多学科合作诊疗系统治疗孕妇心理问题诱发的躯体功能障碍临床回顾性研究

目的 探讨孕产妇由心理问题诱发的躯体功能障碍[孕产期心身障碍(PSD)]临床创新技术疗效.方法 对2016年1月至2017年2月在天津市滨海新区大港妇女儿童保健中心、广州市越秀区妇幼保健院、烟台市烟台山医院、天津市河北区妇女儿童保健和计划生育服务中心、临安市妇幼保健计划生育服务中心、扬州市妇幼保健院孕产妇心身健康门诊研究基地应用多学科合作模式的生理调控、心理调节、音乐调理(PPM)干预措施(基于产科)治疗罹患孕产期PSD的283例孕妇的临床疗效进行回顾性分析.结果 治疗显效率为60.78%(172/283),治疗有效率为31.44%(89/283);治疗无效率为7.78%(22/283);总有效率为92.23%(261/283).结论 应用多学科合作模式的PPM干预措施(基于产科)治疗孕产期PSD,疗效显著;同时对焦虑、抑郁亦起到治疗作用.     

Sleep rebound attenuates context-dependent behavioural sensitization induced by amphetamine

We have recently demonstrated that paradoxical sleep deprivation (PSD) potentiates the induction of amphetamine (AMPH)-induced behavioural sensitization by increasing its conditioned component. In the present study, the effects of sleep rebound (induced by 24 h recovery period from PSD) were studied on AMPH-induced behavioural sensitization. Sleep rebound attenuated the acute locomotor-stimulating effect of AMPH. AMPH-induced behavioural sensitization was context-specific and was also attenuated by sleep rebound. These results strengthen the notion that sleep conditions can influence AMPH-induced behavioural sensitization.     

Homers regulate drug-induced neuroplasticity: implications for addiction

Drug addiction is a chronic, relapsing disorder, characterized by an uncontrollable motivation to seek and use drugs. Converging clinical and preclinical observations implicate pathologies within the corticolimbic glutamate system in the genetic predisposition to, and the development of, an addicted phenotype. Such observations pose cellular factors regulating glutamate transmission as likely molecular candidates in the etiology of addiction. Members of the Homer family of proteins regulate signal transduction through, and the trafficking of, glutamate receptors, as well as maintain and regulate extracellular glutamate levels in corticolimbic brain regions. This review summarizes the existing data implicating the Homer family of protein in acute behavioral and neurochemical sensitivity to drugs of abuse, the development of drug-induced neuroplasticity, as well as other behavioral and cognitive pathologies associated with an addicted state.     

针刺联合氟西汀对卒中后抑郁症疗效及HPA轴功能的影响

目的:观察针刺联合氟西汀治疗卒中后抑郁症(PSD)的疗效并探讨其神经内分泌机制。方法:40例PSD患者随机分为两组,对照组20例单纯使用氟西汀治疗6周,研究组20例采用针刺结合氟西汀治疗6周。观察两组疗效和治疗前后血浆ACTH、CORT的含量变化。结果:治疗后两组临床疗效和ACTH、CORT值均有明显改善,研究组尤甚(P<0.05或0.01)。结论:针刺联合药物治疗PSD和单纯使用药物治疗相比,能够更好地改善患者的抑郁状态,其机理可能与抑制下丘脑-垂体-肾上腺(HPA)轴功能亢进有关。     

Characterization of protein kinase C isoforms in primary cultured cerebellar granule cells

Protein kinase C (PKC) is a family of serine/threonine kinases comprised of 10 isoforms. Although commercial antibodies are available for all 10 isoforms, the specificity of these antibodies has been questioned. We have identified immunoblot conditions in which commercially purchased PKC antibodies are specific for their respective isoform. We then used these conditions to determine that PKC isoforms alpha, betaI, betaII, delta, epsilon, gamma, lambda, theta, and zeta are present in rat primary cultured cerebellar granule cells (CGCs) 6-14 days in vitro (DIV). This PKC profile is identical to that observed in cerebellar homogenates taken from 6-, 14- and 21-day-old rats. Western blot analysis indicated that the classical and the atypical PKC isoforms were more prevalent in the cytosolic subcellular fraction compared to the particulate fraction under basal conditions. Immunoreactivity for the novel isoforms tended to be higher in the particulate fraction under basal conditions. Phorbol 12-myristate 13-acetate (PMA) treatment resulted in translocated immunoreactivity from the cytosolic to the particulate fraction for all of the classical and novel PKC isoforms, but not for the atypical isoforms. However, the degree of translocation as well as the speed of translocation varied among the isoforms. The stability of the individual isoforms after PMA-induced activation also varied among the isoforms. Differences in these parameters were dependent upon culture batches and PKC isoform groups. We have identified experimental conditions in which reproducible results can be obtained with primary cultured CGCs in the study of PKC. We discuss possible solutions for problems encountered when utilizing primary cultured neurons to study PKC-mediated signal transduction.     

Vesicular glutamate (VGlut), GABA (VGAT), and acetylcholine (VACht) transporters in basal forebrain axon terminals innervating the lateral hypothalamus

The basal forebrain (BF) is known to play important roles in cortical activation and sleep, which are likely mediated by chemically differentiated cell groups including cholinergic, gamma-aminobutyric acid (GABA)ergic and other unidentified neurons. One important target of these cells is the lateral hypothalamus (LH), which is critical for arousal and the maintenance of wakefulness. To determine whether chemically specific BF neurons provide an innervation to the LH, we employed anterograde transport of 10,000 MW biotinylated dextran amine (BDA) together with immunohistochemical staining of the vesicular transporter proteins (VTPs) for glutamate (VGluT1, -2, and -3), GABA (VGAT), or acetylcholine (ACh, VAChT). In addition, we applied triple staining for the postsynaptic proteins (PSPs), PSD-95 with VGluT or Gephyrin (Geph) with VGAT, to examine whether the BDA-labeled varicosities may form excitatory or inhibitory synapses in the LH. Axons originating from BDA-labeled neurons in the magnocellular preoptic nucleus (MCPO) and substantia innominata (SI) descended within the medial forebrain bundle and extended collateral varicose fibers to contact LH neurons. In the LH, the BDA-labeled varicosities were immunopositive (+) for VAChT ( approximately 10%), VGluT2 ( approximately 25%), or VGAT ( approximately 50%), revealing an important influence of newly identified glutamatergic together with GABAergic BF inputs. Moreover, in confocal microscopy, VGluT2+ and VGAT+ terminals were apposed to PSD-95+ and Geph+ profiles respectively, indicating that they formed synaptic contacts with LH neurons. The important inputs from glutamatergic and GABAergic BF cells could thus regulate LH neurons in an opposing manner to stimulate vs. suppress cortical activation and behavioral arousal reciprocally.