Cortical Plasticity Induced by Spike-Triggered Microstimulation in Primate Somatosensory Cortex

Electrical stimulation of the nervous system for therapeutic purposes, such as deep brain stimulation in the treatment of Parkinson’s disease, has been used for decades. Recently, increased attention has focused on using microstimulation to restore functions as diverse as somatosensation and memory. However, how microstimulation changes the neural substrate is still not fully understood. Microstimulation may cause cortical changes that could either compete with or complement natural neural processes, and could result in neuroplastic changes rendering the region dysfunctional or even epileptic. As part of our efforts to produce neuroprosthetic devices and to further study the effects of microstimulation on the cortex, we stimulated and recorded from microelectrode arrays in the hand area of the primary somatosensory cortex (area 1) in two awake macaque monkeys. We applied a simple neuroprosthetic microstimulation protocol to a pair of electrodes in the area 1 array, using either random pulses or pulses time-locked to the recorded spiking activity of a reference neuron. This setup was replicated using a computer model of the thalamocortical system, which consisted of 1980 spiking neurons distributed among six cortical layers and two thalamic nuclei. Experimentally, we found that spike-triggered microstimulation induced cortical plasticity, as shown by increased unit-pair mutual information, while random microstimulation did not. In addition, there was an increased response to touch following spike-triggered microstimulation, along with decreased neural variability. The computer model successfully reproduced both qualitative and quantitative aspects of the experimental findings. The physiological findings of this study suggest that even simple microstimulation protocols can be used to increase somatosensory information flow.     

FURTHER OBSERVATIONS ON JUVENILE AND ADULT HEDERA

Robbins , William J. (The New York Botanical Garden, New York, N. Y.) Further observations on juvenile and adult Hedera. Amer. Jour. Bot. 47(6) : 485–491. Illus. 1960.—Plants of arborescent Hedera helix sprayed with gibberellic acid produced juvenile shoots. Juvenile characters appeared in December to March from applications of gibberellic acid made from May to July. Gibberellic acid modified inflorescences toward a vegetative condition. Previous reports that seeds of arborescent Hedera helix produce juvenile plants were confirmed. Seedlings of a variant, Hedera helix ‘238th Street,‘ which has adult-shaped leaves on a vine type of growth produced vines with lobed leaves. Heavy pruning of arborescent Hedera helix caused the production of juvenile shoots.     

EFFECTS OF X IRRADIATION ON LEMNA PERPUSILLA

Posner , Herbert B., and William S. Hillman . (Yale U., New Haven, Conn.) Effects of x irradiation on Lemna perpusilla. Amer. Jour. Bot. 47(6): 506–511. Illus. 1960.—The effects of x rays on the multiplication rates (MR), percent flowering (Fl%) and gross morphology of aseptically grown cultures of Lemna perpusilla, strain 6746, were studied. MR values are unaffected by doses of less than 300 r but are progressively depressed as the dose increases. The effect of a given dose on short-term MR values is the same at the 2 dosage intensities used, 500 and 2000 r/min. The inhibitory effect of intermediate doses on long-term growth is delayed; high doses have an “immediate” effect. Bleaching of fronds and cessation of growth occur in all cultures given 5,000 r or higher. Radiosensitivity is not altered by addition of yeast extract and casein hydrolysate to the medium. Depressed Fl% and seed production appear to be consequences of lowered MR. Morphological aberrations such as small size, epinasty and wrinkling are temporary. Frond-sequence may be altered by x rays but this aberration is permanent. Various aspects of the results are discussed.     

Circadian clock adjustment to plant iron status depends on chloroplast and phytochrome function

Plant chloroplasts are not only the main cellular location for storage of elemental iron (Fe), but also the main site for Fe, which is incorporated into chlorophyll, haem and the photosynthetic machinery. How plants measure internal Fe levels is unknown. We describe here a new Fe‐dependent response, a change in the period of the circadian clock. In Arabidopsis, the period lengthens when Fe becomes limiting, and gradually shortens as external Fe levels increase. Etiolated seedlings or light‐grown plants treated with plastid translation inhibitors do not respond to changes in Fe supply, pointing to developed chloroplasts as central hubs for circadian Fe sensing. Phytochrome‐deficient mutants maintain a short period even under Fe deficiency, stressing the role of early light signalling in coupling the clock to Fe responses. Further mutant and pharmacological analyses suggest that known players in plastid‐to‐nucleus signalling do not directly participate in Fe sensing. We propose that the sensor governing circadian Fe responses defines a new retrograde pathway that involves a plastid‐encoded protein that depends on phytochromes and the functional state of chloroplasts.