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S M Bawin

Publications and source records attributed to S M Bawin.

14 recordsLinked to original sources
PubMed1996

Extremely-low-frequency magnetic fields disrupt rhythmic slow activity in rat hippocampal slices.

Several studies have indicated that weak, extremely-low-frequency (ELF; 1-100 Hz) magnetic fields affect brain electrical activity and memory processes in man and laboratory animals. Our studies sought to determine whether ELF magnetic fields could couple directly with brain tissue and affect neuronal activity in vitro. We used rat hippocampal slices to study field effects on a specific brain activity known as rhythmic slow activity (RSA), or theta rhythm, which occurs in 7-15 s bursts in the hippocampus during memory functions. RSA, which, in vivo, is a cholinergic activity, is induced in hippocampal slices by perfusion of the tissue with carbachol, a stable analog of acetylcholine. We previously demonstrated that the free radical nitric oxide (NO), synthesized in carbachol-treated hippocampal slices, lengthened and destabilized the intervals between successive RSA episodes. Here, we investigate the possibility that sinusoidal ELF magnetic fields could trigger the NO-dependent perturbation of the rate of occurrence of the RSA episodes. Carbachol-treated slices were exposed for 10 min epochs to 1 or 60 Hz magnetic fields with field intensities of 5.6, 56, or 560 microT (rms), or they were sham exposed. All exposures took place in the presence of an ambient DC field of 45 microT, with an angle of -66 degrees from the horizontal plane. Sinusoidal 1 Hz fields at 56 and 560 microT, but not at 5.6 microT, triggered the irreversible destabilization of RSA intervals. Fields at 60 Hz resulted in similar, but not statistically significant, trends. Fields had no effects on RSA when NO synthesis was pharmacologically inhibited. However, field effects could take place when extracellular NO, diffusing from its cell of origin to the extracellular space,was chelated by hemoglobin. These results suggest that ELF magnetic fields exert a strong influence on NO systems in the brain; therefore, they could modulate the functional state of a variety of neuronal ensembles.

Animals↗
PubMed1994

Nitric oxide modulates rhythmic slow activity in rat hippocampal slices.

We investigated the role of nitric oxide (NO) in controlling the rate of occurrence of muscarinic rhythmic slow activity (RSA) episodes induced by carbachol in rat hippocampal slices. Typically, a series of several short intervals (< 40 s) between RSA episodes alternated with one or two longer intervals. Treatments with inhibitors of NO synthesis (NG-nitro- or NG-methyl-L-arginine) or with hemoglobin shortened and stabilized all intervals. By contrast, applications of an NO donor (sodium nitroprusside) or membrane permeant cGMP analogs (8-bromo-cGMP or dibutyryl-cGMP) during blockade of NO synthesis lengthened and destabilized the intervals. The importance of cholinergic mechanisms in learning and memory is well known and our findings suggest that NO could influence synaptic plasticity by modulating the occurrence of a muscarinic component of hippocampal RSA.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1993

Roles of the NMDA and quisqualate/kainate receptors in the induction and expression of kindled bursts in rat hippocampal slices.

We used combinations of NMDA and quisqualate/kainate (Q/K) receptor antagonists and low Mg2+ (0.1 mM) solutions to study the respective roles of these receptors during in vitro kindling of interictal bursts in the CA3 area of rat hippocampal slices. Intracellular and extracellular recordings in CA3 showed that Q/K receptors were not necessary for the induction of kindling once the Mg2+ block of NMDA was alleviated, but that the expression of bursts kindled via NMDA-driven mechanisms was Q/K-dependent.

Animals↗
PubMed1991

Transition from normal to epileptiform activity in kindled rat hippocampal slices.

