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F Nadim

Publications and source records attributed to F Nadim.

18 recordsLinked to original sources
PubMed2001

Synaptic depression mediates bistability in neuronal networks with recurrent inhibitory connectivity.

When depressing synapses are embedded in a circuit composed of a pacemaker neuron and a neuron with no autorhythmic properties, the network can show two modes of oscillation. In one mode the synapses are mostly depressed, and the oscillations are dominated by the properties of the oscillating neuron. In the other mode, the synapses recover from depression, and the oscillations are primarily controlled by the synapses. We demonstrate the two modes of oscillation in a hybrid circuit consisting of a biological pacemaker and a model neuron, reciprocally coupled via model depressing synapses. We show that across a wide range of parameter values this network shows robust bistability of the oscillation mode and that it is possible to switch the network from one mode to the other by injection of a brief current pulse in either neuron. The underlying mechanism for bistability may be present in many types of circuits with reciprocal connections and synaptic depression.

Animals↗
PubMed2001

The mechanism and applicability of in situ oxidation of trichloroethylene with Fenton's reagent.

Fenton's reagent is the result of reaction between hydrogen peroxide (H(2)O(2)) and ferrous iron (Fe(2+)), producing the hydroxyl radical (-*OH). The hydroxyl radical is a strong oxidant capable of oxidizing various organic compounds. The mechanism of oxidizing trichloroethylene (TCE) in groundwater and soil slurries with Fenton's reagent and the feasibility of injecting Fenton's reagent into a sandy aquifer were examined with bench-scale soil column and batch experiment studies. Under batch experimental conditions and low pH values ( approximately 3), Fenton's reagent was able to oxidize 93-100% (by weight) of dissolved TCE in groundwater and 98-102% (by weight) of TCE in soil slurries. Hydrogen peroxide decomposed rapidly in the test soil medium in both batch and column experiments. Due to competition between H(2)O(2) and TCE for hydroxyl radicals in the aqueous solutions and soil slurries, the presence of TCE significantly decreased the degradation rate of H(2)O(2) and was preferentially degraded by hydroxyl radicals. In the batch experiments, Fenton's reagent was able to completely dechlorinate the aqueous-phase TCE with and without the presence of soil and no VOC intermediates or by-products were found in the oxidation process. In the soil column experiments, it was found that application of high concentrations of H(2)O(2) with addition of no Fe(2+) generated large quantities of gas in a short period of time, sparging about 70% of the dissolved TCE into the gaseous phase with little or no detectable oxidation taking place. Fenton's reagent completely oxidized the dissolved phase TCE in the soil column experiment when TCE and Fenton's regent were simultaneously fed into the column. The results of this study showed that the feasibility of injecting Fenton's reagent or H(2)O(2) as a Fenton-type oxidant into the subsurface is highly dependent on the soil oxidant demand (SOD), presence of sufficient quantities of ferrous iron in the application area, and the proximity of the injection area to the zone of high aqueous concentration of the target contaminant. Also, it was found that in situ application of H(2)O(2) could have a gas-sparging effect on the dissolved VOC in groundwater, requiring careful attention to the remedial system design.

Hydrogen Peroxide↗
PubMed2001

Long-term investigation of atmospheric mercury contamination in Connecticut.

Atmospheric mercury was monitored from January 1997 through the end of December 1999 in eight sampling locations in Connecticut. Four sampling locations were chosen along the shores of Long Island Sound and four were chosen in interior sections of Connecticut. Sampling locations were chosen to represent both rural and urban sectors. Average concentrations of gaseous and particulate mercury were found to be 2.06 ng/m3 and 10.5 pg/m3, respectively. The weekly average wet deposition fluxes of mercury and methylmercury over the three-year sampling period were measured to be 611 and 11 microg/ha/week, respectively. Concentrations of gaseous, particulate and wet flux of mercury were found to be significantly higher in urban areas than the rural sampling locations. There was, however, no significant difference between the mean gaseous and particulate concentrations of mercury in coastal and inland sampling locations. No significant difference was observed either between the wet fluxes of total mercury in coastal and inland sampling locations and there was no spatial gradient for mercury concentration and deposition. The data of this study suggest that vehicular traffic and localized emission sources in urban areas play a significant role in determining the atmospheric concentration of mercury in Connecticut.

