Simultaneous electrochemical and unit recording measurements: Characterization of the effects of d-amphetamine and ascorbic acid on neostriatal neurons

Simultaneous electrochemical measurements and recordings of single-unit activity were obtained from the neostriatum of immobilized, locally anesthetized rats. Electrical cross-talk between the two systems was minimized by the use of carbon-fiber voltammetric electrodes, which generate very small currents during electrolysis, and by the careful isolation of the recording apparatus. An intraperitoneal (i.p.) injection of 2.5 mg/kg d-amphetamine (d-AMPH) typically inhibited unit activity and produced a corresponding mirror-image increase in oxidation current. Both the depression of firing rate and the elevated electrochemical signal were maximal approximately 25 min after d-AMPH administration. In contrast, both unit activity and oxidation current were elevated after administration of 7.5 mg/kg d-AMPH with the maximum change in firing rate occurring significantly sooner than the peak electrochemical response. In view of evidence that the d-AMPH-induced voltammetric signal is similar to that for ascorbic acid (AA), but not dopamine (DA), a separate group of 12 animals received 1000 mg/kg AA (i.p.). In all cases, AA increased the electrochemical signal and in 7 animals this response was accompanied by an increase in firing rate. Our results, which demonstrate the feasibility of combining in vivo electrochemistry with single-unit electrophysiology, suggest that a d-AMPH-induced release of DA cannot completely explain the dose-dependent biphasic shift in neuronal activity produced by this drug in the neostriatum. Moreover, AA appears to be an effective modulator of neostriatal activity.     

Trace element regulation of immunity and infection

Nutritional deficiency is associated with impaired immunocompetence and increased susceptibility to infection. Among other nutrients, several trace elements have been shown to regulate immune responses. Zinc deficiency results in lymphoid atrophy and decreased capacity to respond to many T-dependent antigens. Plaque forming cell response to heterologous red cells is decreased as is the function of B cells. The generation of cytotoxic spleen cells following in vivo immunization with tumor cells is reduced, whereas natural killer cell activity and antibody-dependent cell mediated cytotoxicity are largely unchanged. Iron deficiency is associated with slight reduction in rosette-forming T cells, impaired lymphocyte proliferation response to mitogens and antigens, and decreased bactericidal capacity of neutrophils. Copper deficiency results in decreased antibody-forming cell response and increased susceptibility to a variety of microorganisms. Selenium deficiency reduces T cell dependent antibody responses, particularly in association with vitamin E deficiency. Thymic hormone activity is reduced in deficiencies of zinc, copper and selenium. Excess intake of many essential trace elements also depresses immune responses. Many of the heavy metals produce impaired cell-mediated immunity. These effects of trace elements on immunity and infection may have important fundamental and clinical implications.