南宁市初三学生焦虑抑郁状况调查

目的 了解南宁市初三学生焦虑、抑郁水平及其与考试焦虑的关系,为对学生进行有针对性的心理干预提供参考。方法 于2021年5月-6月,采用简单随机抽样方法,在南宁市每个区/县内随机抽取一个初中学校,以每个学校初三年级中3个班级的学生为调查对象。采用考试焦虑量表（TAS）、焦虑自评量表（SAS）和抑郁自评量表（SDS）进行调查,采用Pearson相关分析考察各量表评分的相关性。结果 共2 080名学生参与此次调查,回收有效问卷1 826份（87.79%）。其中,999名（54.71%）初三学生感受到考试带来的不适感,检出存在焦虑和抑郁情绪者分别有577人（31.60%）、830人（45.45%）。女生TAS评分高于男生［（16.75±6.78）分vs.（15.08±6.97）分,t=-5.136,P<0.01］,女生SAS评分高于男生［（46.05±10.43）分vs.（44.16±10.87）分,t=-3.769,P<0.01］,女生SDS评分高于男生［（52.34±12.44）分vs.（49.98±12.17）分,t=-4.039,P<0.01］。相关分析显示,初三学生SAS、SDS评分与TAS评分均呈正相关（r=0.574、0.531,P均<0.01）,控制年龄和性别后,相关性仍存在（r=0.570、0.526,P均<0.01）。结论 南宁市初三学生的焦虑和抑郁症状检出率较高,且与考试焦虑均呈正相关。另外,女生的焦虑和抑郁水平均高于男生。     

辅助生殖技术对儿童体格和孤独症行为的影响：一项3年纵向随访研究

背景 辅助生殖技术日益成熟,并广泛应用于临床。辅助生殖技术诞生的新生儿越来越多,这类儿童的健康问题也需要更多关注。目的 探讨辅助生殖技术对儿童体格和孤独症行为的影响,提高对辅助生殖儿童孤独症行为的关注度。方法 从病历信息系统中,按时间顺序选取2018年8月-2019年8月在安徽医科大学附属巢湖医院产科出生的辅助生殖新生儿（辅助生殖组）588例为研究对象。从病历信息系统中选取同一时间段该院产科自然受孕出生的600名新生儿为对照组。收集所有新生儿的性别、出生时母亲的年龄和受教育年限、出生孕周、出生体质量、出生身长以及3岁时体质量和身高数据,并在3岁随访时进行克氏孤独症行为量表（CABS）评定。结果 辅助生殖组母亲受教育年限长于对照组母亲受教育年限［（12.04±1.96）年vs.（11.34±2.90）年,t=-4.887,P<0.01］,出生孕周和出生体质量均低于对照组［（38.68±2.56）周vs.（39.53±2.91）周,t=5.315,P<0.01,（3 273.27±720.39）g vs.（3 158.29±701.74）g,t=2.792,P<0.05］。两组出生身长差异无统计学意义［（49.97±5.94）cm vs.（50.07±6.08）cm,t=-0.287,P>0.05］。3岁时,辅助生殖组体质量和身高均低于对照组［（16.16±2.53）kg vs.（16.96±1.67）kg,t=6.393,P<0.01,（95.81±4.50）cm vs.（97.47±7.49）cm,t=4.626,P<0.01］。对照组和辅助生殖组分别筛查出6例（1.00%）和15例（2.55%）存在孤独症行为,差异有统计学意义（χ²=4.113,P<0.05）。结论 辅助生殖技术可能对儿童体格和神经发育存在影响。     

