Biomedical subjects

L Zablow

Publications and source records attributed to L Zablow.

15 recordsLinked to original sources

PubMed2001

Rapid increase in clusters of presynaptic proteins at onset of long-lasting potentiation.

A change in the efficiency of synaptic communication between neurons is thought to underlie learning. Consistent with recent studies of such changes, we find that long-lasting potentiation of synaptic transmission between cultured hippocampal neurons is accompanied by an increase in the number of clusters of postsynaptic glutamate receptors containing the subunit GluR1. In addition, potentiation is accompanied by a rapid and long-lasting increase in the number of clusters of the presynaptic protein synaptophysin and the number of sites at which synaptophysin and GluR1 are colocalized. These results suggest that potentiation involves rapid coordinate changes in the distribution of proteins in the presynaptic neuron as well as the postsynaptic neuron.

Actins↗

PubMed2001

Visualization of changes in presynaptic function during long-term synaptic plasticity.

Controversy exists regarding the site of modification of synaptic transmission during long-term plasticity in the mammalian hippocampus. Here we used a fluorescent marker of presynaptic activity, FM 1-43, to directly image changes in presynaptic function during both short-term and long-term forms of plasticity at presynaptic boutons of CA3-CA1 excitatory synapses in acute hippocampal slices. We demonstrated enhanced presynaptic function during long-term potentiation (LTP) induced either chemically (with tetraethylammonium), or by high-frequency (200-Hz) electrical stimulation. Both of these forms of LTP required activation of L-type voltage-gated calcium channels and NMDA receptors in the postsynaptic CA1 neuron. These results thus implied that a long-lasting increase in the efficacy of synaptic transmission is likely to depend, at least in part, on enhanced transmitter release from the presynaptic neuron.

Animals↗

PubMed1999

Cyclic AMP induces functional presynaptic boutons in hippocampal CA3-CA1 neuronal cultures.

Long-term forms of synaptic plasticity that may underlie learning and memory have been suggested to depend on changes in the number of synapses between presynaptic and postsynaptic neurons. Here we have investigated a form of synaptic plasticity in cultures of hippocampal CA3 and CA1 neurons related to the late phase of long-term potentiation, which depends on cAMP and protein synthesis. Using the fluorescent dye FM 1-43 to label active presynaptic terminals, we find that a membrane permeable analog of cAMP enhances the number of active presynaptic terminals and that this effect requires protein synthesis.

Animals↗

PubMed1992

Evaluation of cellular mechanisms for modulation of calcium transients using a mathematical model of fura-2 Ca2+ imaging in Aplysia sensory neurons.

A theoretical model of [Ca++]i diffusion, buffering, and extrusion was developed for Aplysia sensory neurons, and integrated with the measured optical transfer function of our fura-2 microscopic recording system, in order to fully simulate fura-2 video or photomultiplier tube measurements of [Ca++]i. This allowed an analysis of the spatial and temporal distortions introduced during each step of fura-2 measurements of [Ca++]i in cells. In addition, the model was used to evaluate the plausibility of several possible mechanisms for modulating [Ca++]i transients evoked by action potentials. The results of the model support prior experimental work (Blumenfeld, Spira, Kandel, and Siegelbaum, 1990. Neuron. 5: 487-499), suggesting that 5-HT and FMRFamide modulate action potential-induced [Ca++]i transients in Aplysia sensory neurons through changes in Ca++ influx, and not through changes in [Ca++]i homeostasis or release from internal stores.

Action Potentials↗

PubMed1990

Interaction of intracellular ion buffering with transmembrane-coupled ion transport.

The role of the Na/Ca exchanger in the control of cellular excitability and tension development is a subject of current interest in cardiac physiology. It has been suggested that this coupled transporter is responsible for rapid changes in intracellular calcium activity during single beats, generation of plateau currents, which control action potential duration, and control of intracellular sodium during Na/K pump suppression, which may occur during terminal states of ischemia. The actual behavior of this exchanger is likely to be complex for several reasons. First, the exchanger transports two ionic species and thus its instantaneous flux rate depends on both intracellular sodium and calcium activity. Secondly, the alteration in intracellular calcium activity, which is caused by a given transmembrane calcium flux, and which controls the subsequent exchanger rate, is a complex function of available intracellular calcium buffering. The buffers convert the ongoing transmembrane calcium fluxes into changes in activity that are a small and variable fraction of the change in total calcium concentration. Using a number of simple assumptions, we model changes in intracellular calcium and sodium concentration under the influence of Na/Ca exchange, Na/K ATPase and Ca-ATPase pumps, and passive sodium and calcium currents during periods of suppression and reactivation of the Na/K ATPase pump. The goal is to see whether and to what extent general notions of the role of the Na/Ca exchanger used in planning and interpreting experimental studies are consistent with its function as derived from current mechanistic assumptions about the exchanger. We find, for example, that based on even very high estimates of intracellular calcium buffering, it is unlikely that Na/Ca exchange alone can control intracellular sodium during prolonged Na/K pump blockade. It is also shown that Na/Ca exchange can contaminate measurements of Na/K pump currents under a variety of experimental conditions. The way in which these and other functions are affected by the dissociation constants and total capacity of the intracellular calcium buffers are also explored in detail.

