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J D Jirsch

Publications and source records attributed to J D Jirsch.

3 recordsLinked to original sources

High-frequency oscillations during human focal seizures.

Discrete high-frequency oscillations (HFOs) in the range of 100-500 Hz have previously been recorded in human epileptic brains using depth microelectrodes. We describe for the first time similar oscillations in a cohort of unselected focal epileptic patients implanted with EEG macroelectrodes. Spectral analysis and visual inspection techniques were used to study seizures from 10 consecutive patients undergoing pre-surgical evaluation for medically refractory focal epilepsy. Four of these patients had focal seizure onset in the mesial temporal lobe, and in all 12 of their seizures, well-localized, segmental, very high frequency band (VHF: 250-500 Hz) oscillations were visually identified near the time of seizure onset from contacts in this zone. Increased high-frequency band (HF: 100-200 Hz) activity compared with the background was distinguished both visually and with spectral analysis later in the seizures of 3/4 mesial temporal patients, involving contacts in the generator region and, in one patient, areas of contralateral peri-hippocampal propagation. Three patients with well-defined neocortical seizure-onset areas also demonstrated focal HF or VHF oscillations confined to the seizure-onset channels during their eight seizures. No discrete HF or VHF activity was present in the poorly localized seizures from the remaining three patients. These results show that discrete HFOs can be recorded from human focal epileptic brain using depth macroelectrodes, and that they occur mostly in regions of primary epileptogenesis and rarely in regions of secondary spread. Absent high-frequency activity seems to indicate poor localization, whereas the presence of focal HFOs near the time of seizure onset may signify proximity to the epileptogenic focus in mesial temporal lobe and neocortical seizures. We postulate that focal HFOs recorded with depth macroelectrodes reflect the partial synchronization of very local oscillations such as those previously studied using microelectrodes, and result from interconnected small neuronal ensembles. Our finding that localized HFOs occur in varying anatomical structures and pathological conditions perhaps indicates commonality to diverse epileptogenic aetiologies.

Adult↗

Cation regulation of anion current activated by cell swelling in two types of human epithelial cancer cells.

1. In epithelial cells, hyposmotic stress induces visible cell swelling and large Cl- currents, which deactivate on return to isotonic solutions and are abolished by 0.1-0.5 mM DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid). During depolarizing voltage clamp pulses, the currents activate rapidly and show time-dependent relaxation with associated tail currents on return to negative potentials. 2. We used whole-cell and outside-out patch recording to study volume activation of Cl- currents in the epithelial cancer cell lines H69AR and HeLa S5. In a 210 or 160 mosmol l-1 hyposmotic bathing solution containing 90 mM NaCl, 1 mM Ca2+ and 1 mM Mg2+, current relaxation was rapid, occurred positive to the Cl- reversal potential and reduced current to < 30% of its peak level at +100 mV. 3. Replacement of most bath inorganic cations by N-methyl-D-glucamine (NMDG) at constant Cl- concentration and osmolarity eliminated most of the current relaxation and caused an increase in steady-state current levels. Steady-state current was 85 +/- 6% of peak current at +100 mV in NMDG-Cl bath solution. This ratio fell to 55 +/- 2% (n = 5) when 1 mM Mg2+ was re-added to the bath. 4. Re-addition of Mg2+ or other Group II metals (Ca2+, Sr2+, Ba2+) induced immediate changes in current relaxation in a dose- and species-dependent manner. Concentrations of Mg2+ as low as 0.1 mM were effective in causing Cl- current relaxation. The IC50 for steady-state current block by external Mg2+ was 1.75 mM.(ABSTRACT TRUNCATED AT 250 WORDS)

Anions↗

ATP is not required for anion current activated by cell swelling in multidrug-resistant lung cancer cells.

During whole cell recording with 4 mM ATP and 0.1 mM GTP in the pipette, outwardly rectifying Cl- currents (155 +/- 20.5 pA/pF) were repetitively activated on reduction of bath solution osmolarity from 290 mosM (control) to 210 mosM. These currents were sensitive to 0.1-1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. Omission of ATP from the pipette solution reduced the current magnitude to 42.7 +/- 9.5 pA/pF and prevented repetitive activation. More hyposmotic solutions (160 mosM) usually elicited current repetitively despite an ATP-free pipette solution. In cells depleted of ATP (to < 5% of control) by preincubation with 2-deoxyglucose (10 mM) and rotenone (100 nM), hyposmotic solutions failed to activate significant current. Cell volume increased to 230 +/- 18% of control (19.1 +/- 1.2 microns) in 210 mosM bath (normal cells) but only to 114 +/- 13% of control in ATP-depleted cells exposed to 160 mosM solution. This failure of ATP-depleted cells to swell in hypotonic external solutions was reversed by overnight pretreatment with cytochalasin D (2 micrograms/ml; n = 6) but not by colchicine (250 microM; n = 8). In outside-out patches of membrane dialyzed with zero ATP and excised from swollen cells, we observed sustained activation of a 53-pS outwardly rectifying channel (chord conductance, +100 mV; open probability approximately 1.0). In cell-attached patches from normal and ATP-depleted cells, we activated similar channels by suction. ATP does not appear to be an absolute requirement for the activation of this Cl- channel in H69AR cells but may be essential for the normal volume response and channel activation mediated through cytoskeletal elements within cells.

Adenosine Triphosphate↗