事件相关电位P300在颅脑损伤患者认知功能障碍评定中的应用

目的 探讨事件相关电位P300在颅脑损伤患者认知功能障碍评定中的应用价值。方法 选取2021年1月-9月在绵阳市第三人民医院神经外科保守治疗、并符合诊断标准的颅脑损伤患者36例作为研究组,同期在医院其他患者家属和护工中招募健康对照组共36名。采用Oddball范式对受试者进行事件相关电位P300检测,采用蒙特利尔认知评估量表（MoCA）和简易精神状态评价量表（MMSE）评定受试者的认知功能。比较两组P300的潜伏期、波幅以及MoCA和MMSE评分,比较P300潜伏期、MoCA和MMSE对颅脑损伤患者认知功能障碍的检出率。结果 研究组MoCA和MMSE评分均低于对照组［（18.08±4.29）分vs.（27.36±1.20）分,（22.53±3.54）分vs.（28.11±1.09）分,t=-12.510、-9.041,P均<0.05］;研究组P300潜伏期高于对照组［（406.08±26.95）ms vs.（367.08±22.50）ms,t=6.665,P<0.05］,波幅低于对照组［（7.76±0.90）μV vs.（9.87±0.99）μV,t=-9.459,P<0.05］。在研究组中,P300潜伏期阳性检出率和MoCA对认知功能障碍的检出率均高于MMSE对认知功能障碍的检出率（χ²=5.675、7.604,P均<0.05）。结论 事件相关电位P300或许可作为评估颅脑损伤患者认知功能障碍的客观临床指标。     

成都市基层医院孤独症谱系障碍早期筛查技能培训效果的多中心研究

目的 了解孤独症谱系障碍（ASD）早期筛查技能培训对提高基层医院儿保科医护人员ASD早期筛查能力的效果。方法 于2021年9月，对成都市各县（市、区）共20家基层医院儿保科工作人员进行ASD早期筛查技能培训。以培训前后各基层医院向上级医院转诊的疑似ASD患儿人数、确诊ASD人数以及转诊的ASD患儿平均诊断年龄作为指标，评价培训效果。结果 培训后，基层医院转诊的疑似ASD患儿人数多于培训前，差异有统计学意义［（16.65±11.60）人vs.（3.40±2.23）人，t=5.431，P<0.01］。确诊ASD人数多于培训前，差异有统计学意义［（6.85±4.93）人vs.（2.45±1.67）人，t=4.171，P<0.01］。诊断年龄方面，培训后，ASD患儿平均诊断年龄小于培训前，差异有统计学意义［（34.95±11.67）个月vs.（42.2±14.64）个月，t=-2.553，P=0.019］。结论 对基层医院儿保科医护人员进行ASD早期筛查技能培训，可能有助于提高其ASD早期筛查能力。     

留守中学生社会支持与网络成瘾的“量-效”趋势研究

目的 了解留守中学生社会支持水平和网络成瘾现状及其之间的关系,为有针对性地进行网络成瘾干预、降低网络成瘾风险提供参考。方法 采用分层整群随机抽样方法抽取重庆市渝东南地区某县6所中学的3 532名学生为研究对象,其中留守学生1 945人（55.07%）,非留守学生1 587人（44.93%）。采用自编一般情况问卷、中学生网络成瘾诊断量表（DSIA-MSS）、青少年社会支持量表（ASSRS）进行评定,并分析ASSRS评分与网络成瘾的关联趋势。结果 ①留守组网络成瘾检出率高于非留守组（22.98% vs. 16.13%,χ²=25.732,P<0.01）;②留守组ASSRS评分低于非留守组［（66.81±15.92）分vs.（68.19±16.18）分,t=2.544,P=0.011］;③在非留守、单亲外出和双亲外出三种留守状态下,不同ASSRS评分等级的中学生网络成瘾检出率差异均有统计学意义（χ²=35.220、37.662、31.434,P均<0.01）;④中学生ASSRS评分与网络成瘾存在“量效”趋势,即ASSRS评分等级越高,网络成瘾风险越低（P<0.01）。结论 留守中学生存在更突出的网络成瘾问题,且社会支持水平与网络成瘾检出率具有明显的相关性,表现为负性“量效”趋势关系。     