Air Pollutants↗
PubMed2001

The differential diagnosis of crystals in the retina.

Crystalline deposits in the retina may be associated with a wide variety of systemic disorders such as oxalosis, cystinosis, hyperornithinaemia and Sjögren-Larsson syndrome. Refractile crystalline deposits may also be a manifestation of drug toxicity like the antineoplastic agent tamoxifen, the anesthetic methoxyflurane and the oral tanning agent canthaxanthine. Crystals may also occur in drug abusers who inject multiple crushed tablets of methadone or meperidine intravenously (talc retinopathy). The differential diagnosis of retinal crystals also includes primary ocular diseases like Bietti's crystalline retinopathy, calcified macular drusen, idiopathic parafoveal telangiectasis and longstanding retinal detachment. This article will review the most common causes of crystalline retinopathies, their etiologies, pathologies and clinical characteristics.

Crystallization↗
PubMed2001

Estimation of wet, dry and bulk deposition of atmospheric nitrogen in Connecticut.

Atmospheric nitrogen species including NO3-, NH4+ and total nitrogen in air and precipitation samples were collected with low-volume filter packs and wet deposition collectors from March 1999 through the end of December 2000 in seven sampling locations in Connecticut. Three sampling locations were chosen along the shores of Long Island Sound and four were chosen in interior sections of Connecticut. Sampling sites were chosen to represent both rural and urban sectors. Wet deposition flux of nitrogen species was calculated using wet concentrations, the volume of collected precipitation and the opening surface area of the Aerochemetrics wet deposition collector. The dry deposition flux of nitrogen species was estimated with the application of the dry deposition inferential model (DDIM). Bulk deposition of nitrogen was collected with the aid of a device based on the Swedish IVL Sampler. The dry deposition fluxes of NO3-, NH4+ and total nitrogen were found to be significantly higher in urban areas than the rural sampling locations. There was, however, no significant difference between the wet deposition fluxes of different nitrogen species in rural and urban sampling locations. When inland and coastal sites were compared, the dry deposition fluxes of NH4+ and total nitrogen were significantly higher in inland locations and there was no significant difference between coastal and inland sampling locations for wet deposition fluxes of nitrogen species. No significant difference was observed between the bulk deposition and the sum of the wet and dry deposition fluxes of total nitrogen at rural sampling locations. In urban sampling locations, the bulk deposition flux of total nitrogen was significantly lower than the sum of dry and wet deposition fluxes. There appears to be a similar seasonal trend in wet and dry deposition fluxes of total nitrogen in Connecticut with high and low deposition fluxes occurring in summer and winter periods, respectively.

Air Pollutants↗
PubMed2000

The role of short-term synaptic dynamics in motor control.

During the past few years, much attention has been given to the role of short-term synaptic plasticity, in particular depression and facilitation, in sculpting network activity. A recent study shows that synaptic depression in rhythmic motor networks could switch the control of network frequency from intrinsic neuronal properties to the synaptic dynamics. Short-term synaptic plasticity is also involved in the stabilization and reconfiguration of motor circuits and in the initiation, maintenance and modulation of motor programs.

Animals↗
PubMed1999

Coordination of fast and slow rhythmic neuronal circuits.

Interactions among rhythmically active neuronal circuits that oscillate at different frequencies are important for generating complex behaviors, yet little is known about the underlying cellular mechanisms. We addressed this issue in the crab stomatogastric ganglion (STG), which contains two distinct but interacting circuits. These circuits generate the gastric mill rhythm (cycle period, approximately 10 sec) and the pyloric rhythm (cycle period, approximately 1 sec). When the identified modulatory projection neuron named modulatory commissural neuron 1 (MCN1) is activated, the gastric mill motor pattern is generated by interactions among MCN1 and two STG neurons [the lateral gastric (LG) neuron and interneuron 1]. We show that, during MCN1 stimulation, an identified synapse from the pyloric circuit onto the gastric mill circuit is pivotal for determining the gastric mill cycle period and the gastric-pyloric rhythm coordination. To examine the role of this intercircuit synapse, we replaced it with a computational equivalent via the dynamic-clamp technique. This enabled us to manipulate better the timing and strength of this synapse. We found this synapse to be necessary for production of the normal gastric mill cycle period. The synapse acts, during each LG neuron interburst, to boost rhythmically the influence of the modulatory input from MCN1 to LG and thereby to hasten LG neuron burst onset. The two rhythms become coordinated because LG burst onset occurs with a constant latency after the onset of the triggering pyloric input. These results indicate that intercircuit synapses can enable an oscillatory circuit to control the speed of a slower oscillatory circuit, as well as provide a mechanism for intercircuit coordination.

