Articles by Hilary S. McCarren in JoVE
Évaluer les changements dans volatils anesthésie générale sensibilité des souris après l'intervention pharmacologique local ou systémique 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 Perte du réflexe de redressement a longtemps servi comme un substitut de comportement standard pour la perte de conscience, aussi appelé l'hypnose, chez les animaux de laboratoire. Altérations de la sensibilité anesthésique volatil causés par des interventions pharmacologiques peuvent être détectés avec un système d'évaluation à haut débit soigneusement contrôlé, qui peut être adapté pour la livraison de toute thérapeutique inhalé.
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.