We previously demonstrated kindling of synchronized bursts (ISs) by repeated sine-wave stimulation (SW: 2-5 sec, 60 Hz, 20-50 microA, every 5 min) in the CA2/3 area of rat hippocampal slices. Here we report the behavior of individual CA2/3 neurons during the kindling procedure. Intra- and extracellular recordings were obtained concurrently before, during and following SW. Test pulses and SWs were applied in CA2/3 or CA1 stratum radiatum. Neuronal response to to intracellular stimulation was tested by 100 msec depolarizing dc pulses or by 2-20 sec sinusoidal currents. The role of the N-methyl-D-aspartate (NMDA) receptor in the transition from normal responses to ISs was assessed by perfusing the slices with a specific antogonist (DL-2-amino-5-phosphono-valeric acid, APV, 50-200 microM). Our results show that kindling of ISs occurred in two steps: (1) via NMDA-dependent depolarizations during SW, or during SW-induced afterdischarges, and (2) through the recruitment of secondary, late EPSPs (1EPSPs), between consecutive SWs. ISs developed from the 1EPSPs, while the early responses (action potentials, EPSPs, and population spikes) remained unchanged. Kindling of ISs occurred with no changes in resting membrane potential, membrane resistance, or threshold of action potentials. APV did not block kindled ISs, but considerably reduced their amplitude and duration, and increased their frequency. These latter findings suggest that APV-insensitive mechanisms, activated through NMDA-dependent processes, were responsible for the triggering of ISs, and that NMDA receptor systems participated in the control of their rate of occurrence.

2-Amino-5-phosphonovalerate↗
PubMed1986

Long-term effects of sinusoidal extracellular electric fields in penicillin-treated rat hippocampal slices.

Rat hippocampal slices in 0, 0.25, 1.5 or 3 mM penicillin were exposed briefly to extracellular sinusoidal electric fields (20 s, 5 and 60 Hz, 20-40 mV/cm in tissue). Fields induced long-term (min) changes in population spike amplitudes in the CA1 cell layer. Post-field effects included both depression of strongly epileptiform responses and potentiation of weakly epileptiform and normal responses. Endogenous extracellular fields may participate in the dynamic regulation of the course of seizures.

Animals↗
PubMed1986

Comparison between the effects of extracellular direct and sinusoidal currents on excitability in hippocampal slices.

The amplitude of population spikes in the CA1 cell layer of rat hippocampal slices was transiently altered during stimulation of the tissue with DC and sinusoidal extracellular electric fields parallel to the dendrosomatic axis of the CA1 pyramidal neurons. Field threshold was about 50 mV/cm in the tissue. Independently, long-lasting (min) increases in population spike amplitude followed sinusoidal fields as low as 7 mV/cm parallel or perpendicular to the cell axis.

Animals↗
PubMed1984

Influences of sinusoidal electric fields on excitability in the rat hippocampal slice.

The influence of extracellular sinusoidal electric fields on the amplitude of population spikes evoked by single test pulses in excitatory pathways to CA1 pyramidal neurons was studied in rat hippocampal slices. The fields in the tissue were of the order of EEG gradients. Stimulation at 5 Hz, a frequency representative of hippocampal theta activity, was compared with 60 Hz, which is often used in kindling procedures. Brief stimulation (5-30 s) with both 5 and 60 Hz fields (20-70 mV/cmp-p in the perfusing solution) often produced a long-term increase (longer than 10 min) of the population spike. Fields at 60 Hz, but not at 5 Hz, also induced short-term depression (1-6 min) or transient post-field excitation (15-30 s). Prolonged stimulation (3 min) emphasized this frequency dependent response: fields at 5 Hz induced long-lasting potentiation while fields at 60 Hz always resulted in progressive depression persisting for a few minutes after the end of stimulation. These effects appeared as a global response of CA1 neurons. Antidromic responses studied during blockade of synaptic transmission (0.2 mM Ca2+, 4 mM Mg2+) were depressed during and following 3 min field stimulation at either frequency, which could reflect failing calcium mechanisms in the tissue. The field influence on the potential evoked by synaptic or antidromic stimulation was independent of the phase of the sine wave at which the test pulse was delivered, arguing against a direct polarization of the cell membrane by the fields. The experimental evidence suggests a functional role for EEG-like fields in hippocampal excitability.

Animals↗
PubMed1982

Effects of weak amplitude-modulated microwave fields on calcium efflux from awake cat cerebral cortex.

