The effect of Fe doping (<20%) on the Mn site in the ferromagnetic (x=0.37) and the antiferromagnetic (x=0.53) phases of La1−xCaxMnO3 has been studied. Upon doping, no appreciable structure changes have been found in either series. However, conduction and ferromagnetism have been consistently suppressed by Fe doping. Colossal magnetoresistance has been shifted to lower temperatures, and in some cases enhanced by Fe doping. These results are not due to the strong lattice effects commonly seen in doping of the La sites. Rather, replacement of Mn3+ by Fe3+ depopulates the hopping electrons, and weakens the double exchange. The effect of Fe doping can be explained in terms of the band structure.

The effect of Fe doping (<20%) on the Mn site in the ferromagnetic ((Formula presented)) and the antiferromagnetic ((Formula presented)) phases of (Formula presented) has been studied. The same ionic radii of (Formula presented) and (Formula presented) cause no structure change in either series, yet conduction and ferromagnetism have been consistently suppressed by Fe doping. Colossal magnetoresistance has been shifted to lower temperatures, and in some cases enhanced by Fe doping. Doping with Fe bypasses the usually dominant lattice effects, but depopulates the hopping electrons and thus weakens the double exchange. © 1996 The American Physical Society.

Structural, transport, and magnetic properties of (Formula presented)(Formula presented)(Formula presented) (0≤x≤1) have been studied to probe the consequence of strong lattice distortion and reduced double exchange. Charge ordering has been observed over a large composition range of 0.30≤x≤0.80. For 0.33≤x≤0.40, at low temperatures, a magnetic field induces a first-order antiferromagnetic semiconductor to ferromagnetic metal transition and reduces the resistance by several orders of magnitude. These results illustrate the competition between double exchange and mechanisms that promote charge localization. © 1996 The American Physical Society.

Background: N-methyl-d-aspartate (NMDA) receptor hypofunction has been implicated in the pathophysiology of schizophrenia and its associated neurocognitive impairments. The high rate of cigarette smoking in schizophrenia raises questions about how nicotine