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Köçkar, Hakan (Balikesir Author), A series of CoNiCu/Cu multilayers was potentiostatically electrodeposited on strong (100) textured Cu substrates from the electrolytes with different Ni concentrations. The x-ray diffraction (XRD) data showed that all studied samples exhibited a face centred cubic (fcc) structure. According to scanning electron microscopy (SEM) images, the surface morphology of the films is affected by their Ni content. The chemical analysis by energy dispersive x-ray spectroscopy (EDX) demonstrates that as the Ni ion concentration in the electrolyte is increased, the Ni content of the film increases while the Co and Cu contents decrease. Magnetoresistance (MR) measurements were carried out at room temperature in the magnetic fields of +/- 12 kOe. The samples grown from the electrolytes with the Ni concentration of up to 0.3 M exhibited giant magnetoresistance (GMR). For the samples grown from 0.3 M Ni, anisotropic magnetoresistance (AMR) begins to appear. The GMR decreased with increasing Ni concentration and the AMR appeared. For the 2.0 M Ni concentration, MR converted from GMR to AMR. Furthermore, the magnetization measurements made by a vibrating sample magnetometer (VSM) showed that the antiferromagnetic coupling between ferromagnetic layers weakened with increasing the Ni concentrations., Balikesir University Research - 2005/18 State Planning Organization (DPT) - 2005K120170

The dopamine transporter (DAT) is a key mediator of dopaminergic neurotransmission and a major target for amphetamine. We found previously that protein kinase C (PKC) beta regulates amphetamine-mediated dopamine efflux. Here, using PKCbeta wild-type (WT) and knockout (KO) mice, we report a novel role for PKCbeta in amphetamine-induced regulation of DAT trafficking and activity. PKCbeta KO mice have less striatal surface DAT, [3H]dopamine uptake, and amphetamine-stimulated dopamine efflux, yet higher novelty-induced locomotor activity than WT mice. Although a short exposure (or =90 s) to amphetamine rapidly increases striatal surface DAT and [3H]dopamine uptake in WT mice, this treatment decreases surface DAT and [3H]dopamine uptake in KO mice. Increases in surface DAT and [3H]dopamine uptake are not evident in KO mice until a longer exposure (60 min) to amphetamine, by which time WT mice exhibit decreased surface DAT and dopamine uptake. The slowness of amphetamine-induced striatal DAT trafficking in PKCbeta KO mice was mimicked by the use of a specific PKCbeta inhibitor, LY379196, in WT mice. Furthermore, PKCbeta KO mice exhibit reduced locomotor responsiveness to amphetamine compared with WT, which could be explained by reduced surface DAT and delayed amphetamine-induced DAT trafficking in KO mice. Our results indicate that PKCbeta is crucial for proper trafficking of DAT to the surface and for functioning of DAT and amphetamine signaling, providing new insight into the role of PKCbeta as an important regulator of dopaminergic homeostasis.

RATIONALE: Psychostimulants are often used in close temporal proximity to nicotine and have been reported to enhance acutely nicotine’s desirability in humans. OBJECTIVE: To investigate the acute associations between amphetamine and nicotine, we examined the potentiative interactions between clinically-relevant, low doses of these drugs on locomotor activity and dopamine overflow in the rat. METHODS: Locomotor activity was measured by telemetry in the home cage environment, and dopamine overflow was evaluated in striatal slice preparations from female Holtzman rats. RESULTS: When administered simultaneously, nicotine and amphetamine produced a predominantly additive effect on locomotor behavior. However amphetamine, when given 2-4 hours prior to nicotine, strongly potentiated nicotine-induced locomotor activity. Correspondingly, nicotine given 1-4 h prior to amphetamine, robustly enhanced amphetamine-stimulated locomotor activity when, even when the effects of the nicotine pretreatment dissipated. Acute nicotine pretreatment similarly potentiated the effects of dopamine transporter ligands, cocaine, nomifensine, and methamphetamine, but not a direct dopamine receptor agonist. Consistent with the behavioral studies, in vivo nicotine pretreatment exaggerated amphetamine-induced dopamine efflux from rat striatal slices. Likewise, in vivo pretreatment of rats with amphetamine potentiated nicotine-induced dopamine efflux from striatal slices. Direct pretreatment of striatal tissue by nicotine also potentiated subsequent amphetamine-stimulated dopamine overflow, further suggesting that the nicotine-amphetamine interaction occurs at the level of the dopamine terminal. CONCLUSION: Overall, the present data demonstrate that acute interactions of nicotine and other psychomotor stimulants produce potentiative effects and that these transient interactions may play a role in the frequent co-use and abuse of nicotine and other stimulants.