Animals↗
PubMed1999

Synaptic depression creates a switch that controls the frequency of an oscillatory circuit.

Synaptic depression is a form of short-term plasticity exhibited by many synapses. Nonetheless, the functional significance of synaptic depression in oscillatory networks is not well understood. We show that, in a recurrent inhibitory network that includes an intrinsic oscillator, synaptic depression can give rise to two distinct modes of network operation. When the maximal conductance of the depressing synapse is small, the oscillation period is determined by the oscillator component. Increasing the maximal conductance beyond a threshold value activates a positive-feedback mechanism that greatly enhances the synaptic strength. In this mode, the oscillation period is determined by the strength and dynamics of the depressing synapse. Because of the regenerative nature of the feedback mechanism, the circuit can be switched from one mode of operation to another by a very small change in the maximal conductance of the depressing synapse. Our model was inspired by experimental work on the pyloric network of the lobster. The pyloric network produces a simple motor rhythm generated by a pacemaker neuron that receives feedback inhibition from a depressing synapse. In some preparations, elimination of the synapse had no effect on the period of the rhythm, whereas in other preparations, there was a significant decrease in the period. We propose that the pyloric network can operate in either of the two modes suggested by the model, depending on the maximal conductance of the depressing synapse.

Action Potentials↗
PubMed1999

Network oscillations generated by balancing graded asymmetric reciprocal inhibition in passive neurons.

We describe a novel mechanism by which network oscillations can arise from reciprocal inhibitory connections between two entirely passive neurons. The model was inspired by the activation of the gastric mill rhythm in the crab stomatogastric ganglion by the modulatory commissural ganglion neuron 1 (MCN1), but it is studied here in general terms. One model neuron has a linear current-voltage (I-V) curve with a low (L) resting potential, and the second model neuron has a linear current-voltage curve with a high (H) resting potential. The inhibitory connections between them are graded. There is an extrinsic modulatory excitatory input to the L neuron, and the L neuron presynaptically inhibits the modulatory neuron. Activation of the extrinsic modulatory neuron elicits stable network oscillations in which the L and H neurons are active in alternation. The oscillations arise because the graded reciprocal synapses create the equivalent of a negative-slope conductance region in the I-V curves for the cells. Geometrical methods are used to analyze the properties of and the mechanism underlying these network oscillations.

Animals↗
PubMed1998

Frequency control of a slow oscillatory network by a fast rhythmic input: pyloric to gastric mill interactions in the crab stomatogastric nervous system.

The stomatogastic nervous system of the crab, Cancer borealis, produces a slow gastric mill rhythm and a fast pyloric rhythm. When the gastric mill rhythm is not active, stimulation of the modulatory commissural ganglion neuron 1 (MCN1) activates a gastric mill rhythm in which the lateral gastric (LG) neuron fires in antiphase with interneuron 1 (Int1). We present theoretical and experimental data that indicate that the period of the MCN1 activated gastric mill rhythm depends on the strength and time course of the MCN1 evoked slow excitatory synaptic potential (EPSP) in the LG neuron, and on the strength of inhibition of Int 1 by the pacemaker of the pyloric network. This work demonstrates a new mechanism by which a slow network oscillator can be controlled by a much faster oscillatory neuron or network and suggests that modulation of the slow oscillator can occur by direct action on the neurons and synapses of the slow oscillator, or indirectly by actions on the fast oscillator and its synaptic connection with the slow oscillator.

