[1]

朱大年.神经系统功能活动的基本原理//姚泰.生理学.北京: 人民卫生出版社, 2005: 410-411.
[2]

胡刚.镇静催眠药//杨世杰.药理学.北京: 人民卫生出版社, 2005: 196-197.
[3] Olsen RW, Sieghart W. GABAA receptors: Subtypes provide diver-sity of function and pharmacology. Neuropharmacology, 2009, 56(1): 141-148.  doi: 10.1016/j.neuropharm.2008.07.045
[4] Lüddens H, Seeburg PH, Korpi ER. Impact of beta and gamma variants on ligand-binding properties of gamma-aminobutyric acid type A receptors. Mol Pharmacol, 1994, 45(5): 810-814.
[5] Wingrove PB, Wafford KA, Bain C, et al. The modulatory action of loreclezole at the gamma-aminobutyric acid type A receptor is determined by a single amino acid in the beta 2 and beta 3 subunit. Proc Natl Acad Sci USA, 1994, 91(10): 4569-4573.  doi: 10.1073/pnas.91.10.4569
[6] Korpi ER, Kuner T, Seeburg PH, et al. Selective antagonist for the cerebellar granule cell-specific gamma-aminobutyric acid type A receptor. Mol Pharmacol, 1995, 47(2): 283-289.
[7] Pirker S, Schwarzer C, Wieselthaler A, et al. GABAA receptors: immunocytochemical distribution of 13 subunits in the adult rat brain. Neuroscience, 2000, 101(4): 815-850.  doi: 10.1016/S0306-4522(00)00442-5
[8] Uusi-Oukari M, Korpi ER. Regulation of GABAA receptor subunit expression by pharmacological agents. Pharmacol Rev, 2010, 62(1): 97-135.
[9] Yee BK, Keist R, von Boehmer L, et al. A schizophrenia-related sensorimotor deficit links α3-containing GABAA receptors to a dopamine hyperfunction. Proc Natl Acad Sci USA, 2005, 102(47): 17154-17159.  doi: 10.1073/pnas.0508752102
[10] Smith SS, Gong QH, Hsu FC, et al. GABAA receptor α4 subunit suppression prevents withdrawal properties of an endogenous steroid. Nature, 1998, 392(6679): 926-930.  doi: 10.1038/31948
[11] Holt RA, Bateson AN, Martin IL. Chronic treatment with diazepam or abecarnil differently affects the expression of GABAA receptor subunit mRNAs in the rat cortex. Neuropharmacology, 1996, 35(9-10): 1457-1463.  doi: 10.1016/S0028-3908(96)00064-0
[12] Collinson N, Kuenzi FM, Jarolimek W, et al. Enhanced learning and memory and altered GABAergic synaptic transmission in mice lacking the alpha 5 subunit of the GABAA receptor. J Neurosci, 2002, 22(13) : 5572-5580.  doi: 10.1523/JNEUROSCI.22-13-05572.2002
[13] Korpi ER, Kleingoor C, Kettenmann H, et al. Benzodiazepine-induced motor impairment linked to point mutation in cerebellar GABAA receptor. Nature. 1993, 361(6410): 356-359.  doi: 10.1038/361356a0
[14] Jurd R, Arras M, Lambert S, et al. General anesthetic actions in vivo strongly attenuated by a point mutation in the GABAA receptor β3 subunit. FASEB J, 2003, 17(2): 250-252.  doi: 10.1096/fj.02-0611fje
[15] Reynolds DS, Rosahl TW, Cirone J, et al. Sedation and anesthesia mediated by distinct GABAA receptor isoforms. J Neurosci, 2003, 23(24): 8608-8617.  doi: 10.1523/JNEUROSCI.23-24-08608.2003
[16] Zeller A, Arras M, Lazaris A, et al. Distinct molecular targets for the central respiratory and cardiac actions of the general anesthetics etomidate and propofol. FASEB J, 2005, 19(12): 1677-1679.  doi: 10.1096/fj.04-3443fje
[17] Cirone J, Rosahl TW, Reynolds DS, et al. γ-aminobutyric acid type A receptor β2 subunit mediates the hypothermic effect of etomidate in mice. Anesthesiology, 2004, 100(6): 1438-1445.  doi: 10.1097/00000542-200406000-00016
[18] Homanics GE, DeLorey TM, Firestone LL, et al. Mice devoid of γ-aminobutyrate type A receptor β3 subunit have epilepsy, cleft palate, and hypersensitive behavior. Proc Natl Acad Sci USA, 1997, 94(8): 4143-4148.  doi: 10.1073/pnas.94.8.4143
[19] Günther U, Benson J, Benke D, et al. Benzodiazepine-insensitive mice generated by targeted disruption of the γ2 subunit gene of γ-aminobutyric acid type A receptors. Proc Natl Acad Sci USA, 1995, 92(17): 7749-7753.  doi: 10.1073/pnas.92.17.7749
[20] Mihalek RM, Bowers BJ, Wehner JM, et al. GABAA receptor delta subunit knockout mice have multiple defects in behavioral responses to ethanol. Alcohol Clin Exp Res, 2001, 25(12): 1708-1718.
