Data Fabrication and Data Falsification in the paper entitled "Regulation of DARPP-32 dephosphorylation at PKA and Cdk5-sites by NMDA and AMPA receptors", authored by Nishi, A., Bibb, J.A., Matsuyama, S., Hamada, M., Higushi, H., Nairn, A.C. and Greengard. P., and published in the Journal of Neurochemistry. [J. Neurochem. (2002) Vol. 5, pp832-841].

The paper entitled "Regulation of DARPP-32 dephosphorylation at PKA and Cdk5-sites by NMDA and AMPA receptors", authored by Nishi, A., Bibb, J.A., Matsuyama, S., Hamada, M., Higushi, H., Nairn, A.C. and Greengard. P., and published in the Journal of Neurochemistry. [J. Neurochem. (2002) Vol. 5, pp832-841] describes the study the effects of ionotropic glutamate NMDA and AMPA receptors on DARPP-32 phosphorylation in neostriatal slices and purported to show that activation of NMDA and AMPA receptors caused the decrease of phosphorylations of threonone 34 and threonine 75 DARPP-32 mediated by Ca 2+ -dependent activation of calcineurin and protein phosphatase-2A respectively. However, no supporting scientific results were provided. Figures 1A, 1B, 1C and 1D are duplicates of each other. With exactly the same figures depicting exactly the same immunublots, the authors somehow came up with different bar charts that supposedly quantify the extent of DARPP-32 phosphorylation levels under different conditions. Figures 3A and 3C are also duplicates of each other. It is not clear how the reviewer(s) and the Editor of the Journal of Neurochemistry could have missed the glaring evidence of Data Fabrication and and Data Falsification.

Heterogeneity in Use-Dependent Depression of Inhibitory Postsynaptic Potentials in the Rat Neostriatum In Vitro

Radnikow, Gabriele, Jutta Rohrbacher, and Ulrich Misgeld. Heterogeneity in use-dependent depression of inhibitory postsynaptic potentials in the rat neostriatum in vitro. J. Neurophysiol. 77: 427–434, 1997. “Minimal stimulation” was applied to evoke responses in an “all-or-none” fashion in presumed medium spiny neurons of rat neostriatal slices in the presence of antagonists for glutamatergic excitation. For comparison, responses were evoked in the same cells by compound stimulation. Bicuculline (30 μM) blocked responses evoked by minimal stimulation, indicating that they were γ-aminobutyric acid-A (GABAA)-receptor-mediated inhibitory postsynaptic potentials (IPSPs), whereas responses evoked by compound stimulation were only reduced in amplitude. Likewise, R(−)baclofen (1–20 μM) blocked IPSPs evoked by minimal stimulation in all but one cell. On the contrary, responses evoked by compound stimulation were always reduced in amplitude but never blocked. Paired-pulse depression (PPD) of averaged responses to minimal and compound stimulation was observed at a stimulus interval of 300 ms. The GABAB receptor antagonist CGP55845A (0.5 μM) had no effect on PPD evoked by compound stimulation but abolished PPD evoked by minimal stimulation. In a second set of experiments, the two stimulation paradigms were used to evoke responses in neostriatal slices continuously bathed in R(−)baclofen (10–20 μM). In R(−)baclofen a strong PPD was evoked by minimal and by compound stimulation. The amplitude of the response to compound stimulation increased on application of CGP55845A (0.5 μM). At the same time, PPD evoked by compound stimulation decreased. On the contrary, IPSP amplitude and PPD evoked by minimal stimulation remained unchanged. We conclude that two types of GABAergic terminals exist in the rat neostriatum, only one of which is regulated by GABAB receptors. However, the other class of terminals, not regulated by GABAB receptors, displays a much more pronounced PPD.