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Articles by H Peng
Total Records ( 2 ) for H Peng
  B. S Chen , H Peng and S. N. Wu
  Background

Dexmedetomidine (DEX), a selective agonist of 2-adrenergic receptors, is recognized to facilitate analgesia and anaesthesia in humans. Despite the potential for wide use, its effects on ion currents and membrane potential in neurones remain largely unclear.

Methods

We investigated the effects of DEX on ion channels in NG108-15 neuronal cells differentiated with dibutyryl cyclic AMP and in cultured cerebellar neurones.

Results

DEX suppressed the amplitude of delayed rectifier K+ current [IK(DR)] in a concentration-dependent manner with an IC50 value of 4.6 µM in NG108-15 cells. No change in the steady-state inactivation of IK(DR) was evident in the presence of DEX. A minimal binding scheme was also used to evaluate DEX-induced block of IK(DR). Inhibition of IK(DR) by DEX was still observed in cells preincubated with yohimbine (10 µM) or efaroxan (10 µM). DEX depressed the peak amplitude of Na+ current (INa), whereas it had minimal effect on L-type Ca2+ current. Under current-clamp configuration, DEX increased the duration of action potentials (APs). IK(DR) and INa in response to AP waveforms were more sensitive to block by DEX than those elicited during rectangular pulses. In isolated cerebellar granule cells, DEX also effectively suppressed IK(DR).

Conclusions

The effects of DEX are not limited to its interactions with 2-adrenergic receptors. Inhibitory effects on IK(DR) and INa constitute one of the underlying mechanisms through which DEX and its structurally related compounds might affect neuronal activity in vivo.

  Y Yang , J Weiner , Y Liu , A. J Smith , D. J Huss , R Winger , H Peng , P. D Cravens , M. K Racke and A. E. Lovett Racke
 

The extent to which myelin-specific Th1 and Th17 cells contribute to the pathogenesis of experimental autoimmune encephalomyelitis (EAE) is controversial. Combinations of interleukin (IL)-1β, IL-6, and IL-23 with transforming growth factor β were used to differentiate myelin-specific T cell receptor transgenic T cells into Th17 cells, none of which could induce EAE, whereas Th1 cells consistently transferred disease. However, IL-6 was found to promote the differentiation of encephalitogenic Th17 cells. Further analysis of myelin-specific T cells that were encephalitogenic in spontaneous EAE and actively induced EAE demonstrated that T-bet expression was critical for pathogenicity, regardless of cytokine expression by the encephalitogenic T cells. These data suggest that encephalitogenicity of myelin-specific T cells appears to be mediated by a pathway dependent on T-bet and not necessarily pathway-specific end products, such as interferon and IL-17.

 
 
 
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