Joseph B. Watson

Affiliations: 
University of California, Los Angeles, Los Angeles, CA 
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"Joseph Watson"
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Barry J, Sarafian TA, Watson JB, et al. (2020) Mechanisms underlying the enhancement of γ-aminobutyric acid responses in the external globus pallidus of R6/2 Huntington's disease model mice. Journal of Neuroscience Research
Sarafian TA, Ryan CM, Souda P, et al. (2013) Impairment of mitochondria in adult mouse brain overexpressing predominantly full-length, N-terminally acetylated human α-synuclein. Plos One. 8: e63557
Cepeda C, Galvan L, Holley SM, et al. (2013) Multiple sources of striatal inhibition are differentially affected in Huntington's disease mouse models. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 33: 7393-406
Chang JW, Arnold MM, Rozenbaum A, et al. (2012) Synaptoneurosome micromethod for fractionation of mouse and human brain, and primary neuronal cultures. Journal of Neuroscience Methods. 211: 289-95
Cepeda C, Cummings DM, Hickey MA, et al. (2010) Rescuing the Corticostriatal Synaptic Disconnection in the R6/2 Mouse Model of Huntington's Disease: Exercise, Adenosine Receptors and Ampakines. Plos Currents. 2
Watson JB, Hatami A, David H, et al. (2009) Alterations in corticostriatal synaptic plasticity in mice overexpressing human alpha-synuclein. Neuroscience. 159: 501-13
Zhao D, Watson JB, Xie CW. (2004) Amyloid beta prevents activation of calcium/calmodulin-dependent protein kinase II and AMPA receptor phosphorylation during hippocampal long-term potentiation. Journal of Neurophysiology. 92: 2853-8
Chotiner JK, Khorasani H, Nairn AC, et al. (2003) Adenylyl cyclase-dependent form of chemical long-term potentiation triggers translational regulation at the elongation step. Neuroscience. 116: 743-52
Cepeda C, Crawford CA, Margulies JE, et al. (2002) Enhanced epileptogenic susceptibility in a genetic model of reactive synaptogenesis: the spastic Han-Wistar rat. Developmental Neuroscience. 24: 262-71
Campagnoni CW, Landry CF, Pribyl TM, et al. (2001) Identification of genes in the oligodendrocyte lineage through the analysis of conditionally immortalized cell lines. Developmental Neuroscience. 23: 452-63
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