Effects and wavelet spectral entropy analysis of rhubarb extracts rhein on synaptic transmission in rat hippocampal ca1 area in vitro

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Author:
GU Jian-wen()
ZHENG Chong-xun()
ZHANG Ai-hua()
Hiroshi Hasuo()
Takashi Akasu()
YANG Wen-tao()
YANG li-bin()
XIA Xun()
MA Yuan()
Journal Title:
CHINESE MEDICAL JOURNAL
Issue:
Volume 118, Issue 10, 2005
DOI:
Key Word:
rhein;hippocampus CA1;excitatory postsynaptic potential;presynaptic inhibition

Abstract: Background 5-dihydroxyanthraquinone-2-carboxylic acid (rhein) inhibits oxidoreduction induced by reducing nicotingamide adenine dinucleotide in the mitochondria and reducing reactive oxygen species, it also suppresses lipid peroxidation in rat brain homogenates. This study was to assess the effects of anthraquinone derivatives, rhein on synaptic transmission in the rat hippocampal CA1 pyramidal cell layer by intracellular recording.Methods The excitatory postsynaptic potential (EPSP) evoked by stimulation of the Schaffer collaterals in the presence of bicuculline (15 μmol/L) was depressed by application of rhein (0.3-30 μmol/L). The amplitude of the EPSP was restored within 20 minutes after removal of rhein from the supernatant. At a concentration of 30 μmol/L, rhein reduced the amplitude of the EPSP to 42%±3.7% (n=24) of the control. Subsequently, wavelet spectral entropy was used to analyze the EPSP. Results A strong positive correlation was observed between the wavelet spectral entropy and other parameters such as amplitude, slope of rising phase and slope of descending phase of the EPSP. The paired-pulse facilitation (PPF) of the EPSP was significantly increased by rhein (30 μmol/L). The inhibitory postsynaptic potential (IPSP) recorded in the presence of CNQX (20 μmol/L) and APV (40 μmol/L) is not altered by rhein (30 μmol/L). Conclusions Rhein (30 μmol/L) can decrease the frequency but not the amplitude of the miniature EPSP (mEPSP). It is suggested that rhein inhibits excitatory synaptic transmission by decreasing the release of glutamate in rat hippocampal CA1 pyramidal neurons.

  • [1]Toth Z, Hollrigel GS, Gorcs T, et al. Instantaneous perturbation of dentate interneuronal networks by a pressure wave-transient delivered to the neocortex. J Neurosci 1997;17:8106-8117.
  • [2]Benveniste H. The excitotoxin hypothesis in relation to cerebral ischemia. Cerebrovasc Brain Metab Rev 1991;3:213-245.
  • [3]Zauner A, Bullock R. The role of excitatory amino acids in severe brain trauma: opportunities for therapy: a review. J Neurotrauma 1995;12:547-554.
  • [4]Choi DW, Rothman SM. The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death. An Rev Neurosci 1990;13:171-183.
  • [5]Marion DW, Penrod LE, Kelsey SF, et al. Treatment of traumatic brain injury with moderate hypothermia. N Engl J Med 1997;336:540-546.
  • [6]Kontos HA, Povlishock JT. Oxygen radicals in brain injury. Cent Nerv Syst Trauma 1986;3:257-263.
  • [7]Gu J, Zhang X, Fei Z, et al. Rhubarb extracts in treating complications of severe cerebral injury. Chin Med J 2000;113:529-531.
  • [8]Lin XZ, Jin ZH. Effects of sennosides, rhubarb polysaccharides and emodin on the cytoplasmic free calcium in isolated rat brain cells. Yao Xue Xue Bao 1995;30:307-310.
  • [9]Cormier A, Morin C, Zini R, et al. In vitro effects of nicotine on mitochondrial respiration and superoxide anion generation. Brain Res 2001;900:72-79.
  • [10]Sato H, Ishizawa F, Hirayama H, et al. Extra-weak chemiluminescence of drugs. XIV. Quenching effects of anthraquinones on the extra-weak chemilumi-nescence from lipid peroxidation in rat brain homogenates. Yakugaku Zasshi 1992;112:199-202.
  • [11]Takeya M, Hasuo H, Akasu T. Effects of temperature increase on the propagation of presynaptic action potentials in the pathway between the Schaffer collaterals and hippocampal CA1 neurons. Neurosci Res 2002;42:175-185.
  • [12]Katz BB. The release of neural transmitter substances. Liverpool: Liverpool University Press; 1969.
  • [13]Thompson SM, Copogna M, Scanziani M. Presynaptic inhibition in the hippocampus. Trends Neurosci 1993;16:222-227.
  • [14]Behr J, Gloveli T, Schmitz D, et al. Dopamine depresses excitatory synaptic transmission onto rat subicular neurons via presynaptic D1-like dopamine receptors. J Neurophysiol 2000;84:112-119.
  • [15]Debanne D, Guérineau NC, G?hwiler BH, et al. Paired-pulse facilitation and depression at unitary synapses in rat hippocampus: quantal fluctuation affects subsequent release. J Physiol (Lond) 1996;491:163-176.
  • [16]Chang CH, Lin CC, Yang JJ, et al. Anti-inflammatory effects of emodin from ventilago leiocarpa. Am J Chin Med 1996;24:139-142.
  • [17]Reinert MM, Bullock R. Clinical trials in head injury. Neurol Res 1999;21:330-338.
  • [18]Benveniste HJ, rgensen MB, Sandberg M, et al. Ischemic damage in hippocampal CA1 is dependent on glutamate release and intact innervation from CA3. J Cereb Blood Flow Metab 1989;9:629-639.
  • [19]McIntosh TK, Saatman KE, Raghupathi R. Calcium and the pathogenesis of traumatic CNS injury: Cellular and molecular mechanisms. Neuroscientist 1997;3:169-175.
  • [20]Mattson MP, Scheff SW. Endogenous neuroprotection factors and traumatic brain injury: mechanisms of action and implications for therapy. J Neurotrauma 1994;11:3-33.
  • [21]Fineman I, Hovda DA, Smith M, et al. Concussive brain injury is associated with a prolonged accumulation of calcium: a 45 Ca autoradiographic study. Brain Res 1993;624:94-102.
  • [22]Kakarieka A, Braakman R, Schakel EH. Clinical significance of the finding of subarachnoid blood on CT scan after head injury. Acta Neurochir (Wien) 1994;129:1-5.
  • [23]McIntosh TK, Juhler M, Wieloch T. Novel pharmacologic strategies in the treatment of experimental traumatic brain injury: 1998. J Neurotrauma 1998;15:731-769.
  • [24]Lyeth BG, Gong Q-Z, Shields S, et al. Group I metabotropic glutamate antagonist reduces acute neuronal degeneration and behavioral deficits after traumatic brain injury in rats. Exp Neurol 2001;169:191-199.
  • [25]Hall ED. Free radicals and lipid peroxidation. In: Neurotrauma, Narayan RK, Wilberger JE, Povlishock JT, eds. New York: McGraw-Hill; 1996:1405-1419.
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