In JoVE (1)
Articles by Hilary S. McCarren in JoVE
局所または全身薬理学的介入後のマウスの揮発性全身麻酔の感度変化を評価する Hilary S. McCarren1,2,4, Jason T. Moore1,3,4, Max B. Kelz1,2,3,4 1Department of Anesthesiology and Critical Care, Perelman School of Medicine, University of Pennsylvania, 2Department of Pharmacology, Perelman School of Medicine, University of Pennsylvania, 3Department of Neuroscience, Perelman School of Medicine, University of Pennsylvania, 4Center for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania 立ち直り反射の消失は、長い実験動物でも催眠呼ばれる、意識不明のための標準的な行動の代理を務めています。薬理学的介入によって引き起こされる揮発性麻酔薬感受性における変化は、任意の吸入治療剤の送達のために適合させることができる注意深く制御されたハイスループット評価システムを用いて検出することができる。
Other articles by Hilary S. McCarren on PubMed
Mouse Behavioral Endophenotypes for Schizophrenia Brain Research Bulletin. Sep, 2010 | Pubmed ID: 20433908 An endophenotype is a heritable trait that is generally considered to be more highly, associated with a gene-based neurological deficit than a disease phenotype itself. Such, endophenotypic deficits may therefore be observed in the non-affected relatives of disease patients. Once endophenotypes have been established for a given illness, such as schizophrenia, mechanisms of, action may then be established and treatment options developed in order to target such measures. The, current paper describes and assesses the merits and limitations of utilizing behavioral and, electrophysiological endophenotypes of schizophrenia in mice. Such endophenotypic deficits include: decreased auditory event related potential (ERP) amplitude and gating (specifically, that of the P20, N40, P80 and P120); impaired mismatch negativity (MMN); changes in theta and gamma frequency, analyses; decreased pre-pulse inhibition (PPI); impaired working and episodic memories (for instance, novel object recognition [NOR], contextual and cued fear conditioning, latent inhibition, Morris and, radial arm maze identification and nose poke); sociability; and locomotor activity. A variety of, pharmacological treatments, including ketamine, MK-801 and phencyclidine (PCP) can be used to, induce some of the deficits described above, and numerous transgenic mouse strains have been, developed to address the mechanisms responsible for such endophenotypic differences. We also, address the viability and validity of using such measures regarding their potential clinical implications, and suggest several practices that could increase the translatability of preclinical data.