Two phases of the contingent negative variation in humans: association with motor and mental functions.

The question of the relationship between contingent negative variation and the mechanisms controlling motor and mental functions has received inadequate study. The aims of the present work were to investigate the relationship between the early and late phases of contingent negative variation and the state of motor and mental functions in patients with Parkinson's disease and to study the effects of levodopa on contingent negative variation. Patients with Parkinson's disease showed significant decreases in the amplitudes and areas of both phases of contingent negative variation as compared with subjects of similar age.

Intracellular regulation of neuronal nicotinic cholinoreceptors.

Experiments on isolated superior cervical ganglia from rats were used to study the effects of substances affecting intracellular second messengers on membrane currents evoked by iontophoretic application of acetylcholine (ACh currents) and on excitatory postsynaptic currents (EPSC) induced by single discharges of preganglionic nerve fibers. These studies showed that the adenylate cyclase activator forskolin, the phosphodiesterase inhibitor isobutylmethylxanthine (IMBX), and the protein kinase C activator phorbol ester decreased the amplitude of the ACh current. Neither IMBX nor phorbol ester had any effect on the amplitude or decay time constant of EPSC, while forskolin increased the amplitude of EPSC without altering its decay time constant.

The endoplasmic reticulum and mitochondria as elements of the mechanism of intracellular signaling in the nerve cell.

Experimental data obtained in our laboratory from studies of intracellular signals arising within nerve cells during excitation are summarized. Measurements of transmembrane ion currents in conditions of fixed membrane potential and intracellular free Ca ion concentrations, using fluorescent probes, yielded the time and spatial characteristics of transient elevations in the Ca concentration (the "calcium signal") in various types of mouse and rat neurons. These studies showed that intracellular structures-the endoplasmic reticulum and mitochondria-had significant roles in forming these signals; these structures can take up Ca from the cytosol and liberate Ca into the cytosol; the contribution of these processes was extremely variable, depending on the internal organization of different functional types of neurons.