Electroencephalogram activity in the anoxic turtle brain.

The anoxia-tolerant turtle brain slowly undergoes a complex sequence of changes in electroencephalogram (EEG) activity as the brain systematically downregulates its energy demands. Following N2 respiration, the root mean square voltage rapidly fell, reaching approximately 20% of normoxic levels after approximately 100 min of anoxia. During the first 20- to 40-min transition period, the power of the EEG decreased substantially, particularly in the 12- to 24-Hz band, with low-amplitude slow wave activity predominating (3-12 Hz). Bursts of high voltage rhythmic slow (approximately 3-8 Hz) waves were seen during the 20- to 100-min period of anoxia, accompanied by large sharp waves. During the next 400 min of N2 respiration, two distinct patterns of electrical activity characterized the anoxic turtle brain: 1) a sustained but depressed activity level, with an EEG amplitude approximately 20% of the normoxic control and with total EEG power reduced by one order of magnitude at all frequencies, and 2) short (3-15 s) periodic (0.5-2/min) bursts of mixed-frequency activity that interrupted the depressed activity state. We speculate that the EEG patterns seen during sustained anoxia represent the minimal or basic electrical activities that are compatible with the survival of the anoxic turtle brain as an integrated unit, which allow the brain to return to normal functioning when air respiration resumed.

Is there an error correcting code in the base sequence in DNA?

Modern methods of encoding information into digital form include error check digits that are functions of the other information digits. When digital information is transmitted, the values of the error check digits can be computed from the information digits to determine whether the information has been received accurately. These error correcting codes make it possible to detect and correct common errors in transmission. The sequence of bases in DNA is also a digital code consisting of four symbols: A, C, G, and T. Does DNA also contain an error correcting code? Such a code would allow repair enzymes to protect the fidelity of nonreplicating DNA and increase the accuracy of replication. If a linear block error correcting code is present in DNA then some bases would be a linear function of the other bases in each set of bases. We developed an efficient procedure to determine whether such an error correcting code is present in the base sequence. We illustrate the use of this procedure by using it to analyze the lac operon and the gene for cytochrome c. These genes do not appear to contain such a simple error correcting code.

What causes ion channel proteins to fluctuate open and closed?

Ion channels in the cell membrane spontaneously switch from states that are closed to the flow of ions such as sodium, potassium, and chloride to states that are open to the flow of these ions. The durations of times that an individual ion channel protein spends in the closed and open states can be measured by the patch clamp technique. We explore two basic issues about the molecular properties of ion channels: 1) If the switching between the closed and open state is an inherently random event, what does the patch clamp data tell us about the structure or motions in the ion channel protein? 2) Is this switching random?

Membrane potential fluctuations of human T-lymphocytes have fractal characteristics of fractional Brownian motion.

The voltage across the cell membrane of human T-lymphocyte cell lines was recorded by the whole cell patch clamp technique. We studied how this voltage fluctuated in time and found that these fluctuations have fractal characteristics. We used the Hurst rescaled range analysis and the power spectrum of the increments of the voltage (sampled at 0.01-sec intervals) to characterize the time correlations in these voltage fluctuations. Although there was great variability in the shape of these fluctuations from different cells, they all could be represented by the same fractal form. This form displayed two different regimes. At short lags, the Hurst exponent H = 0.76 +/- 0.05 (SD) and, at long lags, H = 0.26 +/- 0.04 (SD). This finding indicated that, over short time intervals, the correlations were persistent (H > 0.5), that is, increases in the membrane voltage were more likely to be followed by additional increases. However, over long time intervals, the correlations were antipersistent (H < 0.5), that is, increases in the membrane voltage were more likely to be followed by voltage decreases. Within each time regime, the increments in the fluctuations had characteristics that were consistent with those of fractional Gaussian noise (fGn), and the membrane voltage as a function of time had characteristics that were consistent with those of fractional Brownian motion (fBm).

Using fractals and nonlinear dynamics to determine the physical properties of ion channel proteins.

Three examples are given of how concepts from fractals and nonlinear dynamics have been used to analyze the voltages and currents recorded through ion channels in an attempt to determine the physical properties of ion channel proteins. (1) Early models had assumed that the switching of the ion channel protein from one conformational state to another can be represented by a Markov process that has no long-term correlations. However, one support for the existence of long-term correlations in channel function is that the currents recorded through individual ion channels have self-similar properties. These fractal properties can be characterized by a scaling function determined from the distribution of open and closed time intervals, which provides information on the distribution of activation energy barriers between the open and closed conformational substates of the ion channel protein and/or on how those energy barriers change in time. (2) Another support for such long-term correlations is that the whole-cell membrane voltage recorded across many channels at once may also have a fractal form. The Hurst rescaled range analysis of these fluctuations provides information on the type and degree of correlation in time of the functioning of ion channels. (3) The early models had also assumed that the switching from one state to another is an inherently random process driven by the energy from thermal fluctuations. More recently developed models have shown that deterministic dynamics may also produce the same distributions of open and closed times as those previously attributed to random events. This raises the possibility that the deterministic atomic and electrostatic forces play a role in switching the channel protein from one conformational shape to another. Debate exists about whether random, fractal, or deterministic models best represent the functioning of ion channels. However, fractal and deterministic dynamics provide a new approach to the study of ion channels that should be seriously considered by neuroscientists.

Action potentials pass severed earthworm MGA segments reconnected by laser and electric field pulses.

Active and passive electrical signals transmit across the earthworm (Lumbricus terrestris) medial giant axon (MGA) segment after reconnection induced by laser and electric field pulses. Laser pulses of 308 nm, 15 ns pulse duration, and pulse energy 5-50 microJ in the objective plane induced axon reconnection in 12 of 133 (9%) preparations. Electric field pulses of 200-800 V, 100 microseconds duration, induced axon reconnection in 15 of 188 (8%) preparations. Electrical continuity is possible after the reconnection of severed axons induced by laser and electric field pulses.

Electric-field-induced reconnection of severed axons.

We report the first successful axon reconnection in the earthworm (Lumbricus terrestris) medial giant axon (MGA) by electric fields generated by electrical pulses of 10-100 microseconds duration and 80-200 V amplitude. Reconnection was documented by light and electron microscopy, and by transport of Lucifer yellow dye across the reconnected MGA segments. Direct repair of a severed nerve axon promises the advantages of preserving axon viability and distal connections.

Laser-induced reconnection of severed axons.

After their axons have been severed, nerve cells can achieve functional recovery either by regrowth of the injured cells or by direct repair of the injured cell at the site of injury. Direct repair of a severed axon promises the advantages of preserving the viability and existing connections of the axon distal to the injury. We report here the first successful axon reconnection in the earthworm (Lumbricus terrestris) medial giant axon (MGA) in vitro system (1) by the application of well-focused 15 nsec, 5 to 50 muJ/pulse, 308 nm laser pulses. Axon reconnection is documented by light and electron microscopy, as well as by transfer of the iontophoretically injected fluorescent dye, Lucifer Yellow, across the reconnected MGA segments.