Animals↗
PubMed1998

Frequency regulation of a slow rhythm by a fast periodic input.

Many nervous systems contain rhythmically active subnetworks that interact despite oscillating at widely different frequencies. The stomatogastric nervous system of the crab Cancer borealis produces a rapid pyloric rhythm and a considerably slower gastric mill rhythm. We construct and analyze a conductance-based compartmental model to explore the activation of the gastric mill rhythm by the modulatory commissural neuron 1 (MCN1). This model demonstrates that the period of the MCN1-activated gastric mill rhythm, which was thought to be determined entirely by the interaction of neurons in the gastric mill network, can be strongly influenced by inhibitory synaptic input from the pacemaker neuron of the fast pyloric rhythm, the anterior burster (AB) neuron. Surprisingly, the change of the gastric mill period produced by the pyloric input to the gastric mill system can be many times larger than the period of the pyloric rhythm itself. This model illustrates several mechanisms by which a fast oscillatory neuron may control the frequency of a much slower oscillatory network. These findings suggest that it is possible to modify the slow rhythm either by direct modulation or indirectly by modulating the faster rhythm.

Action Potentials↗
PubMed1997

Temporal dynamics of graded synaptic transmission in the lobster stomatogastric ganglion.

Synaptic transmission between neurons in the stomatogastric ganglion of the lobster Panulirus interruptus is a graded function of membrane potential, with a threshold for transmitter release in the range of -50 to -60 mV. We studied the dynamics of graded transmission between the lateral pyloric (LP) neuron and the pyloric dilator (PD) neurons after blocking action potential-mediated transmission with 0.1 microM tetrodotoxin. We compared the graded IPSPs (gIPSPs) from LP to PD neurons evoked by square pulse presynaptic depolarizations with those potentials evoked by realistic presynaptic waveforms of variable frequency, amplitude, and duty cycle. The gIPSP shows frequency-dependent synaptic depression. The recovery from depression is slow, and as a result, the gIPSP is depressed at normal pyloric network frequencies. Changes in the duration of the presynaptic depolarization produce nonintuitive changes in the amplitude and time course of the postsynaptic responses, which are again frequency-dependent. Taken together, these data demonstrate that the measurements of synaptic efficacy that are used to understand neural network function are best made using presynaptic waveforms and patterns of activity that mimic those in the functional network.

Animals↗
PubMed1997

A slow outward current activated by FMRFamide in heart interneurons of the medicinal leech.

The endogenous neuropeptide FMRFamide (Phe-Met-Arg-Phe-NH2) can accelerate the oscillation of reciprocally inhibitory pairs of interneurons that pace heartbeat in the medicinal leech. A model based on all available biophysical data of a two-cell heart interneuron oscillator provides a theoretical basis for understanding this modulation. Previously observed modulation of K+ currents by FMRFamide cannot account for this acceleratory effect in the model. This observation prompted the present reexamination of K+ currents in heart interneurons. We devised better methods for separation of the various components of K+ current and more accurately measured their activation and deactivation kinetics. Moreover, we demonstrated that FMRFamide activates a previously undetected K+ current (IKF), which has very slow activation and deactivation kinetics. Addition of physiologically measured amounts of IKF to the model two-cell oscillator can account for the acceleratory effect of FMRFamide.

Animals↗
PubMed1996

Uniform growth and neuronal integration.

1. The cable equations were analyzed to determine the effects of two patterns of uniform growth on the passive and active integrative properties of neurons. 2. During uniform isoelectrotonic growth, the diameters of all neuronal processes increase as the square of their increase in length, while the specific electrical properties and branch terminal conditions of the neuron remain constant. An analytic inductive proof is given to show that, for any neuron, uniform isoelectrotonic growth increases the input conductance everywhere by the cube of the growth factor, but leaves the active and passive spread of membrane potential within the neuron unchanged. The spread of membrane voltage is unchanged because this pattern of growth enables both the axial and membrane currents everywhere in the cell to increase by the cube of the growth factor. Synaptic inputs would evoke the same responses in the isoelectrotonically larger cell as in the smaller cell if the total postsynaptic conductance of the synapse increased with the dendritic membrane area. 3. During uniform isometric growth, the diameter and lengths of all processes increase by the same factor, while the specific electrical properties and branch terminal conditions remain constant. This pattern of uniform growth increases the input conductance by the square of the growth factor, and also increases the attenuation, delay, and low-pass filtering of the cell's responses. Voltage attenuation increases with isometric growth because the axial current increases in proportion to growth, while the membrane current increases in proportion to the square of the growth factor. Isometric growth reduces the ability of distal synaptic inputs to affect the membrane potential at proximal integrating sites, even after the synaptic conductance has increased to compensate for the increased input conductance. 4. These two patterns of uniform growth help define the consequences of all types of uniform growth for neuronal integration and responsiveness.

