The molluscan neuropeptide FMRF-amide (10 to 50 microM) decreases the duration of the Ca2+-dependent action potential recorded in the cell body of identified neurons of the snail Helix aspersa (cells D3 and E2). In these neurons, FMRF-amide evokes a decrease of the Ca2+ current resulting from a decrease in Ca2+ conductance. In another single neuron, cell E11, FMRF-amide, besides evoking a decrease of the Ca2+ conductance, induces a decrease of the S-current (Klein, M., J. S. Camardo, and E. R. Kandel (1982) Proc. Natl. Acad Sci. U. S. A. 79: 5713–5717), a K+ current controlled by cyclic AMP. However, in this E11 cell, FMRF-amide also evokes a decrease of the amplitude of the Ca2+ spike plateau. As discussed in the preceding paper (Paupardin-Tritsch, D., L. Colombaioni, P. Deterre, and H. M. Gerschenfeld (1985) J. Neurosci. 5: 2522–2532), it is suggested that these FRMF-amide-induced modulations of ionic conductances involved in the Ca2+-dependent spike recorded in these neuronal somata may intervene in processes of presynaptic inhibition and facilitation.

Significance: The correct interplay between mitochondria and nuclear functions is essential to generate the mature functional six-layered structure of the mammalian cerebral cortex. Thus, alteration in this interaction results in pathological conditions such as cancer or neurodevelopmental disorders. The molecules and signaling mechanisms responsible for the nucleus–mitochondria communication and functional coordination are still largely unknown. The here-reported nuclear and mitochondrial localization of Forkhead box g1 (Foxg1), a transcription factor essential for brain development and cerebral cortex layering, provides insights on the molecular mechanisms through which Foxg1 acts as a link among mitochondrial function, neuronal differentiation, and pathological conditions.

A mini review of the toxicity of Thallium (Tl) at low doses is herein presented. Thallium has severe toxicity. Although its acute biological effects have been widely investigated and are well known, its biological effects on human health and in cell cultures at low doses (<100 μg/L) due, for example, to Tl chronic exposure via consumption of contaminated water or foods, have often been overlooked or underestimated. Relatively few papers have been published on this topic and are herein reviewed to provide a focused scientific opinion in the light of current worldwide regulatory issues.

Dopamine (10 to 50 microM) modulates in two different ways the duration of the Ca2+-dependent action potential recorded in the cell body of identified neurons of the snail Helix aspersa. In some neurons (cells E13 and F1) dopamine increases the amplitude of their Ca2+-dependent spike plateau by decreasing the S-current (Klein, M., J.S. Camardo, and E. R. Kandel (1982) Proc. Natl. Acad. Sci. U.S.A. 79: 5713–5717), a K+ current controlled by cyclic AMP. In another neuron (cell D2), dopamine decreases the Ca2+-dependent plateau of the somatic action potential by evoking a decrease in Ca2+-current resulting from a decrease in Ca2+ conductance. Both modulatory effects could be observed in the same single neuron in which dopamine induces decreases of both the Ca2+ conductance and cyclic AMP-dependent K+ conductance. Nevertheless, in these cells (such as cell F5) dopamine only evokes a decrease of the amplitude of the Ca2+ spike plateau. Since the modulation of the duration of the Ca2+ action potential recorded in the neuronal soma has been shown to constitute a good model of events taking place at synaptic endings, it is suggested that these modulatory mechanisms evoked by dopamine may be involved in processes of presynaptic facilitation and inhibition.