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M Pekel

Publications and source records attributed to M Pekel.

8 recordsLinked to original sources

Optokinetic eye movements elicited by radial optic flow in the macaque monkey.

We recorded spontaneous eye movements elicited by radial optic flow in three macaque monkeys using the scleral search coil technique. Computer-generated stimuli simulated forward or backward motion of the monkey with respect to a number of small illuminated dots arranged on a virtual ground plane. We wanted to see whether optokinetic eye movements are induced by radial optic flow stimuli that simulate self-movement, quantify their parameters, and consider their effects on the processing of optic flow. A regular pattern of interchanging fast and slow eye movements with a frequency of 2 Hz was observed. When we shifted the horizontal position of the focus of expansion (FOE) during simulated forward motion (expansional optic flow), median horizontal eye position also shifted in the same direction but only by a smaller amount; for simulated backward motion (contractional optic flow), median eye position shifted in the opposite direction. We relate this to a change in Schlagfeld typically observed in optokinetic nystagmus. Direction and speed of slow phase eye movements were compared with the local flow field motion in gaze direction (the foveal flow). Eye movement direction matched well the foveal motion. Small systematic deviations could be attributed to an integration of the global motion pattern. Eye speed on average did not match foveal stimulus speed, as the median gain was only approximately 0.5-0.6. The gain was always lower for expanding than for contracting stimuli. We analyzed the time course of the eye movement immediately after each saccade. We found remarkable differences in the initial development of gain and directional following for expansion and contraction. For expansion, directional following and gain were initially poor and strongly influenced by the ongoing eye movement before the saccade. This was not the case for contraction. These differences also can be linked to properties of the optokinetic system. We conclude that optokinetic eye movements can be elicited by radial optic flow fields simulating self-motion. These eye movements are linked to the parafoveal flow field, i.e., the motion in the direction of gaze. In the retinal projection of the optic flow, such eye movements superimpose retinal slip. This results in complex retinal motion patterns, especially because the gain of the eye movement is small and variable. This observation has special relevance for mechanisms that determine self-motion from retinal flow fields. It is necessary to consider the influence of eye movements in optic flow analysis, but our results suggest that direction and speed of an eye movement should be treated differently.

Animals

Optic flow processing in monkey STS: a theoretical and experimental approach.

How does the brain process visual information about self-motion? In monkey cortex, the analysis of visual motion is performed by successive areas specialized in different aspects of motion processing. Whereas neurons in the middle temporal (MT) area are direction-selective for local motion, neurons in the medial superior temporal (MST) area respond to motion patterns. A neural network model attempts to link these properties to the psychophysics of human heading detection from optic flow. It proposes that populations of neurons represent specific directions of heading. We quantitatively compared single-unit recordings in area MST with single-neuron simulations in this model. Predictions were derived from simulations and subsequently tested in recorded neurons. Neuronal activities depended on the position of the singular point in the optic flow. Best responses to opposing motions occurred for opposite locations of the singular point in the visual field. Excitation by one type of motion is paired with inhibition by the opposite motion. Activity maxima often occur for peripheral singular points. The averaged recorded shape of the response modulations is sigmoidal, which is in agreement with model predictions. We also tested whether the activity of the neuronal population in MST can represent the directions of heading in our stimuli. A simple least-mean-square minimization could retrieve the direction of heading from the neuronal activities with a precision of 4.3 degrees. Our results show good agreement between the proposed model and the neuronal responses in area MST and further support the hypothesis that area MST is involved in visual navigation.

Animals

Neuronal responses in the motion pathway of the macaque monkey to natural optic flow stimuli.

Neurones in higher visual motion areas in the superior temporal sulcus (STS) of the macaque monkey respond to abstract random dot optic flow stimuli. Higher motion areas may not only represent, but in a next computational stage also analyse the flow field to determine, for instance, the direction of heading for navigation purposes. Real world visual scenes differ in several aspects from these abstract optic flow stimuli. We tested the neuronal response to naturalistic optic flow stimuli which simulated egomotion in different virtual environments and contained different numbers of visual cues. Neuronal activity depended mainly on the position of the focus of expansion rather than on other visual cues. This finding supports the hypothesis that higher motion areas within the STS analyse optic flow in natural scenes and can thus signal the direction of heading.

Animals

Voltage-activated calcium channel currents of rat DRG neurons are reduced by mercuric chloride (HgCl2) and methylmercury (CH3HgCl).

The actions of bath applied mercuric chloride (HgCl2) and methylmercury (CH3HgCl) on voltage-activated calcium channel currents (VACCCs) were tested, using the whole cell patch clamp recording technique with cultured dorsal root ganglion (DRG) neurons from 2-4 day old rat pups. Both metal compounds reduced the current irreversibly in a concentration dependent fashion, reaching a new (lower) steady state within 3 to 5 min after application. Inorganic mercury was more effective in reducing the VACCCs with an IC50 of 1.3 microM, while the IC50 for methylmercury was 2.6 microM. But the threshold concentrations were below 0.25 microM for both metal compounds and the calcium channel currents were reduced by more than 90% with concentrations of 5 microM and 20 microM, respectively. The Hill coefficient for both dose-response relationship was calculated as approximately 1. Calcium channel currents were reduced over the entire voltage range, but the current-voltage relation shifted to more positive potentials in a concentration dependent manner, the effect being more pronounced with HgCl2 than with CH3HgCl (1 microM HgCl2: 10 mV shift, 5 microM CH3HgCl: 5 mV shift). At higher concentrations (> or = 2 microM for HgCl2, and > or = 10 microM for CH3HgCl) an unidentified membrane current was observed. The inorganic mercury caused an inward current, while the organic mercury compound generated a biphasic current with a transient inward and a long lasting outward component. Our results suggest that mercury compounds affect the electrical properties of neurons and thereby decrease cognitive and motor performance.