Electrophysiology↗
PubMed1995

Heartbeat control in the medicinal leech: a model system for understanding the origin, coordination, and modulation of rhythmic motor patterns.

We have analyzed in detail the neuronal network that generates heartbeat in the leech. Reciprocally inhibitory pairs of heart interneurons form oscillators that pace the heartbeat rhythm. Other heart interneurons coordinate these oscillators. These coordinating interneurons, along with the oscillators interneurons, form an eight-cell timing oscillator network for heartbeat. Still other interneurons, along with the oscillator interneurons, inhibit heart motor neurons, sculpting their activity into rhythmic bursts. Critical switch interneurons interface between the oscillator interneurons and the other premotor interneurons to produce two alternating coordination states of the motor neurons. The periods of the oscillator interneurons are modulated by endogenous RFamide neuropeptides. We have explored the ionic currents and graded and spike-mediated synaptic transmission that promote oscillation in the oscillator interneurons and have incorporated these data into a conductance-based computer model. This model has been of considerable predictive value and has led to new insights into how reciprocally inhibitory neurons produce oscillation. We are now in a strong position to expand this model upward, to encompass the entire heartbeat network, horizontally, to elucidate the mechanisms of FMRFamide modulation, and downward, to incorporate cellular morphology. By studying the mechanisms of motor pattern formation in the leech, using modeling studies in conjunction with parallel physiological experiments, we can contribute to a deeper understanding of how rhythmic motor acts are generated, coordinated, modulated, and reconfigured at the level of networks, cells, ionic currents, and synapses.

Animals↗
PubMed1995

Modeling the leech heartbeat elemental oscillator. I. Interactions of intrinsic and synaptic currents.

We have developed a biophysical model of a pair of reciprocally inhibitory interneurons comprising an elemental heartbeat oscillator of the leech. We incorporate various intrinsic and synaptic ionic currents based on voltage-clamp data. Synaptic transmission between the interneurons consists of both a graded and a spike-mediated component. By using maximal conductances as parameters, we have constructed a canonical model whose activity appears close to the real neurons. Oscillations in the model arise from interactions between synaptic and intrinsic currents. The inhibitory synaptic currents hyperpolarize the cell, resulting in activation of a hyperpolarization-activated inward current Ih and the removal of inactivation from regenerative inward currents. These inward currents depolarize the cell to produce spiking and inhibit the opposite cell. Spike-mediated IPSPs in the inhibited neuron cause inactivation of low-threshold Ca++ currents that are responsible for generating the graded synaptic inhibition in the opposite cell. Thus, although the model cells can potentially generate large graded IPSPs, synaptic inhibition during canonical oscillations is dominated by the spike-mediated component.

Animals↗
PubMed1995

Modeling the leech heartbeat elemental oscillator. II. Exploring the parameter space.

In the previous paper, we described a model of the elemental heartbeat oscillator in the leech. Here, the parameters of our model are explored around the baseline canonical model. The maximal conductances of the currents and the reversal potential of the leak current are varied to reveal the effects of individual currents and the interaction between synaptic and intrinsic currents in the model. The model produces two distinct modes of oscillation as the parameters are varied, S-mode and G-mode. These two modes are defined, their origin is identified, and the parameter space is mapped into S-mode and G-mode oscillation and no oscillation. Finally, we will make predictions for how the period can be modulated in heart interneurons.

Animals↗