新冠肺炎疫情下浏阳市精神疾病患者家属焦虑抑郁情况及影响因素

目的 了解新冠肺炎疫情期间精神疾病患者家属焦虑、抑郁情况及影响因素。方法 采用横断面研究，通过立意抽样和分层抽样的方法，选取2020年3月18日-28日浏阳市精神病医院门诊患者家属116名和住院患者家属111名。采用焦虑自评量表（SAS）、抑郁自评量表（SDS）和自行设计的一般资料问卷进行调查，并对数据进行单因素和多因素Logistic回归分析。结果 共回收问卷239份，其中有效问卷227份，有效问卷回收率为94.98%。检出存在焦虑症状者29人，焦虑检出率为12.78%；检出存在抑郁症状者40人，抑郁检出率为17.62%。Logistic回归分析显示，家属年龄≥60岁（OR=4.454，P=0.041）、睡眠质量评价为中等及以下（OR=17.922、153.728，P<0.01）、患者疫情期间居家休息（OR=5.597，P=0.004）是家属存在焦虑症状的危险因素；睡眠质量评价为中等及以下（OR=7.806、15.105，P<0.01）、受教育程度低（OR=0.137、0.205，P<0.05）、患者疫情期间居家休息（OR=2.868，P=0.022）是家属存在抑郁症状的危险因素。结论 新冠肺炎疫情期间精神疾病患者家属存在一定程度的焦虑、抑郁情绪。其中，年龄≥60岁、睡眠质量不佳、患者居家休息、受教育程度低是家属存在焦虑和抑郁的危险因素。     

抗抑郁药临床试验受试者脱落情况及影响因素

目的 分析抗抑郁药临床试验受试者脱落情况,讨论受试者脱落的影响因素。方法 对广州医科大学附属脑科医院2013年-2020年完成的9项抗抑郁药临床试验受试者资料进行回顾性分析,采用自编调查表采集受试者人口学资料、疾病特点及试验完成情况,分析受试者的脱落情况及影响因素。结果 共入组157例,完成120例,脱落37例。脱落原因分别为：疗效差13例（35.14%）,发生不良反应12例（32.43%）,撤回知情同意书8例（21.62%）,失访4例（10.81%）。相关分析结果显示,受试者脱落与焦虑程度（r=0.224,P<0.01）和不良事件（r=0.158,P<0.05）呈正相关,与受教育程度（r=-0.209,P<0.01）和总体疗效（r=-0.545,P<0.01）呈负相关。二元Logistic回归分析结果显示,受教育程度（β=-0.611,OR=0.543,P<0.05）、就诊次数（β=-1.831,OR=0.160,P<0.01）和总体疗效（β=-2.286,OR=0.102,P<0.01）是受试者脱落的影响因素。结论 受教育程度低、首次就诊、疗效不佳、焦虑程度重以及发生不良事件是抗抑郁药临床试验受试者脱落的影响因素。     

医学生焦虑、抑郁情绪对网络游戏障碍的影响：性别的调节作用

目的 探究焦虑、抑郁情绪对医学生网络游戏障碍的影响以及性别在其中的调节效应，为预防和干预医学生网络游戏障碍提供参考。方法 于2021年11月，选取四川省某医学院校11 771名医学生作为研究对象，通过问卷星网络平台，采用焦虑自评量表（SAS）、抑郁自评量表（SDS）和简式网络游戏障碍量表（IGDS9-SF）进行评定，采用多元分层回归分析性别在焦虑、抑郁情绪和网络游戏障碍关系中的调节作用。结果 ①男生SDS评分低于女生（t=-8.302，P<0.01），IGDS9-SF评分高于女生（t=33.384，P<0.01）。②医学生SAS评分与SDS评分呈正相关（r=0.735，P<0.01），SAS和SDS评分与IGDS9-SF评分均呈正相关（r=0.288、0.238，P均<0.01）。③焦虑、抑郁情绪可以正向预测网络游戏障碍（β=0.245、0.058，t=18.864、4.444，P均<0.01）。④性别在焦虑情绪与网络游戏障碍之间具有调节作用（β=-0.194，t=-4.518，P<0.01）。结论 焦虑、抑郁情绪对医学生网络游戏障碍有正向预测作用。焦虑情绪对医学生网络游戏障碍的影响受到性别的调节，相比于女生，焦虑情绪对男生网络游戏障碍的影响更大。     