[21] Maziere M, Hantraye P, Prenant C, et al. Synthesis of ethyl 8-fluo-ro-5, 6-dihydro-5-[11C]methyl-6-oxo-4H-imidazo[1, 5-a][1, 4]benzodiazepine-3-carboxylate (RO 15.1788-11C): A specific radi-oligand for the in vivo study of central benzodiazepine receptors by positron emission tomography. Int J Appl Radiat Isot, 1984, 35(10): 973-976.  doi: 10.1016/0020-708X(84)90215-1
[22] Suzuki K, Inoue O, Hashimoto K, et al. Computer-con-trolled large scale production of high specific activity[11C]RO 15-1788 for PET studies of benzodiazepine receptors. Int J Appl Radiat Isot, 1985, 36(12): 971-976.  doi: 10.1016/0020-708X(85)90258-3
[23] Debruyne D, Abadie P, Barre L, et al. Plasma pharmacokinetics and metabolism of the benzodiazepine antagonist[11C] Ro 15-1788 (flumazenil) in baboon and human during positron emission tomography studies. Eur J Drug Metab Pharmacokinet, 1991, 16(2): 141-152.
[24] Chugani D, Muzik O, Juhász C, et al. Postnatal maturation of human GABAA receptors measured with positron emission tomog-raphy. Ann Neurol, 2001, 49(5): 618-626.  doi: 10.1002/ana.1003
[25] Salmi E, Kaisti K, Metsähonkala L, et al. Sevoflurane and propofol increase 11C-flumazenil binding to gamma-aminobutyric acidA receptors in humans. Anesth Analg, 2004, 99(5): 1420-1426.
[26] Prevett MC, Lammertsma AA, Brooks DJ, et al. Benzodiazepine-GABAA receptors in idiopathic generalized epilepsy measured[11C] flumazenil and positron emission tomography. Epilepsia, 1995, 36(2): 113-121.  doi: 10.1111/j.1528-1157.1995.tb00969.x
[27] Koepp MJ, Richardson MP, Brooks DJ, et al. Central benzodi-azepine/γ-aminobutyric acid A receptors in idiopathic generalized epilepsy: an[11C] flumazenil positron emission tomography study. Epilepsia, 1997, 38(10): 1089-1097.  doi: 10.1111/j.1528-1157.1997.tb01198.x
[28] Odano I, Halldin C, Karlsson P, et al.[18F] flumazenil binding to central benzodiazepine receptor studies by PET- Quantitative anal-ysis and comparisons with[11C] flumazenil-. NeuroImage, 2009, 45(3): 891-902.  doi: 10.1016/j.neuroimage.2008.12.005
[29] Dedeurwaerdere S, Gregoire MC, Vivash L, et al. In-vivo imaging characteristics of two fluorinated flumazenil radiotracers in the rat. Eur J Nucl Med Mol Imaging, 2009, 36(6): 958-965.  doi: 10.1007/s00259-009-1066-4
[30] Gründer G, Siessmeier T, Lange-Asschenfeldt C, et al.[18F] Fluo-roethylflumazenil: a novel tracer for PET imaging of human benzo-diazepine receptors. Eur J Nucl Med, 2001, 28(10): 1463-1470.  doi: 10.1007/s002590100594
[31] Comar D, Maziere M, Cepeda C, et al. The kinetics and displace-ment of[11C] flunitrazepam in the brain of the living baboon. Eur J Pharmacol, 1981, 75(1): 21-26.  doi: 10.1016/0014-2999(81)90340-X
[32] Comar D, Maziere M, Godot JM, et al. Visualisation of 11C-fluni-trazepam displacement in the brain of the live baboon. Nature, 1979, 280(5720): 329-331.  doi: 10.1038/280329a0
[33] Ishiwata K, Yanai K, Ido T, et al. Synthesis and biodistribution of[11C] fludiazepam for imaging benzodiazepine receptors. Int J Rad Appl Instrum B, 1988, 15(4): 365-371.  doi: 10.1016/0883-2897(88)90005-0
[34] Bottlaender M, Brouillet E, Varastet M, et al. In vivo high intrinsic efficacy of triazolam: a positron emission tomography study in non-human primates. J Neurochem, 1994, 62(3): 1102-1111.
[35] Dobbs FR, Banks W, Fleishaker JC, et al. Studies with[11C] alprazolam: an agonist for the benzodiazepine receptor. Nucl Med Biol, 1995, 22(4): 459-466.