Calcium (45Ca2+) efflux was studied from preloaded cortex in cats immobilized under local anesthesia, and exposed to a 3.0-mW/cm2 450-MHz field, sinusoidally amplitude modulated at 16 Hz modulation depth 85%). Tissue dosimetry showed a field of 33 V/m in the interhemispheric fissure (rate of energy deposition 0.29 W/kg). Field exposure lasted 60 min. By comparison with controls, efflux curves from field exposed brains were disrupted by waves of increased 45Ca2+ efflux. These waves were irregular in amplitude and duration, but many exhibited periods of 20-30 min. They continued into the postexposure period. Binomial probability analysis indicates that the field-exposed efflux curves constitute a different population from controls at a confidence level of 0.96. In about 70% of cases, initiation of field exposure was followed by increased end-tidal CO2 excretion for about 5 min. However, hypercapnea induced by hypoventilation did not elicit increased 45Ca2+ efflux. Thus this increase with exposure does not appear to arise as a secondary effect of raised cerebral CO2 levels. Radioactivity measurements in cortical samples after superfusion showed 45Ca2+ penetration at about 1.7 mm/hr, consistent with diffusion of the ion in free solution.

Animals↗
PubMed1978

Ionic factors in release of 45Ca2+ from chicken cerebral tissue by electromagnetic fields.

Electrical stimulation with radiofrequency fields amplitude-modulated at brain wave frequencies increased 45Ca2+ efflux from isolated chicken cerebral tissue. The response was not sensitive to variations of the calcium concentration (0-4.16 mM) in the bathing solution but was enhanced by addition of H+ (0.108 mM HCl) and inhibited in the absence of normal bicarbonate levels (2.4 mM). Addition of lanthanum to the bicarbonate-free solution restored electrical responsiveness, but the stimulus decreased instead of increasing 45Ca2+ efflux. It is suggested that low-frequency, weak, extracellular electric gradients may be transduced in a specific class of extracellular negative binding sites normally occupied by Ca2+ and susceptible to competitive H+ binding.

Animals↗
PubMed1976

Sensitivity of calcium binding in cerebral tissue to weak environmental electric fields oscillating at low frequency.

Weak sinusoidal electric fields modify the calcium efflux from freshly isolated chick and cat cerebral tissues bathed in Ringer's solution, at 36 degrees. Following incubation (30 min) with radioactive calcium (45Ca2+), each sample, immersed in fresh solution, was exposed for 20 min to fields at 1, 6, 16, 32, or 75 Hz, with electric gradients of 5, 10, 56, and 100 V/m in air. 45Ca2+ efflux in the solution was then measured in 0.2 ml aliquots and compared with efflux from unexposed control samples. Field exposures resulted in a general trend toward a reduction in the release of the preincubated 45Ca2+. Both frequency and amplitude sensitivities were observed. Maximum decreases occurred at 6 and 16 Hz (12-15%). Thresholds were around 10 and 56 V/m for chick and cat tissues, respectively. Similar but nonsignificant trends occurred during other field exposures. All results were statistically compared with matched samples of controls. Tissue gradients could not be measured, but estimates were of the order of 0.1 muV/cm. The susceptibility of the electrochemical equilibrium in the neuronal membrane to small extracellular perturbations is discussed and a possible role for weak intrinsic cerebral fields in neuronal excitability is suggested.

Animals↗
PubMedDate not supplied

Induction of delayed synchronized bursts in hippocampal slices by weak sine-wave stimulation; role of the NMDA receptor.

Weak (20-50 microA) sine-wave stimulation at 60 Hz (SWS) of either the mossy fibers or the Schaffer collaterals promoted epileptiform synchronized bursts in the CA2/3 area of rat hippocampal slices in the absence of epileptogenic agents. Following brief SWSs (2-10 sec every 5 min), delayed synchronized bursts (DSBs) were triggered by weak test pulses in either pathway and transmitted to CA1. The long (2-10 sec) refractory periods which followed synchronized bursts in CA2/3 limited their rate of occurrence. Furthermore, SWS decreased the activity for several minutes in slices that exhibited frequent bursts. DSBs were reversibly blocked by perfusion with the N-methyl-D-aspartate (NMDA) specific antagonist DL-2-amino-5-phosphono-valeric acid (APV). The involvement of NMDA receptors was further suggested by the facilitation of CA2/3 synchronized bursts in medium with NMDA (5 microM) or lacking magnesium, and by iontophoresis of NMDA in the CA2/3 stratum radiatum. The findings that SWS-induced DSBs persisted for hours in undisturbed slices, and that bursts abolished by APV reappeared during washout in control solution, suggest long-term changes in the CA2/3 synaptic region.

2-Amino-5-phosphonovalerate↗