85.71%) neurons in an epileptiform pattern. The increased discharges were not significantly changed after UII (30.0 nmol/L) was applied into the perfusate for 2 min. (3) Pretreatment with picrotoxin (PIC, 50 mu mol/L) , a selective blocker of Cl(-) channel, led to an increase in the SDR of all 8/8 (100%) neurons. The increased discharges were not influenced by the UII (30.0 nmol/L) applied. (4) Application of nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mu mol/L) into the perfusate for 2 min also significantly augmented the SDR of 14/16 (87.5%) neurons , then UII (30.0 nmol/L) applied into the perfusate reduced the increased the SDR of all 14/14 ( 100% ) neurons. Conclusion These results suggest that UII may decrease neuronal activity by potentiating GABA(A) receptor-mediated Cl(-) current in hippocampal CA1 neurons, and involved with the mediation of nitric oxide.