[36] Frost JJ, Wagner HN Jr, Dannals RF, et al. Imaging benzodiazepine receptors in man with[11C] suriclone by positron emission tomogra-phy. Eur J Pharmacol, 1986, 122(3): 381-383.  doi: 10.1016/0014-2999(86)90422-X
[37] la Fougère C, Rominger A, Förster S, et al. PET and SPECT in epilepsy: A critical review. Epilepsy Behav, 2009, 15(1): 50-55.  doi: 10.1016/j.yebeh.2009.02.025
[38] Savic I, Persson A, Roland P, et al. In-vivo demonstration of reduced benzodiazepine receptor binding in human epileptic foci. Lancet, 1988, 2(8616): 863-866.
[39] Muzik O, da Silva EA, Juhasz C, et al. Intracranial EEG versus flumazenil and glucose PET in children with extratemporal lobe epilepsy. Neurology, 2000, 54(1): 171-179.
[40] Koepp MJ, Labbé C, Richardson MP, et al. Regional hippocampal[11C] flumazenil PET in temporal lobe epilepsy with unilateral and bilateral hippocampal sclerosis. Brain, 1997, 120(10): 1865-1876.  doi: 10.1093/brain/120.10.1865
[41] Hammers A, Koepp MJ, Richardson MP, et al. Central benzodi-azepine receptors in malformations of cortical development: A quantitative study. Brain, 2001, 124(8): 1555-1565.  doi: 10.1093/brain/124.8.1555
[42] Koepp MJ, Hammers A, Labbe C, et al. 11C-flumazenil PET in patients with refractory temporal lobe epilepsy and normal MRI. Neurology, 2000, 54(2): 332-339.
[43] Savic I, Widen L, Thorell JO, et al. Cortical benzodiazepine recep-tor binding in patients with generalized and partial epilepsy. Epilepsia, 1990, 31(6): 724-730.  doi: 10.1111/j.1528-1157.1990.tb05513.x
[44] Savic I, Pauli S, Thorell JO, et al. In vivo demonstration of altered benzodiazepine receptor density in patients with generalised epilepsy. J Neurol Neurosurg Psychiatry, 1994, 57(7): 797-804.  doi: 10.1136/jnnp.57.7.797
[45] Abadie P, Boulenger JP, Benali K, et al. Relationships between trait and state anxiety and the central benzodiazepine receptor: a PET study. Eur J Neurosci, 1999, 11(4): 1470-1478.
[46] Malizia AL, Cunningham VJ, Bell CJ, et al. Decreased brain GABAA-benzodiazepine receptor binding in panic disorder: prelimi-nary results from a quantitative PET study. Arch Gen Psychiatry, 1998, 55(8): 715-720.  doi: 10.1001/archpsyc.55.8.715
[47] Hasler G, Nugent AC, Carlson PJ, et al. Altered cerebral γ-aminobutyric acid type A-benzodiazepine receptor binding in panic disorder determined by[11C]flumazenil positron emission tomogra-phy. Arch Gen Psychiatry, 2008, 65(10): 1166-1175.  doi: 10.1001/archpsyc.65.10.1166
[48] Klumpers UM, Veltman DJ, Drent ML, et al. Reduced parahip-pocampal and lateral temporal GABAA-[11C] flumazenil binding in major depression: preliminary results. Eur J Nucl Med Mol Imaging, 2010, 37(3): 565-574.  doi: 10.1007/s00259-009-1292-9
[49] Rudolf J, Sobesky J, Ghaemi M, et al. The correlation between cerebral glucose metabolism and benzodiazepine receptor density in the acute vegetative state. Eur J Neurol, 2002, 9(6): 671-677.  doi: 10.1046/j.1468-1331.2002.00468.x
[50] Lingford-Hughes AR, Wilson SJ, Cunningham VJ, et al. GABA-benzodiazepine receptor function in alcohol dependence: a com-bined 11C-flumazenil PET and pharmacodynamic study. Psy-chopharmacology(Berl), 2005, 180(4): 595-606.
[51] Veselis RA, Reinsel RA, Beattie BJ, et al. Midazolam changes cerebral blood flow in discrete brain regions: an H215O positron emission tomography study. Anesthesiology, 1997, 87(5): 1106-1117.  doi: 10.1097/00000542-199711000-00015
[52] Holopainen IE, Metsähonkala E, Kokkonen H, et al. Decreased binding of[11C]flumazenil in Angelman syndrome patients with GABAA receptor β3 subunit deletions. Ann Neurol, 2001, 49(1): 110-113.  doi: 10.1002/1531-8249(200101)49:1<110::AID-ANA17>3.0.CO;2-T
[53]

Asahina N, Shiga T, Egawa K, et al.[11C]flumazenil positron
[54]

emission tomography analyses of brain gamma-aminobutyric acid type A receptors in Angelman syndrome. J Pediatr, 2008, 152(4): 546-549.
[55] Lucignani G, Panzacchi A, Bosio L, et al. GABAA receptor abnor-malities in Prader Willi syndrome assessed with positron emission tomography and[11C] flumazenil. Neuroimage, 2004, 22(1): 22-28.  doi: 10.1016/j.neuroimage.2003.10.050