压力源及压力反应对大学生偏头痛患者日常生活的影响

背景 压力与偏头痛发作密切相关,但既往研究关于压力源及压力反应对大学生偏头痛人群日常生活的影响不明确。目的 探讨压力源及压力反应对大学生偏头痛人群日常生活的影响,以期为改善大学生偏头痛人群的日常生活提供参考。方法 于2018年8月—2019年8月,采用随机抽样,选取符合《国际头痛疾病分类（第3版）》（ICHD-3）偏头痛诊断标准的458名川北医学院在校大学生为研究对象,采用自编问卷收集大学生一般资料和头痛特征,采用头痛影响测试量表（HIT-6）评定偏头痛对大学生日常生活的影响。采用学生生活应激问卷（SLSI）评定压力源及压力反应,采用汉密尔顿焦虑量表（HAMA）和汉密尔顿抑郁量表24项版（HAMD-24）评定大学生的焦虑症状和抑郁症状。采用Pearson相关分析考查HIT-6评分与各量表评分之间的相关性,采用多元线性回归分析大学生偏头痛人群日常生活的影响因素。结果 SLSI中的挫折（r=0.138,P<0.01）、冲突（r=0.168,P<0.01）、压力（r=0.157,P<0.01）、变化（r=0.148,P<0.01）、自我强加（r=0.158,P<0.01）五个维度的压力源以及生理反应（r=0.256,P<0.01）、情绪反应（r=0.241,P<0.01）、行为反应（r=0.164,P<0.01）、HAMA总评分（r=0.192,P<0.01）、HAMD-24总评分（r=0.250,P<0.01）、SLSI总评分（r=0.250,P<0.01）与HIT-6评分均呈正相关,认知反应（r=-0.104,P<0.05）与HIT-6评分呈负相关。多元线性回归分析结果显示,生理反应（β=0.140,P<0.05）、焦虑（β=0.159,P<0.05）、认知反应（β=-0.091,P<0.05）可预测大学生偏头痛人群日常生活受影响的程度。结论 生理反应、认知反应、焦虑可能是大学生偏头痛人群日常生活的影响因素。     

江门市中学生非自杀性自伤行为的流行病学特征及影响因素分析

目的 了解江门市中学生非自杀性自伤（NSSI）行为的流行病学特征及影响因素。方法 于2020年11月-12月,采用分层随机抽样法,抽取江门市1 220名中学生为研究对象。采用自编调查问卷、中学生应对方式量表、Olweus儿童欺负问卷初中版（BVQ）、青少年社会支持量表及流调中心用抑郁量表（CES-D）进行评定。运用二元Logistic回归分析探讨中学生NSSI行为的影响因素。结果 共检出204名（16.72%）中学生曾有过NSSI行为,其中男生67人、女生137人。NSSI组与非NSSI组在性别、学段、住校情况、同伴关系及学习成绩上差异均有统计学意义（χ²=22.162、7.247、6.541、45.787、25.097,P<0.05或0.01）。与非NSSI组相比,NSSI组CES-D评分（t=-14.240）和BVQ评分（t=-5.952）更高,青少年社会支持量表评分更低（t=9.238）,中学生应对方式量表问题应对分量表评分更低（t=7.148）,情绪应对分量表评分更高（t=-7.038）,受校园欺凌、语言欺凌和关系欺凌检出率更高（χ²=34.215,29.785,16.465）,差异均有统计学意义（P均<0.01）。二元Logistic回归分析结果显示,抑郁（OR=1.090,P<0.01）及受校园欺凌（OR=1.492,P<0.05）进入回归模型。结论 江门市中学生NSSI形势严峻,抑郁及受校园欺凌是其发生NSSI行为的危险因素。     

住院老年精神病患者心理状态及影响因素

本文目的是对住院老年精神病患者心理状态及其影响因素进行综述，为临床改善住院老年精神病患者心理状况、提高治疗效果提供参考。随着人口老龄化程度加深，住院老年精神病患者数量也在持续增加，其心理状态及其影响因素需要得到重视。本文结合近年来相关研究分析住院老年精神病患者的心理状态和影响因素，并进一步探讨干预措施。     