Animals

Mercury (Hg2+) and zinc (Zn2+): two divalent cations with different actions on voltage-activated calcium channel currents.

1. We examined the actions of mercury (Hg2+) and zinc (Zn2+) on voltage-activated calcium channel currents of cultured rat dorsal root ganglion (DRG) neurons, using the whole-cell patch clamp technique. 2. Micromolar concentrations of both cations reduced voltage-activated calcium channel currents. Calcium channel currents elicited by voltage jumps from a holding potential of -80 to 0 mV (mainly L- and N-currents) were reduced by Hg2+ and Zn2+. The threshold concentration for Hg2+ effects was 0.1 microM and that for Zn2+ was 10 microM. Voltage-activated calcium channel currents were abolished (> 80%) with 5 microM Hg2+ or 200 microM Zn2+. The peak calcium current was reduced to 50% (IC50) by 1.1 microM Hg2+ or 69 microM Zn2+. While Zn2+ was much more effective in reducing the T-type calcium channel current--activated by jumping from -80 to -35 mV--Hg2+ showed some increased effectiveness in reducing this current. 3. The effects of both cations occurred rapidly and a steady state was reached within 1-3 min. While the action of Zn2+ was not dependent on an open channel state, Hg2+ effects depended partially on channel activation. 4. While both metal cations reduced the calcium channel currents over the whole voltage range, some charge screening effects were detected with Hg2+ and with higher concentrations (> 100 microM) of Zn2+. 5. As Zn2+ in the concentration range used had no influence on resting membrane currents, Hg2+ caused a clear inward current at concentrations > or 2 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Mercury (Hg2+) decreases voltage-gated calcium channel currents in rat DRG and Aplysia neurons.

Inorganic mercury (Hg2+) reduced voltage-gated calcium channel currents irreversibly in two different preparations. In cultured rat dorsal root ganglion (DRG) neurons, studied with the whole cell patch clamp technique, a rapid concentration-dependent decrease in the L/N-type currents to a steady state was observed with an IC50 of 1.1 microM and a Hill coefficient of 1.3. T-currents were blocked with Hg2+ in the same concentration range (0.5-2 microM). With increasing Hg2+ concentrations a slow membrane current was additionally activated, most obviously at concentrations over 2 microM Hg2+. This current was irreversible and might be due to the opening of other (non-specific) ion channels by Hg2+. The current-voltage (I-V) relation of DRG neurons shifted to more positive values, suggesting a binding of Hg2+ to the channel protein and/or modifying its gating properties. In neurons of the abdominal ganglion of Aplysia californica, studied with the two electrode voltage clamp technique, a continuous decrease of calcium channel currents was seen even with the lowest used concentration of Hg2+ (5 microM). A steady state was not reached and the effect was irreversible without any change on resting membrane currents, even with high concentrations (up to 50 microM). No shift of the I-V relation of the calcium channel currents was observed. Effects on voltage-activated calcium channel currents with Hg2+ concentrations such low have not been reported before. We conclude that neurotoxic effects of inorganic mercury could be partially due to the irreversible blockade of voltage-activated calcium channels.

Animals

Strychnine-sensitive glycine receptors in cultured primary neurons from rat neocortex.

After 1 day in vitro (DIV) glycine (1 mM) evoked chloride-dependent membrane currents in about 50% of primary cultured rat neocortical neurons and more than 98% of the cells were glycine-sensitive after 2 DIV lasting for at least up to 12 DIV which was similar to GABA chemosensitivity. Strychnine (IC50 40 nM) and picrotoxin (30 microM) but not bicuculline (50 microM) blocked the glycine-evoked currents. The results provide evidence for a very early expression of glycine receptors on cortical neurons leading to a powerful chloride channel-operating capacity during early development.

Animals

Depolarization of cultured astrocytes by leukotriene B4. Evidence for the induction of a K+ conductance inhibitor.

Since astrocytes have been shown to participate in intracerebral immunological processes we investigated the effect of the immune mediators, leukotrienes (LT) B4, LTC4 and LTD4 on membrane properties of cultured astrocytes from neonatal rat brain. When LTB4 was added to the bath solution the membrane potential slowly decreased from -96 mV to -38 mV. While LTB4 at a concentration of 500 nM was ineffective, depolarization occurred when concentrations of 750 nM and above were used. The depolarizing effect was specific for LTB4, since LTC4 and LTD4, other arachidonic acid derivates, failed to depolarize astrocytes at even higher concentrations (1 microM). When the K+ conductance blocker, Ba2+ (2 mM), was added to the bath solution, astrocytes depolarized to the same degree but no further depolarization was achieved when LTB4 was added. Bath application of Co2+ (1 mM), in order to reduce putative Ca2+ inward currents or reduced internal chloride concentration, did not alter the LTB4-induced depolarization, thus arguing against additional Ca(2+)- or Cl(-)-dependent depolarizing effects. The LTB4-induced depolarization could be markedly reduced, however, by preincubation of the cells with cycloheximide (2 microM), which blocks translation and thereby protein synthesis. Cycloheximide alone had no effect on the membrane potential. These data indicate that, in astrocytes, LTB4 stimulates the synthesis of a protein, which, in turn, inhibits K+ conductances. This effect could impair glial, as well as neuronal, functions during CNS diseases accompanied by immunological processes.

Animals