Biological Transport↗

PubMed1981

The independence of closely spaced discrete experimental spike foci.

Stable spike foci generated by weak penicillin solutions had a minimal area of distribution of 12.5 mm2. Two foci separated by 4 mm on the same gyrus were consistently dependent and simultaneous. An area of "positive surround" between the two spikes did not prevent dependency. This contradicts the hypothesis that "positive surround" prevents spreading of epileptiform discharges. Spike foci separated by 6 mm were almost always independent. Bursts of afterdischarges remained independent if the primary spikes were independent. Postafterdischarge suppression and spreading depression of Leao affected independent spike focus selectively. These experiments suggest that cross-talking between cortical columns is limited to column 1 to 2 mm apart.

Animals↗

PubMed1980

Quantitative studies of spike foci induced by minimal concentrations of penicillin.

The minimal concentrations of penicillin which induce stable recurrent spikes (20,000 U/ml) and which elicit stable recurrent after-discharges (100,000 U/ml) were determined. A quantitative study of the inter-relationships, variability and changes with time of a number of spike parameters (spike latency, spike amplitude, amplitude of prepositivity, spike duration and spike frequency) was performed. The study adds new information on the pathogenesis of the experimental spike focus and serves as baseline for quantitative evaluation of the effects of anticonvulsants on the characteristics of the primary spike focus and on after-discharges.

Animals↗

PubMed1977

The penicillin focus. I. Distribution of potential at the cortical surface.

The potential field of a penicillin focus of controlled size was recorded from a rectangular array of 12 electrodes occupying a 4 X 6 mm area on the exposed anterior sigmoid gyrus of the cat. The array was made with 2 mm interelectrode spacing of 0.4 mm I.D. glass capillary tubes filled with Ringer's in agar, excepting one containing penicillin to create the focus. Early in the development of the focus a negative spike appears at the penicillin electrode reaching amplitudes of as high as 3,000 muV while all of the other electrodes showed no synchronous activity of more than 100 muV. Within the first 15 min spike activity becomes visible at about 100 muV at all the electrodes and after 30 min, waveforms of all activity become quite stable. At the penicillin-containing electrode, at intervals of 2--10 sec each, a negative sharp wave of up to 4 mV occurs, having a shorter rise time than fall time. A smaller positive spike of about 30 msec duration which showed marked variations in amplitude often preceded the stable negative sharp wave. During the rise of the negativity at the penicillin electrode, practically all the surrounding electrodes showed a predominantly positive spike. This was occasionally followed by negativity during the falling phase at the penicillin electrode. Displays of potential surfaces interpolating the average values at the 12 recording points on the cortex at 4 msec intervals demonstrate a relationship between the field of the sharp wave at the penicillin focus which is less than 2 mm in diameter and that of the surrounding electrode which indicates that symmetrically located synaptic inhibitory processes are strongly activated in areas adjacent to the small simultaneous excitation at the penicillin electrode. Degrees of attenuation of interictal spikes that take place between cortex and scalp are estimated from the measured potential distributions. Explanation is offered for the reported apparent discrepancies between the findings at the cortex and the scalp EEG.

Animals↗

PubMed1973

Sensory conduction in peroneal and posterior tibial nerves using averaging techniques.

A method of obtaining pure sensory nerve conduction velocities in the lower extremities is described. This involves the use of electronic summation (signal averaging). Potentials were obtained and velocities calculated from all normal subjects examined. In patients with peripheral neuropathies it was often possible to obtain nerve velocities with signal amplitudes as low as 0·1 μV and these were often slower than those obtained from the normal subjects. The advantages and disadvantages of this method are discussed. It is of significant clinical value in that pure sensory nerve conduction velocities can be measured in the legs when this may be the only valuable parameter in the absence of motor involvement. In addition, investigation of neuropathies at an earlier stage of development and recovery may be facilitated. It is hoped that in the future this technique of obtaining low amplitude responses with an analogue averager can be incorporated with the more routine aspects of nerve conduction testing when clinically indicated.

Action Potentials↗

PubMed1970