Characterization of α,β-Methylene ATP Binding Sites in Mouse Crude Synaptic Membranes

Since ATP has been reported to be a potent excitatory transmitter in the mammalian central nervous system (CNS), we studied the neurochemical characters of the binding sites of

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,

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-methylene ATP, an agonist of P_2X receptors, in mouse crude synaptic membranes. ATP and its related compounds inhibited [³H]

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,

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-methylene ATP binding in a concentration-dependent manner. The potency order in the inhibition of the binding was as follows;

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,

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-methylene

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>

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> ATP ≥ ADP >

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,

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-methylene ATP UTP > 2-methylthio ATP. And adenosine did not affect the binding. The order was different from those reported in peripheral tissues. And Sr²⁺, Ca²⁺, Mg²⁺, and Cd²⁺ enhanced the binding. These results suggest that

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,

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-methylene ATP binding sites in CNS have different characters from those in peripheral tissues.     

Cardiovascular effects of nitric oxide in the rostral ventrolateral medulla of rats

To investigate the cardiovascular role of nitric oxide (NO) in the rostral ventrolateral medulla (RVLM), NOC 18, an NO donor, was microinjected into the RVLM of rats. NOC 18 significantly decreased mean arterial pressure (MAP). Pre-treatment with an NO trapper, carboxy-PTIO, abolished the NOC 18-induced decrease in MAP. Microinjection of

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-NAME, an NO synthase inhibitor, increased MAP.

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-Arginine reduced MAP and inhibited the pressor response induced by

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-NAME. Results suggest that NO acts on the RVLM neurons and plays an important role in cardiovascular regulation.     

Medium- and long-term effects of repeated bicuculline-induced seizures in developing rats on local cerebral energy metabolism

To assess long-term metabolic consequences of recurrent ictal events arising during development, seizures were repeatedly generated in rats at different stages of cerebral maturation. Seizures were induced by i.p. injections of bicuculline for three consecutive days, starting from postnatal day 5 (P5), when the brain is very immature, or from P15, a period at which the brain is more structurally organized. Local cerebral metabolic rates for glucose were measured in 74 structures at P15, P25 and in adults (P60), by the autoradiographic method using 2-

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-[

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]deoxyglucose. Repeated seizures in P5 to P7 pups led to a reduction (16–34%) of glucose consumption at P15, mainly significant in sensory, motor and functionally non-specific areas as well as in cerebellar nuclei. Selective decreases in metabolic activity were still recorded in adults, mostly in auditory system (20%) and cerebellar nuclei (27%). Seizures generated from P15 to P17 led to an overall mortality rate of 62% (versus 22% at P5 to P7). Surviving animals exhibited reduced metabolic rates for glucose (by 7–27%) at P25, significant in 23 structures, and depicting pronounced changes in limbic, hypothalamic, sensory and white matter areas, whereas brain functional activity finally returned to basal values at P60. Therefore, while younger rats seemed to better tolerate repeated bicuculline-induced seizures than older animals, the reverse was true for long-term metabolic effects, and the more immature the brain when seizures arise, the more persistent the functional consequences.     

Distribution of d-amino acid oxidase (DAO) activity in the medulla and thoracic spinal cord of the rat: implications for a role for d-serine in autonomic function

The activity and regional distribution of

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-amino acid oxidase (DAO), an enzyme that inactivates

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-serine, were examined in the medulla and spinal cord of the rat by biochemical and histochemical procedures. DAO activity was noticeably low or absent in the nucleus of the solitary tract, ventrolateral medulla and intramediolateral cell column of the spinal cord. This may be indicative of a neuromodulatory role for endogenous

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-serine (at the NMDA-glycine site) in the central control of blood pressure.     

Effects of

It has been reported that glutamate-induced neurotoxicity is related to an increase in nitric oxide (NO) concentration. An NO-sensitive electrode has been developed to measure NO concentration directly. Using this electrode, we examined NO concentration and neuronal survival after glutamate application in rat cultured cortical neurons. We also examined the effects of NMDA receptor antagonists, MK-801 and ketamine, and the NO synthetase inhibitor,

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-NMMA on NO production and neuronal death. After 7 days in culture, application of glutamate (1 mM) or

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-arginine (0.3 mM) to the cultured medium increased NO concentration, and decreased the number of anti-microtubule-associated protein 2 positive neurons. Both pretreatment with MK-801 (300 μm) and ketamine (300 μm) prevented glutamate-, but not

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-arginine-induced increase in NO concentration and neuronal death.

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-NMMA prevented both glutamate- and

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-arginine-induced NO production and neuronal death. The nitric oxide donor, S-nitroso-N-acetyl-

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,

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-penicillamine (SNAP) also caused neuronal death, and MK-801, ketamine and

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-NMMA did not prevent SNAP-induced toxicity. We have demonstrated excitatory amino acid-induced changes of NO concentration and the parallel relationship between changes of NO concentration and neuronal death. In conclusion, an increase in NO concentration does induce neuronal death, and the inhibition of the production of NO prevents glutamate-induced neuronal death.     

Direct evidence for the role of nitric oxide on the glutamate-induced neuronal death in cultured cortical neurons

It has been reported that glutamate-induced neurotoxicity is related to an increase in nitric oxide (NO) concentration. An NO-sensitive electrode has been developed to measure NO concentration directly. Using this electrode, we examined NO concentration and neuronal survival after glutamate application in rat cultured cortical neurons. We also examined the effects of NMDA receptor antagonists, MK-801 and ketamine, and the NO synthetase inhibitor,

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-NMMA on NO production and neuronal death. After 7 days in culture, application of glutamate (1 mM) or

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-arginine (0.3 mM) to the cultured medium increased NO concentration, and decreased the number of anti-microtubule-associated protein 2 positive neurons. Both pretreatment with MK-801 (300 μm) and ketamine (300 μm) prevented glutamate-, but not

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-arginine-induced increase in NO concentration and neuronal death.

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-NMMA prevented both glutamate- and

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-arginine-induced NO production and neuronal death. The nitric oxide donor, S-nitroso-N-acetyl-

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,

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-penicillamine (SNAP) also caused neuronal death, and MK-801, ketamine and

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-NMMA did not prevent SNAP-induced toxicity. We have demonstrated excitatory amino acid-induced changes of NO concentration and the parallel relationship between changes of NO concentration and neuronal death. In conclusion, an increase in NO concentration does induce neuronal death, and the inhibition of the production of NO prevents glutamate-induced neuronal death.     

Sustained pharmacological inhibition of nitric oxide synthase does not affect the survival of intrastriatal rat fetal mesencephalic transplants

The objective of the present study was to investigate the potential role of the free radical nitric oxide (NO) in the development of fetal rat mesencephalic neurons grafted in a 6-hydroxydopamine (6-OHDA) lesioned rat model of Parkinson's disease. First, using nitric oxide synthase (NOS)-immunocytochemistry and reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry, we investigated the presence of the neuronal isoform of NOS (nNOS) in intrastriatal mesencephalic grafts. During the course of the experiment (16 weeks) an increase in the staining intensity and the number of nNOS/NADPH-d positive cells within the grafts was observed, as well as a gradual maturation of dopaminergic neurons. In addition, within both the host striatal and grafted mesencephalic tissue, a NO-dependent accumulation of cyclic guanosine monophosphate (cGMP) was detected, indicating the presence of guanylate cyclase, i.e., the target-enzyme for NO. Secondly, to determine the impact of NO on the survival of grafted dopaminergic neurons, 6-OHDA lesioned rats received mesencephalic grafts and were subsequently treated with the competitive NOS-inhibitor N^ω-nitro-

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-arginine methylester (

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-NAME). After chronic treatment for 4 weeks, tyrosine hydroxylase immunocytochemistry revealed no apparent differences between the survival of grafted dopaminergic neurons in control- or

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-NAME treated animals, respectively. As the maturation of grafted dopaminergic neurons coincides with a gradual increase in the expression of nNOS within the graft and since dopaminergic cell numbers are not changed upon administration of

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-NAME, it is concluded that endogenously produced and potentially toxic NO does not affect the survival of grafted fetal dopaminergic neurons.     

Characterization of [

Metabotropic glutamate receptors (mGluRs) are thought to mediate diverse processes in brain including synaptic plasticity and excitotoxicity. These receptors are often divided into three groups by their pharmacological profiles. [³H]Glutamate binding in the presence of compounds selective for ionotropic glutamate receptors can be used as a general assay for these receptors; subtypes of this non-ionotropic [³H]glutamate binding differ in both pharmacology and anatomical distribution, and are differentially sensitive to quisqualate. The characteristics of these binding sites are consistent with those of group 1 (high-affinity quisqualate) and group 2 (low-affinity quisqualate) mGluRs. Under our assay conditions, no [³H]glutamate binding to group 3-like (

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-AP4 sensitive) sites could be demonstrated. We have attempted to characterize particular agents which may selectively measure [³H]glutamate binding to mGluR subtypes. We used two isomers of 2-(carboxycyclopropyl)glycine,

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-CCG-I and

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-CCG-II, and the (2S,1′R,2′R,3′R) isomer of 2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV) as competitors of non-ionotropic [³H]glutamate binding sites. DCG-IV clearly distinguishes two binding sites. Quantitative levels of DCG-IV binding by anatomic region correlate with quisqualate-defined binding subtypes: high-affinity DCG-IV binding correlates with low-affinity quisqualate binding, whereas low-affinity DCG-IV binding correlates with high-affinity quisqualate binding.

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-CCG-II displaces only one type of non-ionotropic [³H]glutamate binding, corresponding to high-affinity quisqualate binding. Therefore DCG-IV and

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-CCG-II at appropriate concentrations appear to distinguish binding to putative group 2 vs. group 1 mGluRs.

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-CCG-I displaces both high- and low-affinity quisqualate binding sites, but unlike the other two compounds, does not clearly distinguish between them.     

Selective metabotropic receptor agonists distinguish non-ionotropic glutamate binding sites

Metabotropic glutamate receptors (mGluRs) are thought to mediate diverse processes in brain including synaptic plasticity and excitotoxicity. These receptors are often divided into three groups by their pharmacological profiles. [³H]Glutamate binding in the presence of compounds selective for ionotropic glutamate receptors can be used as a general assay for these receptors; subtypes of this non-ionotropic [³H]glutamate binding differ in both pharmacology and anatomical distribution, and are differentially sensitive to quisqualate. The characteristics of these binding sites are consistent with those of group 1 (high-affinity quisqualate) and group 2 (low-affinity quisqualate) mGluRs. Under our assay conditions, no [³H]glutamate binding to group 3-like (

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-AP4 sensitive) sites could be demonstrated. We have attempted to characterize particular agents which may selectively measure [³H]glutamate binding to mGluR subtypes. We used two isomers of 2-(carboxycyclopropyl)glycine,

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-CCG-I and

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-CCG-II, and the (2S,1′R,2′R,3′R) isomer of 2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV) as competitors of non-ionotropic [³H]glutamate binding sites. DCG-IV clearly distinguishes two binding sites. Quantitative levels of DCG-IV binding by anatomic region correlate with quisqualate-defined binding subtypes: high-affinity DCG-IV binding correlates with low-affinity quisqualate binding, whereas low-affinity DCG-IV binding correlates with high-affinity quisqualate binding.

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-CCG-II displaces only one type of non-ionotropic [³H]glutamate binding, corresponding to high-affinity quisqualate binding. Therefore DCG-IV and

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-CCG-II at appropriate concentrations appear to distinguish binding to putative group 2 vs. group 1 mGluRs.

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-CCG-I displaces both high- and low-affinity quisqualate binding sites, but unlike the other two compounds, does not clearly distinguish between them.